50 results on '"Harjola, Veli-Pekka"'
Search Results
2. miR‐619‐5p and cardiogenic shock in patients with ST‐segment elevation myocardial infarction.
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Escate, Rafael, Padró, Teresa, Suades, Rosa, Sans‐Roselló, Jordi, Devaux, Yvan, Lakkisto, Päivi, Harjola, Veli‐Pekka, Sionis, Alessandro, and Badimon, Lina
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ST elevation myocardial infarction ,CARDIOGENIC shock ,DISEASE risk factors - Abstract
Background: Cardiogenic shock (CS) is a severe myocardial dysfunction secondary to various cardiac conditions including ST‐segment elevation acute myocardial infarction (STEMI) and associated with a high risk of death. Little is known on epigenetic determinants in CS. Here, we investigated plasma miRNAs in relation to CS stratification in STEMI‐patients. Methods: STEMI‐patients (n = 49), with (CS, n = 25) and without CS (non‐CS, n = 24) fulfilling inclusion criteria were included from HSCSP‐cohort (Derivation‐cohort). CS‐miRNAs were analysed by Affymetrix‐microarray and RT‐PCR. Results were validated in a second cohort of CS‐patients (CardShock: n = 35) with similar inclusion/exclusion criteria as the derivation cohort. In silico analysis were performed to identify potential miRNA target genes. Results: Of the 5‐miRNA signature obtained from microarray analysis, miR‐619‐5p showed higher levels in CS than in Non‐CS patients (p =.003) and discriminating power for CS by ROC (AUC:.752, p =.003). miR‐619‐5p directly associated with risk scores [GRACE, p =.001; CardShock, p <.001]. Furthermore, miR‐619‐5p showed discrimination power for death in CS. Thus, miRNA levels were significantly higher in patients with mortality outcome both in the Derivation HSCSP‐cohort (p =.02; AUC:.78 ±.095) and the Validation CardShock‐cohort (p =.017; AUC:.737 ±.086) By in silico analysis, miR‐619‐5p target genes and TNF‐alpha were involved in the regulation of inflammation. miR‐619‐5p and TNF‐alpha levels discriminated mortality outcome in CS‐patients during 30‐day follow‐up (Validation‐Cohort: ROC:.812, p =.002; HR: 9.99, p =.003). Conclusions: Up‐regulation of miR‐619‐5p is found in the plasma of STEMI‐patients with CS and mortality outcome. These findings highlight the specificity of epigenetic regulation of inflammation on the disease severity of MI. [ABSTRACT FROM AUTHOR]
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- 2024
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3. Acute Heart Failure
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Harjola, Veli-Pekka, Bueno, Héctor, Parissis, John T., Dorobanţu, Maria, editor, Ruschitzka, Frank, editor, and Metra, Marco, editor
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- 2016
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4. Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients
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Léopold, Valentine, Gayat, Etienne, Pirracchio, Romain, Spinar, Jindrich, Parenica, Jiri, Tarvasmäki, Tuukka, Lassus, Johan, Harjola, Veli-Pekka, Champion, Sébastien, Zannad, Faiez, Valente, Serafina, Urban, Philip, Chua, Horng-Ruey, Bellomo, Rinaldo, Popovic, Batric, Ouweneel, Dagmar M., Henriques, José P. S., Simonis, Gregor, Lévy, Bruno, Kimmoun, Antoine, Gaudard, Philippe, Basir, Mir Babar, Markota, Andrej, Adler, Christoph, Reuter, Hannes, Mebazaa, Alexandre, and Chouihed, Tahar
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- 2018
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5. Management of cardiogenic shock complicating myocardial infarction
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Mebazaa, Alexandre, Combes, Alain, van Diepen, Sean, Hollinger, Alexa, Katz, Jaon N., Landoni, Giovanni, Hajjar, Ludhmila Abrahao, Lassus, Johan, Lebreton, Guillaume, Montalescot, Gilles, Park, Jin Joo, Price, Susanna, Sionis, Alessandro, Yannopolos, Demetris, Harjola, Veli-Pekka, Levy, Bruno, and Thiele, Holger
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- 2018
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6. Adrenomedullin: a marker of impaired hemodynamics, organ dysfunction, and poor prognosis in cardiogenic shock
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Tolppanen, Heli, Rivas-Lasarte, Mercedes, Lassus, Johan, Sans-Roselló, Jordi, Hartmann, Oliver, Lindholm, Matias, Arrigo, Mattia, Tarvasmäki, Tuukka, Köber, Lars, Thiele, Holger, Pulkki, Kari, Spinar, Jindrich, Parissis, John, Banaszewski, Marek, Silva-Cardoso, Jose, Carubelli, Valentina, Sionis, Alessandro, Harjola, Veli-Pekka, and Mebazaa, Alexandre
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- 2017
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7. Acute heart failure and valvular heart disease: A scientific statement of the Heart Failure Association, the Association for Acute CardioVascular Care and the European Association of Percutaneous Cardiovascular Interventions of the European Society of Cardiology
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Chioncel, Ovidiu, Adamo, Marianna, Nikolaou, Maria, Parissis, John, Mebazaa, Alexandre, Yilmaz, Mehmet Birhan, Hassager, Christian, Moura, Brenda, Bauersachs, Johann, Harjola, Veli‐Pekka, Antohi, Elena‐Laura, Ben‐Gal, Tuvia, Collins, Sean P., Iliescu, Vlad Anton, Abdelhamid, Magdy, Čelutkienė, Jelena, Adamopoulos, Stamatis, Lund, Lars H., Cicoira, Mariantonietta, and Masip, Josep
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HEART valve diseases ,HEART failure ,CARDIOGENIC shock ,CARDIOLOGY ,SYMPTOMS ,RANDOMIZED controlled trials - Abstract
Acute heart failure (AHF) represents a broad spectrum of disease states, resulting from the interaction between an acute precipitant and a patient's underlying cardiac substrate and comorbidities. Valvular heart disease (VHD) is frequently associated with AHF. AHF may result from several precipitants that add an acute haemodynamic stress superimposed on a chronic valvular lesion or may occur as a consequence of a new significant valvular lesion. Regardless of the mechanism, clinical presentation may vary from acute decompensated heart failure to cardiogenic shock. Assessing the severity of VHD as well as the correlation between VHD severity and symptoms may be difficult in patients with AHF because of the rapid variation in loading conditions, concomitant destabilization of the associated comorbidities and the presence of combined valvular lesions. Evidence‐based interventions targeting VHD in settings of AHF have yet to be identified, as patients with severe VHD are often excluded from randomized trials in AHF, so results from these trials do not generalize to those with VHD. Furthermore, there are not rigorously conducted randomized controlled trials in the setting of VHD and AHF, most of the data coming from observational studies. Thus, distinct to chronic settings, current guidelines are very elusive when patients with severe VHD present with AHF, and a clear‐cut strategy could not be yet defined. Given the paucity of evidence in this subset of AHF patients, the aim of this scientific statement is to describe the epidemiology, pathophysiology, and overall treatment approach for patients with VHD who present with AHF. [ABSTRACT FROM AUTHOR]
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- 2023
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8. Soluble urokinase-type plasminogen activator receptor improves early risk stratification in cardiogenic shock
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Hongisto, Mari, Lassus, Johan, Tarvasmäki, Tuukka, Sans-Roselló, Jordi, Tolppanen, Heli, Kataja, Anu, Jäntti, Toni, Sabell, Tuija, Banaszewski, Marek, Silva-Cardoso, Jose, Parissis, John, Jurkko, Raija, Spinar, Jindrich, Castrén, Maaret, Mebazaa, Alexandre, Masip, Josep, Harjola, Veli-Pekka, Universitat Autònoma de Barcelona, HUS Emergency Medicine and Services, Department of Diagnostics and Therapeutics, University of Helsinki, HUS Heart and Lung Center, Department of Medicine, Kardiologian yksikkö, and Clinicum
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Supar ,MYOCARDIAL-INFARCTION ,PREDICTION ,MORTALITY ,Biomarker ,General Medicine ,3126 Surgery, anesthesiology, intensive care, radiology ,Cardiology and Cardiovascular Medicine ,Critical Care and Intensive Care Medicine ,Cardiogenic shock ,Risk stratification ,suPAR - Abstract
Aims Soluble urokinase–type plasminogen activator receptor (suPAR) is a biomarker reflecting the level of immune activation. It has been shown to have prognostic value in acute coronary syndrome and heart failure as well as in critical illness. Considering the complex pathophysiology of cardiogenic shock (CS), we hypothesized suPAR might have prognostic properties in CS as well. The aim of this study was to assess the kinetics and prognostic utility of suPAR in CS. Methods and results SuPAR levels were determined in serial plasma samples (0–96 h) from 161 CS patients in the prospective, observational, multicentre CardShock study. Kinetics of suPAR, its association with 90-day mortality, and additional value in risk-stratification were investigated. The median suPAR-level at baseline was 4.4 [interquartile range (IQR) 3.2–6.6)] ng/mL. SuPAR levels above median were associated with underlying comorbidities, biomarkers reflecting renal and cardiac dysfunction, and higher 90-day mortality (49% vs. 31%; P = 0.02). Serial measurements showed that survivors had significantly lower suPAR levels at all time points compared with nonsurvivors. For risk stratification, suPAR at 12 h (suPAR12h) with a cut-off of 4.4 ng/mL was strongly associated with mortality independently of established risk factors in CS: OR 5.6 (95% CI 2.0–15.5); P = 0.001) for death by 90 days. Adding suPAR12h > 4.4 ng/mL to the CardShock risk score improved discrimination identifying high-risk patients originally categorized in the intermediate-risk category. Conclusion SuPAR associates with mortality and improves risk stratification independently of other previously known risk factors in CS patients.
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- 2022
9. Soluble triggering receptor expressed on myeloid cells-1 is a marker of organ injuries in cardiogenic shock: results from the CardShock Study
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GREAT-Network, CardShock Investigators, Kimmoun, Antoine, Duarte, Kevin, Harjola, Veli-Pekka, Tarvasmäki, Tuukka, Lassus, Johan, Jurkko, Raija, Tolppanen, Heli, Nieminen, Markku S., Järvinen, Kristiina, Nieminen, Tuomo, Pulkki, Kari, Soininen, Leena, Sund, Reijo, Tierala, Ilkka, Tolonen, Jukka, Varpula, Marjut, BOZEC, Erwan, Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Service de Réanimation Médicale [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Cardiovascular and Renal Clinical Trialists [Vandoeuvre-les-Nancy] (INI-CRCT), Institut Lorrain du Coeur et des Vaisseaux Louis Mathieu [Nancy], French-Clinical Research Infrastructure Network - F-CRIN [Paris] (Cardiovascular & Renal Clinical Trialists - CRCT ), Marqueurs cardiovasculaires en situation de stress (MASCOT (UMR_S_942 / U942)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Centre d'investigation clinique plurithématique Pierre Drouin [Nancy] (CIC-P), Centre d'investigation clinique [Nancy] (CIC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Helsingin yliopisto = Helsingfors universitet = University of Helsinki, Helsinki University Hospital [Finland] (HUS), Hôpital Lariboisière-Fernand-Widal [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), The CardShock study was supported by grants from Aarne Koskelo Foundation, the Finnish Cardiac Foundation, and the Finnish State funding for university-level health research., CardShock Investigators and the GREAT network: Katerina Koniari, Astrinos Voumvourakis, Apostolos Karavidas, John Parissis, Jordi Sans-Rosello, Montserrat Vila, Albert Duran-Cambra, Alessandro Sionis, Jiri Parenica, Roman Stipal, Ondrej Ludka, Marie Palsuva, Eva Ganovska, Petr Kubena, Jindrich Spinar, Matias G Lindholm, Christian Hassager, Lars Køber, Tom Bäcklund, Johan Lassus, Raija Jurkko, Heli Tolppanen, Markku S Nieminen, Kristiina Järvinen, Tuomo Nieminen, Kari Pulkki, Leena Soininen, Reijo Sund, Ilkka Tierala, Jukka Tolonen, Marjut Varpula, Tuomas Korva, Mervi Pietilä, Anne Pitkälä, Rossella Marino, Salvatore Di Somma, Marco Metra, Michela Bulgari, Valentina Lazzarini, Valentina Carubelli, Alexandra Sousa, Jose Silva-Cardoso, Carla Sousa, Mariana Paiva, Inês Rangel, Rui Almeida, Teresa Pinho, Maria Júlia Maciel, Marek Banaszewski, Janina Stepinska, Anna Skrobisz, Piotr Góral, Uwe Zeymer, Holger Thiele, HUS Emergency Medicine and Services, Department of Diagnostics and Therapeutics, Helsinki University Hospital Area, University of Helsinki, HUS Heart and Lung Center, Clinicum, Kardiologian yksikkö, HUS Internal Medicine and Rehabilitation, Department of Medicine, Päijät-Häme Welfare Consortium, Department of Clinical Chemistry and Hematology, HUSLAB, and Department of Social Research (2010-2017)
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Inotrope ,medicine.medical_specialty ,Myeloid ,Shock, Cardiogenic ,Renal function ,Hemodynamics ,Inflammation ,PHARMACOLOGICAL INHIBITION ,030204 cardiovascular system & hematology ,03 medical and health sciences ,LIMITS ,0302 clinical medicine ,INFLAMMATION ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,medicine ,Humans ,Prospective Studies ,030212 general & internal medicine ,Myocardial infarction ,Outcome ,Cardiogenic Shock ,business.industry ,Cardiogenic shock ,General Medicine ,medicine.disease ,Triggering Receptor Expressed on Myeloid Cells-1 ,[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Blood pressure ,medicine.anatomical_structure ,3121 General medicine, internal medicine and other clinical medicine ,Cardiology ,STREM ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,Biomarkers - Abstract
Aims Optimal outcome after cardiogenic shock (CS) depends on a coordinated healing response in which both debris removal and extracellular matrix tissue repair play a crucial role. Excessive inflammation can perpetuate a vicious circle, positioning leucocytes as central protagonists and potential therapeutic targets. High levels of circulating Triggering Receptor Expressed on Myeloid cells-1 (TREM-1), were associated with death in acute myocardial infarction confirming excessive inflammation as determinant of bad outcome. The present study aims to describe the association of soluble TREM-1 with 90-day mortality and with various organ injuries in patients with CS. Methods and results This is a post-hoc study of CardShock, a prospective, multicenter study assessing the clinical presentation and management in patients with CS. At the time of this study, 87 patients had available plasma samples at either baseline, and/or 48 h and/or 96-120 h for soluble TREM-1 (sTREM-1) measurements. Plasma concentration of sTREM-1 was higher in 90-day non-survivors than survivors at baseline [median: 1392 IQR: (724-2128) vs. 621 (525-1233) pg/mL, p = 0.008), 48 h (p = 0.019) and 96-120 h (p = 0.029). The highest tertile of sTREM-1 at baseline (threshold: 1347 pg/mL) was associated with 90-day mortality with an unadjusted HR 3.08 CI 95% (1.48-6.42). sTREM-1 at baseline was not associated to hemodynamic parameters (heart rate, blood pressure, use of vasopressors or inotropes) but rather with organ injury markers: renal (estimated glomerular filtration rate, p = 0.0002), endothelial (bio-adrenomedullin, p = 0.018), myocardial (Suppression of Tumourigenicity 2, p = 0.002) or hepatic (bilirubin, p = 0.008). Conclusion In CS patients TREM-1 pathway is highly activated and gives an early prediction of vital organ injuries and outcome. [GRAPHICS] .
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- 2022
10. Prognostic impact of angiographic findings, procedural success, and timing of percutaneous coronary intervention in cardiogenic shock
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Sabell, Tuija, Banaszewski, Marek, Lassus, Johan, Nieminen, Markku S., Tolppanen, Heli, Jäntti, Toni, Kataja, Anu, Hongisto, Mari, Køber, Lars, Sionis, Alessandro, Parissis, John, Tarvasmäki, Tuukka, Harjola, Veli-Pekka, Jurkko, Raija, Universitat Autònoma de Barcelona, HUS Heart and Lung Center, Department of Medicine, Helsinki University Hospital Area, University of Helsinki, Kardiologian yksikkö, Clinicum, HUS Emergency Medicine and Services, and Department of Diagnostics and Therapeutics
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Male ,medicine.medical_specialty ,Acute coronary syndrome ,OCCLUSION ,medicine.medical_treatment ,Short Communication ,Short Communications ,Shock, Cardiogenic ,030204 cardiovascular system & hematology ,Revascularization ,Coronary Angiography ,Percutaneous coronary intervention ,03 medical and health sciences ,0302 clinical medicine ,TERM MORTALITY ,Internal medicine ,Medicine ,Diseases of the circulatory (Cardiovascular) system ,Humans ,030212 general & internal medicine ,Myocardial infarction ,cardiovascular diseases ,PREDICTORS ,Cardiogenic shock ,ARTERY ,Aged ,business.industry ,ELEVATION MYOCARDIAL-INFARCTION ,PCI ,Thrombolysis ,Middle Aged ,medicine.disease ,Prognosis ,3. Good health ,3121 General medicine, internal medicine and other clinical medicine ,RC666-701 ,Conventional PCI ,Cardiology ,Female ,Cardiology and Cardiovascular Medicine ,business ,TIMI - Abstract
Altres ajuts: This study was supported by grants from the Finnish Foundation for Cardiovascular Research, and Aarne Koskelo Foundation, Helsinki, Finland. Roche Diagnostics provided kits for the analysis of NT-proBNP and TnT. The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication. Tuija Sabell (néeJavanainen) received following personal research grants: Acute Coronary Syndromes and secondary prevention grant from the Finnish Cardiac Society, grant supported by Astra Zeneca and grants from Paavo Nurmi Foundation and Paavo Ilmari Ahvenaisen säätiö. Dr Lassus has served on an advisory board for Boehringer Ingelheim, Medix Biochemica, Novartis, Servier, and Vifor Pharma and received lecture fees from Bayer, Boehringer Ingelheim, Pfizer, Novartis, Orion Pharma, and Vifor Pharma. Dr Parissis has received honoraria from Novartis and Orion Pharma. Urgent revascularization is the mainstay of treatment in acute coronary syndrome (ACS) related cardiogenic shock (CS). The aim was to investigate the association of angiographic results with 90-day mortality. Procedural complications of percutaneous coronary intervention (PCI) were also examined. This CardShock (NCT01374867) substudy included 158 patients with ACS aetiology and data on coronary angiography and complications during PCI procedure. Survival analysis was conducted with Kaplan-Meier curves and Cox regression analysis. Median age was 67 ± 11 years, and 77% were men. During 90-day follow-up, 66 (42%) patients died. Patients with one-vessel disease (n = 49) had lower mortality than patients with two-vessel (n = 59) or three-vessel (n = 50) disease (25% vs. 48% vs. 52%, P = 0.011). Successful revascularization [Thrombolysis in Myocardial Infarction (TIMI) Flow 3 post-PCI) was achieved more often in survivors than non-survivors (81% vs. 60%, P = 0.019). The median symptom-to-balloon time was 340 (196-660) minutes, with no difference between survivors and non-survivors. In multivariable mortality analysis, multivessel disease (HR 2.59, CI 1.29-5.18) and TIMI flow
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- 2020
11. Performance of Early Capillary Refill Time Measurement on Outcomes in Cardiogenic Shock: An Observational, Prospective Multicentric Study.
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Merdji, Hamid, Curtiaud, Anais, Aheto, Antoine, Studer, Antoine, Harjola, Veli-Pekka, Monnier, Alexandra, Duarte, Kevin, Girerd, Nicolas, Kibler, Marion, Ait-Oufella, Hafid, Helms, Julie, Mebazaa, Alexandre, Levy, Bruno, Kimmoun, Antoine, and Meziani, Ferhat
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CARDIOGENIC shock ,TIME measurements ,EXTRACORPOREAL membrane oxygenation ,CAPILLARIES ,BLOOD pressure ,LEFT heart ventricle ,EVALUATION research ,MICROCIRCULATION ,HEART physiology ,HEMODYNAMICS ,RETROSPECTIVE studies ,LONGITUDINAL method ,RESEARCH ,RESEARCH methodology ,STROKE volume (Cardiac output) ,COMPARATIVE studies ,APACHE (Disease classification system) - Abstract
Rationale: Identification of cardiogenic shock severity is a critical step to adapt the management level upon admission. Peripheral tissue perfusion signs, simple and reliable markers of tissue hypoperfusion have never been extensively assessed during cardiogenic shock. Objectives: To assess the correlation of capillary refill time values with 90-day mortality in cardiogenic shock patients or the need for venoarterial extracorporeal membrane oxygenation (VA-ECMO) support. Also to assess the correlation between capillary refill time and hemodynamic parameters. Methods: All consecutive patients with cardiogenic shock admitted to the intensive care unit of two tertiary teaching hospitals were included in a prospective observational study. Macro-hemodynamic parameters (such as heart rate, blood pressure, left ventricular ejection fraction, and cardiac index) and peripheral tissue perfusion signs, such as capillary refill time on the index fingertip, mottling, and Pv-aCO2 (the difference between partial pressure of CO2 between venous and arterial blood) were recorded at inclusion (0 hour), 6 hours, 12 hours, 24 hours, and 48 hours. The composite primary endpoint was the association between 90-day mortality or the need for VA-ECMO support. Measurements and Main Results: A total of 61 patients were included; at inclusion, simplified acute physiology score II was 64 (52-77) points. The primary endpoint was met by 42% of patients. Capillary refill time values were significantly higher at all time points in nonsurvivors or patients needing VA-ECMO support. In univariate analysis, capillary refill time > 3 seconds at inclusion was associated with 90-day all-cause mortality or VA-ECMO support (hazard ratio, 12.38; 95% confidence interval, 2.91-52.71). Capillary refill time at inclusion was poorly associated with macrocirculatory parameters but significantly correlated with microcirculatory parameters. Further, capillary refill time added incremental value to Cardshock score, with an AUC combination at 0.93. Conclusions: In patients with cardiogenic shock admitted to the ICU, our preliminary data suggest that a prolonged capillary refill time >3 seconds was associated with an early prediction of 90-day mortality or the need for VA-ECMO support. [ABSTRACT FROM AUTHOR]
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- 2022
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12. Circulating levels of microRNA 423‐5p are associated with 90 day mortality in cardiogenic shock
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Jäntti, Toni, Segersvärd, Heli, Tolppanen, Heli, Tarvasmäki, Tuukka, Lassus, Johan, Devaux, Yvan, Vausort, Mélanie, Pulkki, Kari, Sionis, Alessandro, Bayes‐Genis, Antoni, Tikkanen, Ilkka, Lakkisto, Päivi, and Harjola, Veli‐Pekka
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Male ,Time Factors ,microRNA ,Short Communication ,Shock, Cardiogenic ,Prognosis ,Risk Assessment ,Survival Rate ,MicroRNAs ,miR‐423‐5p ,Risk Factors ,Cause of Death ,Humans ,Female ,Acute coronary syndrome ,Prospective Studies ,Mortality ,Cardiogenic shock ,Biomarkers ,Finland ,Aged ,Follow-Up Studies - Abstract
Aims The role of microRNAs has not been studied in cardiogenic shock. We examined the potential role of miR‐423‐5p level to predict mortality and associations of miR‐423‐5p with prognostic markers in cardiogenic shock. Methods and results We conducted a prospective multinational observational study enrolling consecutive cardiogenic shock patients. Blood samples were available for 179 patients at baseline to determine levels of miR‐423‐5p and other biomarkers. Patients were treated according to local practice. Main outcome was 90 day all‐cause mortality. Median miR‐423‐5p level was significantly higher in 90 day non‐survivors [median 0.008 arbitrary units (AU) (interquartile range 0.003–0.017) vs. 0.004 AU (0.002–0.009), P = 0.003]. miR‐423‐5p level above median was associated with higher lactate (median 3.7 vs. 2.4 mmol/L, P = 0.001) and alanine aminotransferase levels (median 68 vs. 35 IU/L, P
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- 2018
13. Predictive value of plasma proenkephalin and neutrophil gelatinase-associated lipocalin in acute kidney injury and mortality in cardiogenic shock
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Jäntti, Toni, Tarvasmäki, Tuukka, Harjola, Veli-Pekka, Pulkki, Kari, Turkia, Heidi, Sabell, Tuija, Tolppanen, Heli, Jurkko, Raija, Hongisto, Mari, Kataja, Anu, Sionis, Alessandro, Silva-Cardoso, Jose, Banaszewski, Marek, DiSomma, Salvatore, Mebazaa, Alexandre, Haapio, Mikko, Lassus, Johan, Universitat Autònoma de Barcelona, Kardiologian yksikkö, HUS Heart and Lung Center, Helsinki University Hospital Area, University of Helsinki, Clinicum, HUS Emergency Medicine and Services, Department of Medicine, Department of Clinical Chemistry and Hematology, HUSLAB, Department of Diagnostics and Therapeutics, HUS Internal Medicine and Rehabilitation, HUS Abdominal Center, and Nefrologian yksikkö
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BIOMARKER ,medicine.medical_specialty ,PROGNOSIS ,030204 cardiovascular system & hematology ,Lipocalin ,Critical Care and Intensive Care Medicine ,PENK ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,AKI ,Interquartile range ,Oliguria ,Anesthesiology ,Internal medicine ,medicine ,MANAGEMENT ,030212 general & internal medicine ,Mortality ,NGAL ,Cardiogenic shock ,Creatinine ,OUTCOMES ,business.industry ,STATEMENT ,Research ,Hazard ratio ,Acute kidney injury ,lcsh:Medical emergencies. Critical care. Intensive care. First aid ,lcsh:RC86-88.9 ,medicine.disease ,3126 Surgery, anesthesiology, intensive care, radiology ,Prognosis ,chemistry ,3121 General medicine, internal medicine and other clinical medicine ,Cardiology ,medicine.symptom ,business ,Proenkephalin - Abstract
BackgroundAcute kidney injury (AKI) is a frequent form of organ injury in cardiogenic shock. However, data on AKI markers such as plasma proenkephalin (P-PENK) and neutrophil gelatinase-associated lipocalin (P-NGAL) in cardiogenic shock populations are lacking. The objective of this study was to assess the ability of P-PENK and P-NGAL to predict acute kidney injury and mortality in cardiogenic shock.ResultsP-PENK and P-NGAL were measured at different time points between baseline and 48 h in 154 patients from the prospective CardShock study. The outcomes assessed were AKI defined by an increase in creatinine within 48 h and all-cause 90-day mortality. Mean age was 66 years and 26% were women. Baseline levels of P-PENK and P-NGAL (median [interquartile range]) were 99 (71–150) pmol/mL and 138 (84–214) ng/mL. P-PENK > 84.8 pmol/mL and P-NGAL > 104 ng/mL at baseline were identified as optimal cut-offs for AKI prediction and independently associated with AKI (adjusted HRs 2.2 [95% CI 1.1–4.4,p = 0.03] and 2.8 [95% CI 1.2–6.5,p = 0.01], respectively). P-PENK and P-NGAL levels at baseline were also associated with 90-day mortality. For patients with oliguria 6 h before study enrollment, 90-day mortality differed significantly between patients with low and high P-PENK/P-NGAL at baseline (5% vs. 68%,p 24h > 105.7 pmol/L and P-NGAL24h > 151 ng/mL had unadjusted hazard ratios of 5.6 (95% CI 3.1–10.7,p p ConclusionsHigh levels of P-PENK and P-NGAL at baseline were independently associated with AKI in cardiogenic shock patients. Furthermore, oliguria before study inclusion was associated with worse outcomes only if combined with high baseline levels of P-PENK or P-NGAL. High levels of both P-PENK and P-NGAL at 24 h were found to be strong and independent predictors of 90-day mortality.Trial registration: NCT01374867 atwww.clinicaltrials.gov, registered 16 Jun 2011—retrospectively registered
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- 2021
14. Levosimendan Efficacy and Safety : 20 Years of SIMDAX in Clinical Use
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Papp, Zoltán, Álvarez, Julián, Bettex, Dominique, Bouchez, Stefan, Brito, Dulce, Černý, Vladimir, Comin-Colet, Comin-Colet, Josep, Crespo-Leiro, María Generosa, Delgado-Jiménez, Juan F., Édes, István, Eremenko, Alexander, Farmakis, Dimitrios, Fedele, Francesco, Fonseca, Candida, Fruhwald, Sonja, Girardis, Massimo, Guarracino, Fabio, Harjola, Veli-Pekka, Heringlake, Matthias, Herpain, Antoine, Heunks, Leo, Husebye, Tryggve, Ivancan, Višnja, Karason, Kristjan, Kaul, Sundeep, Kivikko, Matti, Kubica, Janek, Masip, Josep, Matskeplishvili, Simon, Mebazaa, Alexandre, Nieminen, Markku S., Oliva, Fabrizio, Papp, Julius G., Parissis, John, Parkhomenko, Alexander, Põder, Pentti, Pölzl, Gerhard, Reinecke, Alexander, Ricksten, Sven-Erik, Riha, Hynek, Rudiger, Alain, Sarapohja, Toni, Schwinger, Robert H. G., Toller, Wolfgang, Tritapepe, Luigi, Tschöpe, Carsten, Wikström, Gerhard, Lewinski, Dirk von, Vrtovec, Bojan, Pollesello, Piero, Agostoni, Piergiuseppe, HUS Emergency Medicine and Services, Helsinki University Hospital Area, University of Helsinki, HUS Heart and Lung Center, and Repositório da Universidade de Lisboa
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0301 basic medicine ,Inotrope ,lcsh:Diseases of the circulatory (Cardiovascular) system ,CALCIUM SENSITIZING DRUG ,Advanced heart failure ,Vasodilator Agents ,RIGHT-VENTRICULAR FUNCTION ,Cardiomyopathy ,TROPONIN-C ,Insuficiència cardíaca ,030204 cardiovascular system & hematology ,hemodynamics ,GLOMERULAR-FILTRATION-RATE ,AMYOTROPHIC-LATERAL-SCLEROSIS ,ARTERY-BYPASS GRAFT ,0302 clinical medicine ,CARDIAC TROPONIN-C ,Medicine and Health Sciences ,Neurohormone ,Cardiac and Cardiovascular Systems ,Myocardial infarction ,media_common ,Regulatory clinical trial ,0303 health sciences ,Kardiologi ,Cardiogenic shock ,Inodilator ,Cardiac surgery ,3. Good health ,Vasodilation ,Treatment Outcome ,317 Pharmacy ,inotrope ,Patient Safety ,Cardiology and Cardiovascular Medicine ,medicine.drug ,medicine.medical_specialty ,Pharmacological Therapy ,Cardiotonic Agents ,acute heart failure ,neurohormone ,Heart failure ,CARDIAC ,EXTRACORPOREAL MEMBRANE-OXYGENATION ,03 medical and health sciences ,DECOMPENSATED HEART-FAILURE ,medicine ,media_common.cataloged_instance ,Diseases of the circulatory (Cardiovascular) system ,Humans ,regulatory clinical trial ,European union ,Intensive care medicine ,inodilator ,Simendan ,030304 developmental biology ,Pharmacology ,Heart Failure ,haemodynamics ,BLOOD-FLOW ,business.industry ,advanced heart failure ,Hemodynamics ,CORONARY BLOOD-FLOW ,Acute heart failure ,Levosimendan ,medicine.disease ,Hemodinàmica ,Myocardial Contraction ,IMPROVES RENAL-FUNCTION ,030104 developmental biology ,lcsh:RC666-701 ,RC666-701 ,3121 General medicine, internal medicine and other clinical medicine ,CORONARY ,business - Abstract
Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc., Levosimendan was first approved for clinical use in 2000, when authorization was granted by Swedish regulatory authorities for the hemodynamic stabilization of patients with acutely decompensated chronic heart failure (HF). In the ensuing 20 years, this distinctive inodilator, which enhances cardiac contractility through calcium sensitization and promotes vasodilatation through the opening of adenosine triphosphate–dependent potassium channels on vascular smooth muscle cells, has been approved in more than 60 jurisdictions, including most of the countries of the European Union and Latin America. Areas of clinical application have expanded considerably and now include cardiogenic shock, takotsubo cardiomyopathy, advanced HF, right ventricular failure, pulmonary hypertension, cardiac surgery, critical care, and emergency medicine. Levosimendan is currently in active clinical evaluation in the United States. Levosimendan in IV formulation is being used as a research tool in the exploration of a wide range of cardiac and noncardiac disease states. A levosimendan oral form is at present under evaluation in the management of amyotrophic lateral sclerosis. To mark the 20 years since the advent of levosimendan in clinical use, 51 experts from 23 European countries (Austria, Belgium, Croatia, Cyprus, Czech Republic, Estonia, Finland, France, Germany, Greece, Hungary, Italy, the Netherlands, Norway, Poland, Portugal, Russia, Slovenia, Spain, Sweden, Switzerland, the United Kingdom, and Ukraine) contributed to this essay, which evaluates one of the relatively few drugs to have been successfully introduced into the acute HF arena in recent times and charts a possible development trajectory for the next 20 years.
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- 2020
15. Circulating dipeptidyl peptidase 3 is a myocardial depressant factor: dipeptidyl peptidase 3 inhibition rapidly and sustainably improves haemodynamics.
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Deniau, Benjamin, Rehfeld, Linda, Santos, Karine, Dienelt, Anke, Azibani, Feriel, Sadoune, Malha, Kounde, Paul R., Samuel, Jane L., Tolpannen, Heli, Lassus, Johan, Harjola, Veli‐Pekka, Vodovar, Nicolas, Bergmann, Andreas, Hartmann, Oliver, Mebazaa, Alexandre, Blet, Alice, and Harjola, Veli-Pekka
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MYOCARDIAL depressants ,HEMODYNAMICS ,CARDIOGENIC shock ,ANGIOTENSIN II ,HEART failure ,THERAPEUTIC use of monoclonal antibodies ,RESEARCH ,ANIMAL experimentation ,RESEARCH methodology ,ARTHRITIS Impact Measurement Scales ,PROTEOLYTIC enzymes ,MEDICAL cooperation ,EVALUATION research ,COMPARATIVE studies ,MENTAL health surveys ,RESEARCH funding ,MICE ,CHEMICAL inhibitors - Abstract
Aims: Acute heart failure is a high mortality disease and its pathophysiology is not completely understood. Dipeptidyl peptidase 3 (DPP3) is a cytosolic enzyme involved in angiotensin II and enkephalins cleavage. The aim of this study was to investigate the association of circulating DPP3 (cDPP3) levels and mortality in cardiogenic shock patients and to determine the effects of high cDPP3 on organ function in a heart failure (HF) model in mice.Methods and Results: cDPP3 was measured in 174 patients in cardiogenic shock and high cDPP3 levels were associated with an increased short-term mortality risk (standardized hazard ratio: 1.4 (1.1-1.8)) and severe organ dysfunction. Additionally, a rapid decrease in cDPP3 in cardiogenic shock patients within 24 h of admission was associated with a favourable outcome. This study showed that injection of DPP3 induced myocardial depression (-10 ± 2% of shortening fraction) and impaired kidney haemodynamics (+0.30 ± 0.02 of renal resistive index) in healthy mice. cDPP3 inhibition by Procizumab, a specific antibody directed against cDPP3, promptly normalized cardiac function and kidney haemodynamics in an acute heart failure mouse model, with a marked reduction in oxidative stress and inflammatory signalling.Conclusion: Our study demonstrated cDPP3 is a newly discovered myocardial depressant factor, the levels of which at admission are associated with mortality in severe HF patients. Furthermore, inhibition of cDPP3 by Procizumab improved haemodynamics in a mouse model of HF. Our results suggest that DPP3 could be a new biomarker and biotarget for severe HF. [ABSTRACT FROM AUTHOR]- Published
- 2020
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16. Serum Lactate and A Relative Change in Lactate as Predictors of Mortality in Patients With Cardiogenic Shock - Results from the Cardshock Study
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John Parissis, Jindrich Spinar, Johan Lassus, Marek Banaszewski, José Silva-Cardoso, Lars Køber, Valentina Carubelli, Harjola Veli-Pekka, Alexandre Mebazaa, Matias Greve Lindholm, Mari Hongisto, diSomma Salvatore, and Alessandro Sionis
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Adult ,Male ,medicine.medical_specialty ,acute heart failure ,medicine.medical_treatment ,A relative change in lactate ,Shock, Cardiogenic ,030204 cardiovascular system & hematology ,Critical Care and Intensive Care Medicine ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,In patient ,Myocardial infarction ,Lactic Acid ,Aged ,Proportional Hazards Models ,Aged, 80 and over ,lactate ,business.industry ,Cardiogenic shock ,cardiogenic shock ,Hazard ratio ,Hemodynamics ,Percutaneous coronary intervention ,030208 emergency & critical care medicine ,prediction ,Middle Aged ,medicine.disease ,mortality ,Confidence interval ,3. Good health ,lactate clearance ,Multivariate Analysis ,Emergency Medicine ,Cardiology ,Population study ,Female ,business ,Anaerobic exercise - Abstract
Introduction: Cardiogenic shock complicating acute myocardial infarction has a very high mortality. Our present study focuses on serial measurement of lactate during admission due to cardiogenic shock and the prognostic effect of lactate and a relative change in lactate in patients after admission and the institution of intensive care treatment. Methods and Results: This is a secondary analysis of the CardShock study. Data on lactate at baseline were available on 217 of 219 patients. In the study population, the median baseline lactate was 2.8 mmol/L (min-max range, 0.5-23.1 mmol/L). At admission, lactate was predictive of 30-day mortality with an adjusted Hazard ratio (HR) of 1.20 mmol/L (95% confidence interval, CI 1.14-1.27). Within the first 24 h of admission, baseline lactate remained predictive of 30-day mortality. Lactate at 6 h had a HR of 1.14 (95% CI 1.06-1.24) and corresponding values at 12 and 24 h had a HR of 1.10 (1.04-1.17), and of HR 1.19 (95% CI 1.07-1.32), respectively. A 50% reduction in lactate within 6 h resulted in a HR of 0.82 (95% CI 0.72-0.94). Corresponding hazard ratios at 12 and 24 h, were 0.87 (95% CI 0.76-0.98) and 0.74 (95% CI 0.60-0.91), respectively. Conclusion: The main findings of the present study are that baseline lactate is a powerful predictor of 30-day mortality, lactate at 6, 12, and 24 h after admission are predictors of 30-day mortality, and a relative change in lactate is a significant predictor of survival within the first 24 h after instituting intensive care treatment adding information beyond the information from baseline values.
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- 2019
17. Hypoalbuminemia is a frequent marker of increased mortality in cardiogenic shock
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Jäntti, Toni, Tarvasmaki, Tuukka, Harjola, Veli-Pekka, Parissis, John, Pulkki, Kari, Javanainen, Tuija, Tolppanen, Heli, Jurkko, Raija, Hongisto, Mari, Kataja, Anu, Sionis, Alessandro, Silva-Cardoso, Jose, Banaszewski, Marek, Spinar, Jindrich, Mebazaa, Alexandre, Lassus, Johan, Kober, Lars, Metra, Marco, Di Somma, Salvatore, Koniari, Katerina, Voumvourakis, Astrinos, Karavidas, Apostolos, Sans-Rosello, Jordi, Vila, Montserrat, Duran-Cambra, Albert, Bulgari, Michela, Lazzarini, Valentina, Parenica, Jiri, Stipal, Roman, Ludka, Ondrej, Palsuva, Marie, Ganovska, Eva, Kubena, Petr, Lindholm, Matias G., Jarvinen, Kristiina, Nieminen, Tuomo, Soininen, Leena, Sund, Reijo, Tierala, Ilkka, Tolonen, Jukka, Varpula, Marjut, University of Helsinki, HYKS Sydän- ja keuhkokeskus, University of Helsinki, Clinicum, University of Helsinki, HYKS Leikkaussalit, teho- ja kivunhoito, University of Helsinki, Department of Medicine, University of Helsinki, Kardiologian yksikkö, University of Helsinki, Department of Diagnostics and Therapeutics, University of Helsinki, Dep. of Internal Medicine (Institute of Clinical Medicine) (-2009), University of Helsinki, Doctoral Programme in Clinical Research, University of Helsinki, Kliinisen kemian yksikkö (-2009), University of Helsinki, Public Health, University of Helsinki, University Management, HUS Heart and Lung Center, Kardiologian yksikkö, Clinicum, HUS Emergency Medicine and Services, Department of Diagnostics and Therapeutics, Department of Medicine, HUS Internal Medicine and Rehabilitation, Kliinisen kemian yksikkö (-2009), University Management, Faculty of Social Sciences, and HUSLAB
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Male ,Physiology ,LEVEL ,Myocardial Infarction ,Blood Pressure ,030204 cardiovascular system & hematology ,Biochemistry ,Vascular Medicine ,LEVELS PREDICT SURVIVAL ,0302 clinical medicine ,Risk Factors ,Cause of Death ,Odds Ratio ,Medicine and Health Sciences ,Coronary Heart Disease ,030212 general & internal medicine ,Myocardial infarction ,Hypoalbuminemia ,Hospital Mortality ,Prospective Studies ,Prospective cohort study ,Cause of death ,Multidisciplinary ,Cardiogenic shock ,Mortality rate ,ASSOCIATION ,Middle Aged ,SERUM-ALBUMIN CONCENTRATION ,ADMISSION ,3. Good health ,Body Fluids ,PROGNOSTIC VALUE ,Treatment Outcome ,Blood ,Shock (circulatory) ,Cardiology ,Medicine ,HEART-FAILURE ,Female ,medicine.symptom ,Anatomy ,Research Article ,medicine.medical_specialty ,Death Rates ,Science ,Shock, Cardiogenic ,3121 Internal medicine ,Blood Plasma ,03 medical and health sciences ,Population Metrics ,Internal medicine ,Albumins ,medicine ,MANAGEMENT ,Humans ,Aged ,Heart Failure ,RISK PREDICTION ,Population Biology ,business.industry ,Biology and Life Sciences ,Proteins ,Odds ratio ,Length of Stay ,medicine.disease ,3126 Surgery, anesthesiology, intensive care, radiology ,MYOCARDIAL-INFARCTION ,3121 General medicine, internal medicine and other clinical medicine ,business ,Ejection Fraction - Abstract
Altres ajuts: VPH was supported by the Aarne Koskelo Foundation (no grant number): http://www. aarnekoskelonsaatio.fi/, and the Finnish Cardiac Foundation (no grant number): https://www. fincardio.fi/. Laboratory kits were provided by Roche Diagnostics. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Introduction The prevalence of hypoalbuminemia, early changes of plasma albumin (P-Alb) levels, and their effects on mortality in cardiogenic shock are unknown. Materials and methods P-Alb was measured from serial blood samples in 178 patients from a prospective multinational study on cardiogenic shock. The association of hypoalbuminemia with clinical characteristics and course of hospital stay including treatment and procedures was assessed. Theprimary outcome was all-cause 90-day mortality. Results Hypoalbuminemia (P-Alb < 34g/L) was very frequent (75%) at baseline in patients with cardiogenic shock. Patients with hypoalbuminemia had higher mortality than patients with normal albumin levels (48% vs. 23%, p = 0.004). Odds ratio for death at 90 days was 2.4 [95% CI 1.5-4.1] per 10 g/L decrease in baseline P-Alb. The association with increased mortality remained independent in regression models adjusted for clinical risk scores developed for cardiogenic shock (CardShock score adjusted odds ratio 2.0 [95% CI 1.1-3.8], IABPSHOCK II score adjusted odds ratio 2.5 [95%CI 1.2-5.0]) and variables associated with hypoalbuminemia at baseline (adjusted odds ratio 2.9 [95%CI 1.2-7.1]). In serial measurements,albumin levels decreased at a similar rate between 0h and 72h in both survivors andnonsurvivors (ΔP-Alb -4.6 g/L vs. 5.4 g/L, p = 0.5). While the decrease was higher for patients with normal P-Alb at baseline (p 0.001 compared to patients with hypoalbuminemia at baseline), the rate of albumin decrease was not associated with outcome. Conclusions Hypoalbuminemia was a frequent finding early in cardiogenic shock, and P-Alb levels decreased during hospital stay. Low P-Alb at baseline was associated with mortality independently of other previously described risk factors. Thus, plasma albumin measurement should be part of the initial evaluation in patients with cardiogenic shock.
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- 2019
18. Treatments targeting inotropy : a position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association of the European Society of Cardiology
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Maack, Christoph, Eschenhagen, Thomas, Hamdani, Nazha, Heinzel, Frank R., Lyon, Alexander R., Manstein, Dietmar J., Metzger, Joseph, Papp, Zoltan, Tocchetti, Carlo G., Yilmaz, M. Birhan, Anker, Stefan D., Balligand, Jean-Luc, Bauersachs, Johann, Brutsaert, Dirk, Carrier, Lucie, Chlopicki, Stefan, Cleland, John G., de Boer, Rudolf A., Dietl, Alexander, Fischmeister, Rodolphe, Harjola, Veli-Pekka, Heymans, Stephane, Hilfiker-Kleiner, Denise, Holzmeister, Johannes, de Keulenaer, Gilles, Limongelli, Giuseppe, Linke, Wolfgang A., Lund, Lars H., Masip, Josep, Metra, Marco, Mueller, Christian, Pieske, Burkert, Ponikowski, Piotr, Ristic, Arsen, Ruschitzka, Frank, Seferovic, Petar M., Skouri, Hadi, Zimmermann, Wolfram H., Mebazaa, Alexandre, and Cardiovascular Centre (CVC)
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Sarcomeres ,Levosimendan ,Heart failure ,Acute decompensated heart failure ,Omecamtiv mecarbil ,Contractility ,Excitation-contraction coupling ,Mitochondria ,Inotropes ,Energetics ,Nitroxyl ,Calcium ,Adrenergic receptors ,Cardiogenic shock - Abstract
Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term.
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- 2019
19. Levosimendan beyond inotropy and acute heart failure: Evidence of pleiotropic effects on the heart and other organs: An expert panel position paper
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Farmakis, Dimitrios, Alvarez, Julian, Ben Gal, Tuvia, Brito, Dulce, Fedele, Francesco, Fonseca, Candida, Gordon, Anthony C., Gotsman, Israel, Grossini, Elena, Guarracino, Fabio, Harjola, Veli-Pekka, Hellman, Yaron, Heunks, Leo, Ivancan, Visnja, Karavidas, Apostolos, Kivikko, Matti, Lomivorotov, Vladimir, Longrois, Dan, Masip, Josep, Metra, Marco, Morelli, Andrea, Nikolaou, Maria, Papp, Zoltan, Parkhomenko, Alexander, Poelzl, Gerhard, Pollesello, Piero, Ravn, Hanne Berg, Rex, Steffen, Riha, Hynek, Ricksten, Sven-Erik, Schwinger, Robert H. G., Vrtovec, Bojan, Yilmaz, M. Birhan, Zielinska, Marzenna, Parissis, John, Clinicum, Anestesiologian yksikkö, Department of Diagnostics and Therapeutics, [Farmakis, Dimitrios -- Parissis, John] Univ Athens, Univ Athens, Dept Cardiol, Heart Failure Unit,Univ Attikon, Athens, Greece -- [Alvarez, Julian] Univ Santiago Compostela, Dept Anesthesia, Santiago De Compostela, Spain -- [Alvarez, Julian] Univ Santiago Compostela, Surg ICU, Santiago De Compostela, Spain -- [Ben Gal, Tuvia] Rabin Med Ctr, Cardiol Clin, Petah Tiqwa, Israel -- [Brito, Dulce] Hosp Santa Maria, Dept Cardiol, Ctr Hosp Lisboa Norte, Lisbon, Portugal -- [Fedele, Francesco] Sapienza Univ Rome, Dept Cardiovasc Resp Nephrol Anesthesiol & Geriat, Rome, Italy -- [Fonseca, Candida] Univ Nova Lisboa, Heart Failure Unit, Dept Internal Med,NOVA Med Sch,Fac Ciencias Med, Hosp Sao Francico Xavier,Ctr Hosp Lisbo Ocidental, Lisbon, Portugal -- [Gordon, Anthony C.] Imperial Coll London, Sect Anaesthet Pain Med & Intens Care, London, England -- [Gotsman, Israel] Hadassah Univ Hosp Jerusalem, Inst Heart, Cardiol Clin, Jerusalem, Israel -- [Grossini, Elena] Univ East Piedmont, Physiol Lab, Novara, Italy -- [Guarracino, Fabio] Azienda Osped Univ Pisana, Dept Anaesthesia & Crit Care Med Cardiothorac Ana, Pisa, Italy -- [Harjola, Veli-Pekka] Univ Helsinki, Helsinki Univ Hosp, Emergency Med, Helsinki, Finland -- [Hellman, Yaron] Carmel Hosp, Heart Failure Serv, Haifa, Israel -- [Heunks, Leo] Radboud Univ Nijmegen, Med Ctr, Dept Intens Care, Nijmegen, Netherlands -- [Ivancan, Visnja] Univ Hosp Ctr, Emergency Cardiol Dept, Zagreb, Croatia -- [Karavidas, Apostolos] G Gennimatas Gen Hosp, Dept Cardiol, Athens, Greece -- [Kivikko, Matti -- Pollesello, Piero] Orion Pharma, Crit Care Proprietary Prod, Espoo, Finland -- [Lomivorotov, Vladimir] State Res Inst Circulat Pathol, Dept Anesthesiol & Intens Care, Novosibirsk, Russia -- [Longrois, Dan] Univ Paris Diderot, Hop Uiversitaires Paris Nord Val Seine, Hop Bichat Claude Bernard, Dept Anesthesie Reanimat Chirurg, Paris, France -- [Masip, Josep] Hosp St Joan Despi Moises Broggi, Intens Care Unit, Barcelona, Spain -- [Metra, Marco] Univ & Civil Hosp, Cardiol Clin, Brescia, Italy -- [Morelli, Andrea] Univ Roma La Sapienza, Dept Anesthesiol & Intens Care, Policlin Umberto 1, Rome, Italy -- [Nikolaou, Maria] Sismanoglio & Amalia Fleming Gen Hosp, Dept Cardiol, Athens, Greece -- [Papp, Zoltan] Univ Debrecen, Fac Med, Dept Cardiol, Div Clin Physiol, Debrecen, Hungary -- [Parkhomenko, Alexander] Inst Cardiol, Dept Anesthesiol, Kiev, Ukraine -- [Parkhomenko, Alexander] Inst Cardiol, Intens Care Unit Cardiac Surg Patients, Kiev, Ukraine -- [Poelzl, Gerhard] Univ Klin Innsbruck, Innere Med 3, Innsbruck, Austria -- [Ravn, Hanne Berg] Rigshosp, Ctr Heart, Dept Cardiothorac Anaesthesia, Copenhagen, Denmark -- [Rex, Steffen] Univ Leuven, Dept Cardiovasc Sci, Leuven, Belgium -- [Riha, Hynek] Inst Clin & Expt Med, Dept Anaesthesiol & Intens Care Med, Cardiothorac Anaesthesiol & Intens Care, Prague, Czech Republic -- [Ricksten, Sven-Erik] Univ Gothenburg, Sahlgrenska Univ Hosp, Inst Clin Sci, Dept Anesthesiol & Intens Care Med, Gothenburg, Sweden -- [Schwinger, Robert H. G.] Klinikum Weiden, Med Klin 2, Weiden, Germany -- [Vrtovec, Bojan] Univ Clin Ctr Ljubljana, Dept Cardiol, Ljubljana, Slovenia -- [Yilmaz, M. Birhan] Cumhuriyet Univ, Dept Cardiol, Sivas, Turkey -- [Zielinska, Marzenna] Med Univ Lodz, Dept Intens Cardiac Therapy, Lodz, Poland, Brito, Dulce Alves -- 0000-0003-1278-1847, Lomivorotov, Vladimir -- 0000-0001-8591-6461, Pollesello, Piero -- 0000-0001-6994-768X, YILMAZ, Mehmet Birhan -- 0000-0002-8169-8628, Zielinska, Marzenna -- 0000-0002-0118-8610, Gordon, Anthony -- 0000-0002-0419-547X, YILMAZ, MEHMET BIRHAN -- 0000-0002-8169-8628, Alvarez, Julian -- 0000-0002-2518-0891, MORELLI, ANDREA -- 0000-0001-6065-1006, Riha, Hynek -- 0000-0002-9861-7361, Gotsman, Israel -- 0000-0001-9608-2298, and Rex, Steffen -- 0000-0002-3536-9321
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Levosimendan ,3121 General medicine, internal medicine and other clinical medicine ,Inotropes ,education ,Heart failure ,Cardioprotection ,Cardiogenic shock ,Organ protection - Abstract
WOS: 000384698300056, PubMed ID: 27498374, Levosimendan is a positive inotrope with vasodilating properties (inodilator) indicated for decompensated heart failure (HF) patients with low cardiac output. Accumulated evidence supports several pleiotropic effects of levosimendan beyond inotropy, the heart and decompensated HF. Those effects are not readily explained by cardiac function enhancement and seem to be related to additional properties of the drug such as anti-inflammatory, anti-oxidative and anti-apoptotic ones. Mechanistic and proof-of-concept studies are still required to clarify the underlying mechanisms involved, while properly designed clinical trials are warranted to translate preclinical or early-phase clinical data into more robust clinical evidence. The present position paper, derived by a panel of 35 experts in the field of cardiology, cardiac anesthesiology, intensive care medicine, cardiac physiology, and cardiovascular pharmacology from 22 European countries, compiles the existing evidence on the pleiotropic effects of levosimendan, identifies potential novel areas of clinical application and defines the corresponding gaps in evidence and the required research efforts to address those gaps. (C) 2016 The Authors. Published by Elsevier Ireland Ltd., Orion Pharma Oyj/Abp (Finland); Medis d.o.o. (Croatia); Biomed JR Ltd. (Israel); TENAX Therapeutics Ltd. (U.S.A.), This project did not receive any financial support, apart from unrestricted grants by Orion Pharma Oyj/Abp (Finland), Medis d.o.o. (Croatia), Biomed JR Ltd. (Israel), and TENAX Therapeutics Ltd. (U.S.A.) that covered the logistic expenses related to the consensus meeting in Athens on Feb. 26-27, 2016. The attendees did not receive any honoraria. P.P. and M.K. are employees of Orion Pharma.
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- 2016
20. Mortality risk prediction in elderly patients with cardiogenic shock: results from the CardShock study.
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Hongisto, Mari, Lassus, Johan, Tarvasmäki, Tuukka, Sionis, Alessandro, Sans‐Rosello, Jordi, Tolppanen, Heli, Kataja, Anu, Jäntti, Toni, Sabell, Tuija, Lindholm, Matias Greve, Banaszewski, Marek, Silva Cardoso, Jose, Parissis, John, Di Somma, Salvatore, Carubelli, Valentina, Jurkko, Raija, Masip, Josep, and Harjola, Veli‐Pekka
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CARDIOGENIC shock ,CARDIOVASCULAR disease related mortality ,OLDER patients - Abstract
Aims: This study aimed to assess the utility of contemporary clinical risk scores and explore the ability of two biomarkers [growth differentiation factor‐15 (GDF‐15) and soluble ST2 (sST2)] to improve risk prediction in elderly patients with cardiogenic shock. Methods and results: Patients (n = 219) from the multicentre CardShock study were grouped according to age (elderly ≥75 years and younger). Characteristics, management, and outcome between the groups were compared. The ability of the CardShock risk score and the IABP‐SHOCK II score to predict in‐hospital mortality and the additional value of GDF‐15 and sST2 to improve risk prediction in the elderly was evaluated. The elderly constituted 26% of the patients (n = 56), with a higher proportion of women (41% vs. 21%, P < 0.05) and more co‐morbidities compared with the younger. The primary aetiology of shock in the elderly was acute coronary syndrome (84%), with high rates of percutaneous coronary intervention (87%). Compared with the younger, the elderly had higher in‐hospital mortality (46% vs. 33%; P = 0.08), but 1 year post‐discharge survival was excellent in both age groups (90% in the elderly vs. 88% in the younger). In the elderly, the risk prediction models demonstrated an area under the curve of 0.75 for the CardShock risk score and 0.71 for the IABP‐SHOCK II score. Incorporating GDF‐15 and sST2 improved discrimination for both risk scores with areas under the curve ranging from 0.78 to 0.84. Conclusions: Elderly patients with cardiogenic shock have higher in‐hospital mortality compared with the younger, but post‐discharge outcomes are similar. Contemporary risk scores proved useful for early mortality risk prediction also in the elderly, and risk stratification could be further improved with biomarkers such as GDF‐15 or sST2. [ABSTRACT FROM AUTHOR]
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- 2021
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21. Circulating levels of 423-5p are associated with 90 day mortality in cardiogenic shock
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Jäntti, Toni, Segersvärd, Heli, Tolppanen, Heli, Tarvasmäki, Tuukka, Lassus, Johan, Devaux, Yvan, Vausort, Mélanie, Pulkki, Kari, Sionis, Alessandro, Bayés-Genís, Antoni, Tikkanen, Ilkka, Lakkisto, Päivi, Harjola, Veli-Pekka, and Universitat Autònoma de Barcelona. Departament de Medicina
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Mir-423-5p ,Acute coronary syndrome ,Mortality ,Prognosis ,Cardiogenic shock ,Microrna - Abstract
Ajuts: This work was supported by grants from the Finnish Foundation for Cardiovascular Research, Aarne Koskelo Foundation, Finnish Foundation for Laboratory Medicine, FinskaLäkaresällskapet, the Liv och Hälsa Foundation, and Finnish state funding for university-level research. The role of microRNAs has not been studied in cardiogenic shock. We examined the potential role of miR-423-5p level to predict mortality and associations of miR-423-5p with prognostic markers in cardiogenic shock. We conducted a prospective multinational observational study enrolling consecutive cardiogenic shock patients. Blood samples were available for 179 patients at baseline to determine levels of miR-423-5p and other biomarkers. Patients were treated according to local practice. Main outcome was 90 day all-cause mortality. Median miR-423-5p level was significantly higher in 90 day non-survivors [median 0.008 arbitrary units (AU) (interquartile range 0.003-0.017) vs. 0.004 AU (0.002-0.009), P = 0.003]. miR-423-5p level above median was associated with higher lactate (median 3.7 vs. 2.4 mmol/L, P = 0.001) and alanine aminotransferase levels (median 68 vs. 35 IU/L, P < 0.001) as well as lower cardiac index (1.8 vs. 2.4, P = 0.04) and estimated glomerular filtration rate (56 vs. 70 mL/min/1.73 m 2, P = 0.002). In Cox regression analysis, miR-423-5p level above median was associated with 90 day all-cause mortality independently of established risk factors of cardiogenic shock [adjusted hazard ratio 1.9 (95% confidence interval 1.2-3.2), P = 0.01]. In cardiogenic shock patients, above median level of miR-423-5p at baseline is associated with markers of hypoperfusion and seems to independently predict 90 day all-cause mortality.
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- 2018
22. Predictive value of the baseline electrocardiogram ST-segment pattern in cardiogenic shock: Results from the CardShock Study.
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Javanainen, Tuija, Tolppanen, Heli, Lassus, Johan, Nieminen, Markku S., Sionis, Alessandro, Spinar, Jindrich, Silva‐Cardoso, José, Greve Lindholm, Matias, Banaszewski, Marek, Harjola, Veli‐Pekka, Jurkko, Raija, Silva-Cardoso, José, and Harjola, Veli-Pekka
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Background: The most common aetiology of cardiogenic shock (CS) is acute coronary syndrome (ACS), but even up to 20%-50% of CS is caused by other disorders. ST-segment deviations in the electrocardiogram (ECG) have been investigated in patients with ACS-related CS, but not in those with other CS aetiologies. We set out to explore the prevalence of different ST-segment patterns and their associations with the CS aetiology, clinical findings and 90-day mortality.Methods: We analysed the baseline ECG of 196 patients who were included in a multinational prospective study of CS. The patients were divided into 3 groups: (a) ST-segment elevation (STE). (b) ST-segment depression (STDEP). (c) No ST-segment deviation or ST-segment impossible to analyse (NSTD). A subgroup analysis of the ACS patients was conducted.Results: ST-segment deviations were present in 80% of the patients: 52% had STE and 29% had STDEP. STE was associated with the ACS aetiology, but one-fourth of the STDEP patients had aetiology other than ACS. The overall 90-day mortality was 41%: in STE 47%, STDEP 36% and NSTD 33%. In the multivariate mortality analysis, only STE predicted mortality (HR 1.74, CI95 1.07-2.84). In the ACS subgroup, the patients were equally effectively revascularized, and no differences in the survival were noted between the study groups.Conclusion: ST-segment elevation is associated with the ACS aetiology and high mortality in the unselected CS population. If STE is not present, other aetiologies must be considered. When effectively revascularized, the prognosis is similar regardless of the ST-segment pattern in ACS-related CS. [ABSTRACT FROM AUTHOR]- Published
- 2018
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23. Current Use and Impact on 30-Day Mortality of Pulmonary Artery Catheter in Cardiogenic Shock Patients: Results From the CardShock Study.
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Sionis, Alessandro, Rivas-Lasarte, Mercedes, Mebazaa, Alexandre, Tarvasmäki, Tuukka, Sans-Roselló, Jordi, Tolppanen, Heli, Varpula, Marjut, Jurkko, Raija, Banaszewski, Marek, Silva-Cardoso, Jose, Carubelli, Valentina, Lindholm, Matias Greve, Parissis, John, Spinar, Jindrich, Lassus, Johan, Harjola, Veli-Pekka, and Masip, Josep
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CARDIOGENIC shock ,PULMONARY artery catheters ,HOSPITAL mortality ,HEMODYNAMICS ,ARTIFICIAL respiration - Abstract
Background: Cardiogenic shock (CS) is the most life-threatening manifestation of acute heart failure. Its complexity and high inhospital mortality may justify the need for invasive monitoring with a pulmonary artery catheter (PAC). Methods: Patients with CS included in the CardShock Study, an observational, prospective, multicenter, European registry, were analyzed, aiming to describe the real-world use of PAC, evaluate its impact on 30-day mortality, and the ability of different hemodynamic parameters to predict outcomes. Results: Pulmonary artery catheter was used in 82 (37.4%) of the 219 patients. Cardiogenic shock patients who managed with a PAC received more frequently treatment with inotropes and vasopressors, mechanical ventilation, renal replacement therapy, and mechanical assist devices (P < .01). Overall 30-day mortality was 36.5%. Pulmonary artery catheter use did not affect mortality even after propensity score matching analysis (hazard ratio = 1.17 [0.59-2.32], P = .66). Cardiac index, cardiac power index (CPI), and stroke volume index (SVI) showed the highest areas under the curve for 30-day mortality (ranging from 0.752-0.803) and allowed for a significant net reclassification improvement of 0.467 (0.083-1.180), 0.700 (0.185-1.282), 0.683 (0.168-1.141), respectively, when added to the CardShock risk score. Conclusions: In our contemporary cohort of CS, over one-third of patients were managed with a PAC. Pulmonary artery catheter use was associated with a more aggressive treatment strategy. Nevertheless, PAC use was not associated with 30-day mortality. Cardiac index, CPI, and SVI were the strongest 30-day mortality predictors on top of the previously validated CardShock risk score. [ABSTRACT FROM AUTHOR]
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- 2020
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24. Epidemiology, pathophysiology and contemporary management of cardiogenic shock – a position statement from the Heart Failure Association of the European Society of Cardiology.
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Chioncel, Ovidiu, Parissis, John, Mebazaa, Alexandre, Thiele, Holger, Desch, Steffen, Bauersachs, Johann, Harjola, Veli‐Pekka, Antohi, Elena‐Laura, Arrigo, Mattia, Gal, Tuvia B., Celutkiene, Jelena, Collins, Sean P., DeBacker, Daniel, Iliescu, Vlad A., Jankowska, Ewa, Jaarsma, Tiny, Keramida, Kalliopi, Lainscak, Mitja, Lund, Lars H, and Lyon, Alexander R.
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CARDIOGENIC shock ,MEDICAL care ,HEART failure ,CLINICAL trial registries ,PERIPARTUM cardiomyopathy ,EPIDEMIOLOGY - Abstract
Cardiogenic shock (CS) is a complex multifactorial clinical syndrome with extremely high mortality, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large spectrum of CS presentations resulting from the interaction between an acute cardiac insult and a patient's underlying cardiac and overall medical condition. Phenotyping patients with CS may have clinical impact on management because classification would support initiation of appropriate therapies. CS management should consider appropriate organization of the health care services, and therapies must be given to the appropriately selected patients, in a timely manner, whilst avoiding iatrogenic harm. Although several consensus‐driven algorithms have been proposed, CS management remains challenging and substantial investments in research and development have not yielded proof of efficacy and safety for most of the therapies tested, and outcome in this condition remains poor. Future studies should consider the identification of the new pathophysiological targets, and high‐quality translational research should facilitate incorporation of more targeted interventions in clinical research protocols, aimed to improve individual patient outcomes. Designing outcome clinical trials in CS remains particularly challenging in this critical and very costly scenario in cardiology, but information from these trials is imperiously needed to better inform the guidelines and clinical practice. The goal of this review is to summarize the current knowledge concerning the definition, epidemiology, underlying causes, pathophysiology and management of CS based on important lessons from clinical trials and registries, with a focus on improving in‐hospital management. [ABSTRACT FROM AUTHOR]
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- 2020
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25. Levels of Growth Differentiation Factor 15 and Early Mortality Risk Stratification in Cardiogenic Shock.
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Hongisto, Mari, Kataja, Anu, Tarvasmäki, Tuukka, Holopainen, Anu, Javanainen, Tuija, Jurkko, Raija, Jäntti, Toni, Kimmoun, Antoine, Levy, Bruno, Mebazaa, Alexandre, Pulkki, Kari, Sionis, Alessandro, Tolppanen, Heli, Wollert, Kai C., Harjola, Veli-pekka, Lassus, Johan, and CardShock investigators
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Background: The aim of this study was to assess the levels, kinetics, and prognostic value of growth differentiation factor 15 (GDF-15) in cardiogenic shock (CS).Methods and Results: Levels of GDF-15 were determined in serial plasma samples (0-120 h) from 177 CS patients in the CardShock study. Kinetics of GDF-15, its association with 90-day mortality, and incremental value for risk stratification were assessed. The median GDF-150h level was 9647 ng/L (IQR 4500-19,270 ng/L) and levels above median were significantly associated with acidosis, hyperlactatemia, renal dysfunction, and higher 90-day mortality (56% vs 28%, P < .001). Serial sampling showed that non-survivors had significantly higher GDF-15 levels at all time points (P < .001 for all). Furthermore, non-survivors displayed increasing and survivors declining GDF-15 levels during the first days in CS. Higher levels of GDF-15 were independently associated with mortality. A GDF-1512h cutoff >7000 ng/L was identified as a strong predictor of death (OR 5.0; 95% CI 1.9-3.8, P = .002). Adding GDF-1512h >7000 ng/L to the CardShock risk score improved discrimination and risk stratification for 90-day mortality.Conclusions: GDF-15 levels are highly elevated in CS and associated with markers of systemic hypoperfusion and end-organ dysfunction. GDF-15 helps to discriminate survivors from non-survivors very early in CS. [ABSTRACT FROM AUTHOR]- Published
- 2019
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26. Acute kidney injury in cardiogenic shock: definitions, incidence, haemodynamic alterations, and mortality.
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Tarvasmäki, Tuukka, Haapio, Mikko, Mebazaa, Alexandre, Sionis, Alessandro, Silva‐Cardoso, José, Tolppanen, Heli, Lindholm, Matias Greve, Pulkki, Kari, Parissis, John, Harjola, Veli‐Pekka, Lassus, Johan, on behalf of the CardShock Study Investigators, Silva-Cardoso, José, Harjola, Veli-Pekka, and CardShock Study Investigators
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CARDIOGENIC shock ,HEMODYNAMIC monitoring ,KIDNEY injuries ,CREATININE ,MORTALITY - Abstract
Copyright of European Journal of Heart Failure is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2018
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27. Current real-life use of vasopressors and inotropes in cardiogenic shock - adrenaline use is associated with excess organ injury and mortality
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Tarvasmäki, Tuukka, Lassus, Johan, Varpula, Marjut, Sionis, Alessandro, Sund, Reijo, Kober, Lars, Spinar, Jindrich, Parissis, John, Banaszewski, Marek, Cardoso, Jose Silva, Carubelli, Valentina, Di Somma, Salvatore, Mebazaa, Alexandre, Harjola, Veli-Pekka, CardShock Study Investigators, Clinicum, Department of Diagnostics and Therapeutics, Department of Medicine, Kardiologian yksikkö, and Department of Social Research (2010-2017)
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Male ,Letter ,Survival ,Propensity score ,ILL PATIENTS ,030204 cardiovascular system & hematology ,Critical Care and Intensive Care Medicine ,0302 clinical medicine ,Inotropes ,SUPPORT ,Vasoconstrictor Agents ,Myocardial infarction ,Hospital Mortality ,Cardiogenic shock ,Middle Aged ,3. Good health ,NOREPINEPHRINE ,Shock (circulatory) ,Cardiology ,adrenaline ,cardiogenic shock ,inotropes ,mortality ,propensity score ,survival ,vasoactive medication ,vasopressors ,HEART-FAILURE ,Female ,medicine.symptom ,medicine.drug ,Vasoactive medication ,Adult ,Mean arterial pressure ,medicine.medical_specialty ,ACUTE MYOCARDIAL-INFARCTION ,Cardiotonic Agents ,Vasopressors ,Epinephrine ,Shock, Cardiogenic ,RENAL DYSFUNCTION ,Adrenaline ,03 medical and health sciences ,Internal medicine ,LOW-DOSE DOPAMINE ,medicine ,MANAGEMENT ,Humans ,Mortality ,Aged ,Tissue Survival ,business.industry ,Hemodynamics ,030208 emergency & critical care medicine ,Levosimendan ,medicine.disease ,3126 Surgery, anesthesiology, intensive care, radiology ,TRENDS ,RANDOMIZED-TRIAL ,Blood pressure ,Heart failure ,3121 General medicine, internal medicine and other clinical medicine ,Dobutamine ,business - Abstract
Background: Vasopressors and inotropes remain a cornerstone in stabilization of the severely impaired hemodynamics and cardiac output in cardiogenic shock (CS). The aim of this study was to analyze current real-life use of these medications, and their impact on outcome and on changes in cardiac and renal biomarkers over time in CS. Methods: The multinational CardShock study prospectively enrolled 219 patients with CS. The use of vasopressors and inotropes was analyzed in relation to the primary outcome, i.e., 90-day mortality, with propensity score methods in 216 patients with follow-up data available. Changes in cardiac and renal biomarkers over time until 96 hours from baseline were analyzed with linear mixed modeling. Results: Patients were 67 (SD 12) years old, 26 % were women, and 28 % had been resuscitated from cardiac arrest prior to inclusion. On average, systolic blood pressure was 78 (14) and mean arterial pressure 57 (11) mmHg at detection of shock. 90-day mortality was 41 %. Vasopressors and/or inotropes were administered to 94 % of patients and initiated principally within the first 24 hours. Noradrenaline and adrenaline were given to 75 % and 21 % of patients, and 30 % received several vasopressors. In multivariable logistic regression, only adrenaline (21 %) was independently associated with increased 90-day mortality (OR 5.2, 95 % CI 1.88, 14.7, p = 0.002). The result was independent of prior cardiac arrest (39 % of patients treated with adrenaline), and the association remained in propensity-score-adjusted analysis among vasopressor-treated patients (OR 3.0, 95 % CI 1.3, 7.2, p = 0.013); this was further confirmed by propensity-score-matched analysis. Adrenaline was also associated, independent of prior cardiac arrest, with marked worsening of cardiac and renal biomarkers during the first days. Dobutamine and levosimendan were the most commonly used inotropes (49 % and 24 %). There were no differences in mortality, whether noradrenaline was combined with dobutamine or levosimendan. Conclusion: Among vasopressors and inotropes, adrenaline was independently associated with 90-day mortality in CS. Moreover, adrenaline use was associated with marked worsening in cardiac and renal biomarkers. The combined use of noradrenaline with either dobutamine or levosimendan appeared prognostically similar.
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- 2016
28. Protein-based cardiogenic shock patient classifier.
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Rueda, Ferran, Borràs, Eva, García-García, Cosme, Iborra-Egea, Oriol, Revuelta-López, Elena, Harjola, Veli-Pekka, Cediel, Germán, Lassus, Johan, Tarvasmäki, Tuukka, Mebazaa, Alexandre, Sabidó, Eduard, and Bayés-Genís, Antoni
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Aims Cardiogenic shock (CS) is associated with high short-term mortality and a precise CS risk stratification could guide interventions to improve patient outcome. Here, we developed a circulating protein-based score to predict short-term mortality risk among patients with CS. Methods and results Mass spectrometry analysis of 2654 proteins was used for screening in the Barcelona discovery cohort (n = 48). Targeted quantitative proteomics analyses (n = 51 proteins) were used in the independent CardShock cohort (n = 97) to derive and cross-validate the protein classifier. The combination of four circulating proteins (Cardiogenic Shock 4 proteins—CS4P), discriminated patients with low and high 90-day risk of mortality. CS4P comprises the abundances of liver-type fatty acid-binding protein, beta-2-microglobulin, fructose-bisphosphate aldolase B, and SerpinG1. Within the CardShock cohort used for internal validation, the C-statistic was 0.78 for the CardShock risk score, 0.83 for the CS4P model, and 0.84 (P = 0.033 vs. CardShock risk score) for the combination of CardShock risk score with the CS4P model. The CardShock risk score with the CS4P model showed a marked benefit in patient reclassification, with a net reclassification improvement (NRI) of 0.49 (P = 0.020) compared with CardShock risk score. Similar reclassification metrics were observed in the IABP-SHOCK II risk score combined with CS4P (NRI =0.57; P = 0.032). The CS4P patient classification power was confirmed by enzyme-linked immunosorbent assay (ELISA). Conclusion A new protein-based CS patient classifier, the CS4P, was developed for short-term mortality risk stratification. CS4P improved predictive metrics in combination with contemporary risk scores, which may guide clinicians in selecting patients for advanced therapies. Download slide Download slide [ABSTRACT FROM AUTHOR]
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- 2019
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29. Circulating levels of microRNA 423‐5p are associated with 90 day mortality in cardiogenic shock.
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Jäntti, Toni, Segersvärd, Heli, Tolppanen, Heli, Tarvasmäki, Tuukka, Lassus, Johan, Devaux, Yvan, Vausort, Mélanie, Pulkki, Kari, Sionis, Alessandro, Bayes‐Genis, Antoni, Tikkanen, Ilkka, Lakkisto, Päivi, and Harjola, Veli‐Pekka
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MICRORNA ,CARDIOGENIC shock ,ACUTE coronary syndrome - Abstract
Aims: The role of microRNAs has not been studied in cardiogenic shock. We examined the potential role of miR‐423‐5p level to predict mortality and associations of miR‐423‐5p with prognostic markers in cardiogenic shock. Methods and results: We conducted a prospective multinational observational study enrolling consecutive cardiogenic shock patients. Blood samples were available for 179 patients at baseline to determine levels of miR‐423‐5p and other biomarkers. Patients were treated according to local practice. Main outcome was 90 day all‐cause mortality. Median miR‐423‐5p level was significantly higher in 90 day non‐survivors [median 0.008 arbitrary units (AU) (interquartile range 0.003–0.017) vs. 0.004 AU (0.002–0.009), P = 0.003]. miR‐423‐5p level above median was associated with higher lactate (median 3.7 vs. 2.4 mmol/L, P = 0.001) and alanine aminotransferase levels (median 68 vs. 35 IU/L, P < 0.001) as well as lower cardiac index (1.8 vs. 2.4, P = 0.04) and estimated glomerular filtration rate (56 vs. 70 mL/min/1.73 m2, P = 0.002). In Cox regression analysis, miR‐423‐5p level above median was associated with 90 day all‐cause mortality independently of established risk factors of cardiogenic shock [adjusted hazard ratio 1.9 (95% confidence interval 1.2–3.2), P = 0.01]. Conclusions: In cardiogenic shock patients, above median level of miR‐423‐5p at baseline is associated with markers of hypoperfusion and seems to independently predict 90 day all‐cause mortality. [ABSTRACT FROM AUTHOR]
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- 2019
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30. Clinical phenotypes and outcome of patients hospitalized for acute heart failure: the ESC Heart Failure Long-Term Registry.
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Chioncel, Ovidiu, Mebazaa, Alexandre, Harjola, Veli-Pekka, Coats, Andrew J., Piepoli, Massimo Francesco, Crespo-Leiro, Maria G., Laroche, Cecile, Seferovic, Petar M., Anker, Stefan D., Ferrari, Roberto, Ruschitzka, Frank, Lopez-Fernandez, Silvia, Miani, Daniela, Filippatos, Gerasimos, and Maggioni, Aldo P.
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BLOOD pressure ,CARDIOGENIC shock ,REPORTING of diseases ,HEART failure ,HOSPITAL care ,PATIENT aftercare ,LONGITUDINAL method ,SCIENTIFIC observation ,PULMONARY edema ,SURVIVAL ,TIME ,PHENOTYPES ,TREATMENT effectiveness ,ACUTE diseases ,ACUTE coronary syndrome - Abstract
Aims: To identify differences in clinical epidemiology, in-hospital management and 1-year outcomes among patients hospitalized for acute heart failure (AHF) and enrolled in the European Society of Cardiology Heart Failure Long-Term (ESC-HF-LT) Registry, stratified by clinical profile at admission. Methods and results: The ESC-HF-LT Registry is a prospective, observational study collecting hospitalization and 1-year follow-up data from 6629 AHF patients. Among AHF patients enrolled in the registry, 13.2% presented with pulmonary oedema (PO), 2.9% with cardiogenic shock (CS), 61.1% with decompensated heart failure (DHF), 4.8% with hypertensive heart failure (HT-HF), 3.5% with right heart failure (RHF) and 14.4% with AHF and associated acute coronary syndromes (ACS-HF). The 1-year mortality rate was 28.1% in PO, 54.0% in CS, 27.2% in DHF, 12.8% in HT-HF, 34.0% in RHF and 20.6% in ACS-HF patients. When patients were classified by systolic blood pressure (SBP) at initial presentation, 1-year mortality was 34.8% in patients with SBP <85 mmHg, 29.0% in those with SBP 85-110 mmHg, 21.2% in patients with SBP 110-140 mmHg and 17.4% in those with SBP >140 mmHg. These differences tended to diminish in the months post-discharge, and 1-year mortality for the patients who survived at least 6 months post-discharge did not vary significantly by either clinical profile or SBP classification. Conclusion Rates of adverse outcomes in AHF remain high, and substantial differences have been found when patients were stratified by clinical profile or SBP. However, patients who survived at least 6 months post-discharge represent a more homogeneous group and their 1-year outcome is less influenced by clinical profile or SBP at admission. [ABSTRACT FROM AUTHOR]
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- 2017
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31. Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology.
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Harjola, Veli‐Pekka, Mebazaa, Alexandre, Čelutkienė, Jelena, Bettex, Dominique, Bueno, Hector, Chioncel, Ovidiu, Crespo‐Leiro, Maria G., Falk, Volkmar, Filippatos, Gerasimos, Gibbs, Simon, Leite‐Moreira, Adelino, Lassus, Johan, Masip, Josep, Mueller, Christian, Mullens, Wilfried, Naeije, Robert, Nordegraaf, Anton Vonk, Parissis, John, Riley, Jillian P., and Ristic, Arsen
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RIGHT heart ventricle , *HEART failure , *CLINICAL trials , *LEFT heart ventricle , *HEART failure treatment , *PULMONARY circulation , *ECHOCARDIOGRAPHY , *HEART ventricle diseases , *PHYSIOLOGY , *DIAGNOSIS , *THERAPEUTICS - Abstract
Acute right ventricular (RV) failure is a complex clinical syndrome that results from many causes. Research efforts have disproportionately focused on the failing left ventricle, but recently the need has been recognized to achieve a more comprehensive understanding of RV anatomy, physiology, and pathophysiology, and of management approaches. Right ventricular mechanics and function are altered in the setting of either pressure overload or volume overload. Failure may also result from a primary reduction of myocardial contractility owing to ischaemia, cardiomyopathy, or arrhythmia. Dysfunction leads to impaired RV filling and increased right atrial pressures. As dysfunction progresses to overt RV failure, the RV chamber becomes more spherical and tricuspid regurgitation is aggravated, a cascade leading to increasing venous congestion. Ventricular interdependence results in impaired left ventricular filling, a decrease in left ventricular stroke volume, and ultimately low cardiac output and cardiogenic shock. Identification and treatment of the underlying cause of RV failure, such as acute pulmonary embolism, acute respiratory distress syndrome, acute decompensation of chronic pulmonary hypertension, RV infarction, or arrhythmia, is the primary management strategy. Judicious fluid management, use of inotropes and vasopressors, assist devices, and a strategy focusing on RV protection for mechanical ventilation if required all play a role in the clinical care of these patients. Future research should aim to address the remaining areas of uncertainty which result from the complexity of RV haemodynamics and lack of conclusive evidence regarding RV-specific treatment approaches. [ABSTRACT FROM AUTHOR]
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- 2016
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32. Recommendations on pre-hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine
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Mebazaa, Alexandre, Yilmaz, M. Birhan, Levy, Phillip, Ponikowski, Piotr, Peacock, W. Frank, Laribi, Said, Ristic, Arsen D., Lambrinou, Ekaterini, Masip, Josep, Riley, Jillian P., McDonagh, Theresa, Mueller, Christian, deFilippi, Christopher, Harjola, Veli‐Pekka, Thiele, Holger, Piepoli, Massimo F., Metra, Marco, Maggioni, Aldo, McMurray, John, and Dickstein, Kenneth
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HEART failure treatment ,HEART failure patients ,CARDIOGENIC shock ,EMERGENCY physicians ,HOSPITAL care - Abstract
Acute heart failure is a fatal syndrome. Emergency physicians, cardiologists, intensivists, nurses and other health care providers have to cooperate to provide optimal benefit. However, many treatment decisions are opinion-based and few are evidenced-based. This consensus paper provides guidance to practicing physicians and nurses to manage acute heart failure in the pre-hospital and hospital setting. Criteria of hospitalization and of discharge are described. Gaps in knowledge and perspectives in the management of acute heart failure are also detailed. This consensus paper on acute heart failure might help enable contiguous practice. [ABSTRACT FROM AUTHOR]
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- 2015
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33. Clinical picture and risk prediction of short-term mortality in cardiogenic shock.
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Harjola, Veli‐Pekka, Lassus, Johan, Sionis, Alessandro, Køber, Lars, Tarvasmäki, Tuukka, Spinar, Jindrich, Parissis, John, Banaszewski, Marek, Silva‐Cardoso, Jose, Carubelli, Valentina, Di Somma, Salvatore, Tolppanen, Heli, Zeymer, Uwe, Thiele, Holger, Nieminen, Markku S, and Mebazaa, Alexandre
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CARDIOGENIC shock , *ACUTE coronary syndrome , *PREDICTION models , *CORONARY angiography , *ETIOLOGY of diseases - Abstract
Aims The aim of this study was to investigate the clinical picture and outcome of cardiogenic shock and to develop a risk prediction score for short-term mortality. Methods and results The CardShock study was a multicentre, prospective, observational study conducted between 2010 and 2012. Patients with either acute coronary syndrome ( ACS) or non- ACS aetiologies were enrolled within 6 h from detection of cardiogenic shock defined as severe hypotension with clinical signs of hypoperfusion and/or serum lactate >2 mmol/L despite fluid resuscitation ( n = 219, mean age 67, 74% men). Data on clinical presentation, management, and biochemical variables were compared between different aetiologies of shock. Systolic blood pressure was on average 78 mmHg (standard deviation 14 mmHg) and mean arterial pressure 57 (11) mmHg. The most common cause (81%) was ACS (68% ST-elevation myocardial infarction and 8% mechanical complications); 94% underwent coronary angiography, of which 89% PCI. Main non- ACS aetiologies were severe chronic heart failure and valvular causes. In-hospital mortality was 37% ( n = 80). ACS aetiology, age, previous myocardial infarction, prior coronary artery bypass, confusion, low LVEF, and blood lactate levels were independently associated with increased mortality. The CardShock risk Score including these variables and estimated glomerular filtration rate predicted in-hospital mortality well (area under the curve 0.85). Conclusion Although most commonly due to ACS, other causes account for one-fifth of cases with shock. ACS is independently associated with in-hospital mortality. The CardShock risk Score, consisting of seven common variables, easily stratifies risk of short-term mortality. It might facilitate early decision-making in intensive care or guide patient selection in clinical trials. Trial registration NCT01374867. [ABSTRACT FROM AUTHOR]
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- 2015
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34. Acute heart failure: Clinical presentation, one-year mortality and prognostic factors
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Rudiger, Alain, Harjola, Veli-Pekka, Müller, Andreas, Mattila, Eero, Säila, Petrus, Nieminen, Markku, and Follath, Ferenc
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HEART failure , *CARDIAC patients , *MORTALITY , *DISEASE risk factors , *SYMPTOMS - Abstract
Abstract: Aims: Acute heart failure (HF) is a common but ill-defined clinical entity. We describe patients hospitalised with acute HF in regard of clinical presentation, mortality, and risk factors for an unfavourable outcome. Methods and results: We conducted a prospective study including 312 consecutive patients from two European centers hospitalised with acute HF, defined as new onset or worsening of symptoms and signs of HF within 7 days. The mean age was 73 years and 56% were men. Twenty-eight percent had de-novo acute HF and 72% a decompensation of chronic HF. Coronary heart disease (CHD) was the most frequent underlying heart disease, elevated blood pressure >150 mmHg and acute ischemia being the most important triggers. Four percent of the patients had cardiogenic shock, 13% presented with pulmonary edema. LV-EF was <35%, 35–50% and >50% in 35%, 32% and 33% of the patients, respectively. ICU-treatment was necessary in 39% of the patients. Thirty-day mortality (11%) was increased in the presence of shock or elevated troponin T levels. Twelve-month all-cause mortality (29%) increased in the presence of shock, left ventricular dysfunction, renal insufficiency, CHD, and age. Conclusions: This prospective study shows that despite modern treatment, morbidity and mortality of patients hospitalised with acute HF remain high. [Copyright &y& Elsevier]
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- 2005
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35. Association of miR-21-5p, miR-122-5p, and miR-320a-3p with 90-Day Mortality in Cardiogenic Shock.
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Hänninen, Mikko, Jäntti, Toni, Tolppanen, Heli, Segersvärd, Heli, Tarvasmäki, Tuukka, Lassus, Johan, Vausort, Mélanie, Devaux, Yvan, Sionis, Alessandro, Tikkanen, Ilkka, Harjola, Veli-Pekka, and Lakkisto, Päivi
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CARDIOGENIC shock ,INTRA-aortic balloon counterpulsation ,ACUTE coronary syndrome ,GLOMERULAR filtration rate ,ALANINE aminotransferase ,MORTALITY - Abstract
Cardiogenic shock (CS) is a life-threatening emergency. New biomarkers are needed in order to detect patients at greater risk of adverse outcome. Our aim was to assess the characteristics of miR-21-5p, miR-122-5p, and miR-320a-3p in CS and evaluate the value of their expression levels in risk prediction. Circulating levels of miR-21-5p, miR-122-5p, and miR-320a-3p were measured from serial plasma samples of 179 patients during the first 5–10 days after detection of CS, derived from the CardShock study. Acute coronary syndrome was the most common cause (80%) of CS. Baseline (0 h) levels of miR-21-5p, miR-122-5p, and miR-320a-3p were all significantly elevated in nonsurvivors compared to survivors (p < 0.05 for all). Above median levels at 0h of each miRNA were each significantly associated with higher lactate and alanine aminotransferase levels and decreased glomerular filtration rates. After adjusting the multivariate regression analysis with established CS risk factors, miR-21-5p and miR-320a-3p levels above median at 0 h were independently associated with 90-day all-cause mortality (adjusted hazard ratio 1.8 (95% confidence interval 1.1–3.0), p = 0.018; adjusted hazard ratio 1.9 (95% confidence interval 1.2–3.2), p = 0.009, respectively). In conclusion, circulating plasma levels of miR-21-5p, miR-122-5p, and miR-320a-3p at baseline were all elevated in nonsurvivors of CS and associated with markers of hypoperfusion. Above median levels of miR-21-5p and miR-320a-3p at baseline appear to independently predict 90-day all-cause mortality. This indicates the potential of miRNAs as biomarkers for risk assessment in cardiogenic shock. [ABSTRACT FROM AUTHOR]
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- 2020
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36. The type of acute heart failure and the costs of hospitalization
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Harjola, Veli-Pekka, Costa, Susana, Sund, Reijo, Ylikangas, Stiina, Siirilä-Waris, Krista, Melin, John, Peuhkurinen, Keijo, and Nieminen, Markku S.
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HOSPITAL costs , *LONGITUDINAL method , *HEART failure treatment , *CARDIOGENIC shock , *HOSPITAL admission & discharge , *MEDICAL economics , *HOSPITAL care , *THERAPEUTICS - Abstract
Abstract: Background: The costs of different classes of acute HF (AHF) are not known. Methods: AHF patients (N =620) were divided in a national, prospective, observational study into five clinical classes: cardiogenic shock, pulmonary oedema, congestive HF, hypertensive HF, and right HF. Index episode and 6-month readmissions were assessed and hospitalization costs were evaluated. Results: The length of index episode, ICU/CCU stay and costs of index episode and cumulative 6-month costs differed significantly between the clinical classes. The highest cumulative 6-month hospitalization costs, 25,963 (15,053–44778) € (mean, 95% confidence interval) incurred in cardiogenic shock, followed by pulmonary oedema, 12,912 (11,006–15,148) €, and congestive HF, 9475 (8550–10,500) €. Conclusions: AHF leads to significant need for hospital care and high costs which differ significantly between clinical classes of AHF. [ABSTRACT FROM AUTHOR]
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- 2010
- Full Text
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37. Kinetics of procalcitonin, C-reactive protein and interleukin-6 in cardiogenic shock – Insights from the CardShock study.
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Kataja, Anu, Tarvasmäki, Tuukka, Lassus, Johan, Sionis, Alessandro, Mebazaa, Alexandre, Pulkki, Kari, Banaszewski, Marek, Carubelli, Valentina, Hongisto, Mari, Jankowska, Ewa, Jurkko, Raija, Jäntti, Toni, Kasztura, Monika, Parissis, John, Sabell, Tuija, Silva-Cardoso, Jose, Spinar, Jindrich, Tolppanen, Heli, and Harjola, Veli-Pekka
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C-reactive protein , *CARDIOGENIC shock , *INTERLEUKIN-6 , *HEART diseases , *INFLAMMATION , *BLOOD lactate - Abstract
Inflammatory responses play an important role in the pathophysiology of cardiogenic shock (CS). The aim of this study was to investigate the kinetics of procalcitonin (PCT), C-reactive protein (CRP), and interleukin-6 (IL-6) in CS and to assess their relation to clinical presentation, other biochemical variables, and prognosis. Levels of PCT, CRP and IL-6 were analyzed in serial plasma samples (0−120 h) from 183 patients in the CardShock study. The study population was dichotomized by PCT max ≥ and < 0.5 μg/L, and IL-6 and CRP max above/below median. PCT peaked already at 24 h [median PCT max 0.71 μg/L (IQR 0.24–3.4)], whereas CRP peaked later between 48 and 72 h [median CRP max 137 mg/L (59–247)]. PCT levels were significantly higher among non-survivors compared with survivors from 12 h on, as were CRP levels from 24 h on (p < 0.001). PCT max ≥ 0.5 μg/L (60% of patients) was associated with clinical signs of systemic hypoperfusion, cardiac and renal dysfunction, acidosis, and higher levels of blood lactate, IL-6, growth-differentiation factor 15 (GDF-15), and CRP max. Similarly, IL-6 > median was associated with clinical signs and biochemical findings of systemic hypoperfusion. PCT max ≥ 0.5 μg/L and IL-6 > median were associated with increased 90-day mortality (50% vs. 30% and 57% vs. 22%, respectively; p < 0.01 for both), while CRP max showed no prognostic significance. The association of inflammatory markers with clinical infections was modest. Inflammatory markers are highly related to signs of systemic hypoperfusion in CS. Moreover, high PCT and IL-6 levels are associated with poor prognosis. • Inflammatory marker levels are considerably elevated during the first days of CS. • PCT peaks early at 24 h, while CRP continues to rise until 48 to 72 h in CS. • High levels of PCT and IL-6 are strongly associated with systemic hypoperfusion in CS. • High inflammatory marker levels are associated with increased mortality in CS. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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38. Organ dysfunction, injury and failure in acute heart failure: from pathophysiology to diagnosis and management. A review on behalf of the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)
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John Parissis, Marek Banaszewski, Christian Mueller, Petar M. Seferovic, Matthieu Legrand, Andreas Schaefer, Wilfried Mullens, Alain Rudiger, Wolfram Doehner, Andreas J. Flammer, Hadi Skouri, Hans-Peter Brunner-La Rocca, Johan Lassus, Valentin Fuhrmann, Veli-Pekka Harjola, Frank Ruschitzka, Gerasimos Filippatos, Mehmet Yilmaz, Zoltán Papp, Ovidiu Chioncel, Mitja Lainscak, Elke Platz, Josep Masip, Johann Bauersachs, Sean P. Collins, Alexandre Mebazaa, University of Zurich, Harjola, Veli-Pekka, [Harjola, Veli-Pekka] Univ Helsinki, Helsinki Univ Hosp, Emergency Med, Helsinki, Finland -- [Mullens, Wilfried] Ziekenhuis Oost Limburg, Dept Cardiol, Genk, Belgium -- [Mullens, Wilfried] Hasselt Univ, Biomed Res Inst, Fac Med & Life Sci, Diepenbeek, Belgium -- [Banaszewski, Marek] Intens Cardiac Therapy Clin, Inst Cardiol, Warsaw, Poland -- [Bauersachs, Johann -- Schaefer, Andreas] Med Sch Hannover, Dept Cardiol & Angiol, Hannover, Germany -- [Brunner-La Rocca, Hans-Peter] Maastricht Univ, Dept Cardiol, Med Ctr, Maastricht, Netherlands -- [Chioncel, Ovidiu] Univ Med & Pharm Carol Davila, Inst Emergency Cardiovasc Dis, Bucharest, Romania -- [Collins, Sean P.] Vanderbilt Univ, Med Ctr, Dept Emergency Med, Nashville, TN USA -- [Doehner, Wolfram] Ctr Stroke Res, Berlin, Germany -- [Doehner, Wolfram] Charite Med Univ, Dept Cardiol, Berlin, Germany -- [Filippatos, Gerasimos S. -- Parissis, John] Univ Athens, Athens Univ Hosp Attikon, Sch Med, Athens, Greece -- [Flammer, Andreas J. -- Ruschitzka, Frank] Univ Zurich Hosp, Univ Heart Ctr, Zurich, Switzerland -- [Fuhrmann, Valentin] Med Univ Vienna, Div Gastroenterol & Hepatol, Vienna, Austria -- [Fuhrmann, Valentin] Univ Med Ctr Hamburg Eppendorf, Dept Intens Care Med, Hamburg, Germany -- [Lainscak, Mitja] Gen Hosp Murska Sobota, Dept Internal Med, Murska Sobota, Slovenia -- [Lainscak, Mitja] Gen Hosp Murska Sobota, Dept Res & Educ, Murska Sobota, Slovenia -- [Lainscak, Mitja] Univ Ljubljana, Fac Med, Ljubljana, Slovenia -- [Lassus, Johan] Univ Helsinki, Helsinki Univ Hosp, Cardiol, Helsinki, Finland -- [Legrand, Matthieu -- Mebazaa, Alexandre] AP HP, INSERM, U942, Paris, France -- [Legrand, Matthieu -- Mebazaa, Alexandre] INI CRCT, Nancy, France -- [Legrand, Matthieu] Univ Paris Denis Diderot, St Louis Hosp, Dept Anaesthesiol, Crit Care & Burn Unit, Paris, France -- [Masip, Josep] Univ Barcelona, Consorci Sanitari Integral Publ Hlth Consortium, Barcelona, Spain -- [Masip, Josep] Hosp Sanitas CIMA, Dept Cardiol, Barcelona, Spain -- [Mueller, Christian] Univ Hosp Basel, Dept Cardiol, Basel, Switzerland -- [Mueller, Christian] Univ Hosp Basel, CRIB, Basel, Switzerland -- [Papp, Zoltan] Univ Debrecen, Div Clin Physiol, Dept Cardiol, Res Ctr Mol Med,Fac Med, Debrecen, Hungary -- [Platz, Elke] Harvard Med Sch, Brigham & Womens Hosp, Dept Emergency Med, Boston, MA USA -- [Rudiger, Alain] Univ Zurich, Univ Zurich Hosp, Cardiosurg Intens Care Unit, Zurich, Switzerland -- [Seferovic, Petar M.] Univ Belgrade, Dept Internal Med, Sch Med, Belgrade, Serbia -- [Seferovic, Petar M.] Univ Belgrade, Heart Failure Ctr, Med Ctr, Belgrade, Serbia -- [Skouri, Hadi] Amer Univ, Div Cardiol, Dept Internal Med, Beirut Med Ctr, Beirut, Lebanon -- [Yilmaz, Mehmet Birhan] Cumhuriyet Univ, Dept Cardiol, Fac Med, Sivas, Turkey -- [Mebazaa, Alexandre] Univ Paris Diderot, Paris, France -- [Mebazaa, Alexandre] Univ Hosp St Louis Lariboisiere, Dept Anaesthesia & Crit Care, Paris, France, YILMAZ, Mehmet Birhan -- 0000-0002-8169-8628, Chioncel, Ovidiu -- 0000-0002-3197-3628, YILMAZ, MEHMET BIRHAN -- 0000-0002-8169-8628, Mebazaa, Alexandre -- 0000-0001-8715-7753, Rudiger, Alain -- 0000-0001-7943-7624, and Flammer, Andreas -- 0000-0002-1373-0630
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INTENSIVE-CARE-UNIT ,LIVER-FUNCTION TESTS ,030204 cardiovascular system & hematology ,law.invention ,0302 clinical medicine ,law ,030212 general & internal medicine ,Myocardial infarction ,Elméleti orvostudományok ,Societies, Medical ,medicine.diagnostic_test ,Cardiogenic shock ,Acute kidney injury ,Disease Management ,EMERGENCY-DEPARTMENT PATIENTS ,Orvostudományok ,Intensive care unit ,3. Good health ,Europe ,Acute Disease ,Cardiology ,10209 Clinic for Cardiology ,medicine.symptom ,3RD UNIVERSAL DEFINITION ,Cardiology and Cardiovascular Medicine ,Diagnostic Imaging ,medicine.medical_specialty ,ACUTE MYOCARDIAL-INFARCTION ,10216 Institute of Anesthesiology ,ACUTE KIDNEY INJURY ,610 Medicine & health ,Heart failure ,2705 Cardiology and Cardiovascular Medicine ,Article ,03 medical and health sciences ,GELATINASE-ASSOCIATED LIPOCALIN ,CARDIOGENIC PULMONARY-EDEMA ,Internal medicine ,medicine ,Humans ,Intensive care medicine ,business.industry ,Organ dysfunction ,medicine.disease ,WORSENING RENAL-FUNCTION ,NATRIURETIC PEPTIDE LEVELS ,Multiple organ failure ,Venous congestion ,Clinical trial ,Liver function tests ,business - Abstract
WOS: 000405571400002, PubMed ID: 28560717, Organ injury and impairment are commonly observed in patients with acute heart failure (AHF), and congestion is an essential pathophysiological mechanism of impaired organ function. Congestion is the predominant clinical profile in most patients with AHF; a smaller proportion presents with peripheral hypoperfusion or cardiogenic shock. Hypoperfusion further deteriorates organ function. The injury and dysfunction of target organs (i.e. heart, lungs, kidneys, liver, intestine, brain) in the setting of AHF are associated with increased risk for mortality. Improvement in organ function after decongestive therapies has been associated with a lower risk for post-discharge mortality. Thus, the prevention and correction of organ dysfunction represent a therapeutic target of interest in AHF and should be evaluated in clinical trials. Treatment strategies that specifically prevent, reduce or reverse organ dysfunction remain to be identified and evaluated to determine if such interventions impact mortality, morbidity and patient-centred outcomes. This paper reflects current understanding among experts of the presentation and management of organ impairment in AHF and suggests priorities for future research to advance the field., Heart Failure Association of the European Society of Cardiology, This work was supported by the Heart Failure Association of the European Society of Cardiology.
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- 2017
39. Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology
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Harjola, V-P, Mebazaa, A, Celutkiene, J, Bettex, D, Bueno, H, Chioncel, O, Crespo-Leiro, MG, Falk, V, Filippatos, G, Gibbs, S, Leite-Moreira, A, Lassus, J, Masip, J, Mueller, C, Mullens, W, Naeije, R, Nordegraaf, AV, Parissis, J, Riley, JP, Ristic, A, Rosano, G, Rudiger, A, Ruschitzka, F, Seferovic, P, Sztrymf, B, Vieillard-Baron, A, Yilmaz, MB, Konstantinides, S, University of Zurich, Harjola, Veli-Pekka, [Harjola, Veli-Pekka] Univ Helsinki, Helsinki Univ Hosp, Dept Emergency Med & Serv, Emergency Med, Helsinki, Finland -- [Mebazaa, Alexandre] Univers Paris Diderot, Sorbonne Paris Cite, Paris, France -- [Mebazaa, Alexandre] AP HP, Inserm U942, Paris, France -- [Mebazaa, Alexandre] Hop Univ St Louis Lariboisiere, AP HP, Dept Anaesthesia & Crit Care, Paris, France -- [Celutkiene, Jelena] Vilnius Univ, Fac Med, Clin Cardiac & Vasc Dis, Vilnius, Lithuania -- [Bettex, Dominique] Univ Zurich Hosp, Inst Anaesthesiol, Zurich, Switzerland -- [Bueno, Hector] Hosp Univ 12 Octubre, CNIC, Madrid, Spain -- [Bueno, Hector] Hosp Univ 12 Octubre, Inst Invest I 12, Madrid, Spain -- [Bueno, Hector] Hosp Univ 12 Octubre, Dept Cardiol, Madrid, Spain -- [Bueno, Hector] Univ Complutense Madrid, E-28040 Madrid, Spain -- [Chioncel, Ovidiu] Univ Med & Pharm Carol Davila, Inst Emergency Cardiovasc Dis, Bucharest, Romania -- [Crespo-Leiro, Maria G.] CHUAC, Complexo Hosp Univ A Coruna, Unidad Insuficiencia Cardiaca Avanzada & Trasplan, La Coruna, Spain -- [Falk, Volkmar] Deutsch Herzzentrum Berlin, Dept Cardiothorac & Vasc Surg, Berlin, Germany -- [Filippatos, Gerasimos] Athens Univ Hosp Attikon, Athens, Greece -- [Gibbs, Simon -- Riley, Jillian P.] Univ London Imperial Coll Sci Technol & Med, London, England -- [Leite-Moreira, Adelino] Univ Porto, Fac Med, Dept Fisiol & Cirurgia Cardiotorac, Rua Campo Alegre 823, P-4100 Oporto, Portugal -- [Lassus, Johan] Univ Helsinki, Helsinki Univ Hosp, Cardiol, Helsinki, Finland -- [Masip, Josep] Univ Barcelona, Hosp St Joan Despi Moises Broggi, Barcelona, Spain -- [Masip, Josep] Univ Barcelona, Hosp Gen Hosp, Barcelona, Spain -- [Mueller, Christian] Univ Basel Hosp, Dept Cardiol, CH-4031 Basel, Switzerland -- [Mueller, Christian] Univ Basel Hosp, CRIB, CH-4031 Basel, Switzerland -- [Mullens, Wilfried] Hasselt Univ, Fac Med & Life Sci, Genk Biomed Res Inst, Dept Cardiol,Ziekenhuis Oost Limburg, Diepenbeek, Belgium -- [Nordegraaf, Anton Vonk] Free Univ Brussels, Dept Phys, Fac Med, 808 Route Lennik, Brussels, Belgium -- [Parissis, John] Vrije Univ Amsterdam, Medisch Centrum, Amsterdam, Netherlands -- [Parissis, John] Attikon Univ Hosp, Athens, Greece -- [Ristic, Arsen] Clin Ctr Serbia, Dept Cardiol, Belgrade, Serbia -- [Ristic, Arsen] Univ Belgrade, Sch Med, Belgrade, Serbia -- [Rosano, Giuseppe] IRCCS San Raffaele Hosp Roma, Rome, Italy -- [Rosano, Giuseppe] St Georges Univ London, Cardiovasc & Cell Sci Inst, London, England -- [Rudiger, Alain] Univ Hosp, Cardiosurg Intens Care Unit, Zurich, Switzerland -- [Ruschitzka, Frank] Univ Heart Ctr Zurich, Dept Cardiol Heart Failure Clin & Transplantat, Zurich, Switzerland -- [Seferovic, Petar] Univ Belgrade, Sch Med, Dept Internal Med, Belgrade, Serbia -- [Seferovic, Petar] Univ Belgrade, Heart Failure Ctr, Med Ctr, Belgrade, Serbia -- [Sztrymf, Benjamin] Hop Univ Paris Sud, AP HP, Hop Antoine Beclere, Reanimat Polyvalente, Clamart, France -- [Vieillard-Baron, Antoine] INSERM U 1018, CESP, UVSQ, Team 5,EpReC Renal & Cardiovasc Epidemiol, Villejuif, France -- [Vieillard-Baron, Antoine] Univ Hosp Ambroise Pare, AP HP, Boulogne, France -- [Yilmaz, Mehmet Birhan] Cumhuriyet Univ, Fac Med, Dept Cardiol, Sivas, Turkey -- [Konstantinides, Stavros] Univ Med Ctr Mainz, CTH, Mainz, Germany -- [Konstantinides, Stavros] Democritus Univ Thrace, Dept Cardiol, Alexandroupolis, Greece, YILMAZ, MEHMET BIRHAN -- 0000-0002-8169-8628, Lamonaca, Palma -- 0000-0003-4891-2255, Celutkiene, Jelena -- 0000-0003-3562-9274, Chioncel, Ovidiu -- 0000-0002-3197-3628, Bueno, Hector -- 0000-0003-0277-7596, YILMAZ, Mehmet Birhan -- 0000-0002-8169-8628, Rudiger, Alain -- 0000-0001-7943-7624, Leite-Moreira, Adelino -- 0000-0001-7808-3596, Mebazaa, Alexandre -- 0000-0001-8715-7753, and Falk, Volkmar -- 0000-0002-7911-8620
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Pulmonary Circulation ,Cardiac & Cardiovascular Systems ,INTENSIVE-CARE-UNIT ,10216 Institute of Anesthesiology ,Ventricular Dysfunction, Right ,RESPIRATORY-DISTRESS-SYNDROME ,Heart failure ,610 Medicine & health ,TROPONIN-T ASSAY ,1102 Cardiovascular Medicine And Haematology ,2705 Cardiology and Cardiovascular Medicine ,ASSIST DEVICE ,Humans ,cardiovascular diseases ,Right ventricular dysfunction ,Cardiogenic shock ,INFERIOR MYOCARDIAL-INFARCTION ,Heart Failure ,Science & Technology ,Right ventricular function ,ACUTE COR-PULMONALE ,Cardiovascular System & Hematology ,CARDIOVASCULAR-DISEASE ,Echocardiography ,Intensive care ,CARDIOGENIC-SHOCK ,Cardiovascular System & Cardiology ,cardiovascular system ,10209 Clinic for Cardiology ,ARTERIAL-HYPERTENSION ,Life Sciences & Biomedicine ,TASK-FORCE - Abstract
WOS: 000373160000002, PubMed ID: 26995592, Acute right ventricular (RV) failure is a complex clinical syndrome that results from many causes. Research efforts have disproportionately focused on the failing left ventricle, but recently the need has been recognized to achieve a more comprehensive understanding of RV anatomy, physiology, and pathophysiology, and of management approaches. Right ventricular mechanics and function are altered in the setting of either pressure overload or volume overload. Failure may also result from a primary reduction of myocardial contractility owing to ischaemia, cardiomyopathy, or arrhythmia. Dysfunction leads to impaired RV filling and increased right atrial pressures. As dysfunction progresses to overt RV failure, the RV chamber becomes more spherical and tricuspid regurgitation is aggravated, a cascade leading to increasing venous congestion. Ventricular interdependence results in impaired left ventricular filling, a decrease in left ventricular stroke volume, and ultimately low cardiac output and cardiogenic shock. Identification and treatment of the underlying cause of RV failure, such as acute pulmonary embolism, acute respiratory distress syndrome, acute decompensation of chronic pulmonary hypertension, RV infarction, or arrhythmia, is the primary management strategy. Judicious fluid management, use of inotropes and vasopressors, assist devices, and a strategy focusing on RV protection for mechanical ventilation if required all play a role in the clinical care of these patients. Future research should aim to address the remaining areas of uncertainty which result from the complexity of RV haemodynamics and lack of conclusive evidence regarding RV-specific treatment approaches.
- Published
- 2016
40. Recommendations on pre-hospitalearly hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine
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Ekaterini Lambrinou, Kenneth Dickstein, Holger Thiele, Alexandre Mebazaa, Theresa McDonagh, Stefan D. Anker, Gerasimos Filippatos, Aldo P. Maggioni, Arsen D. Ristić, Phillip D. Levy, Jillian P. Riley, Massimo F Piepoli, Said Laribi, Abdelouahab Bellou, John J.V. McMurray, Adelino F. Leite-Moreira, Kevin Damman, Marco Metra, Josep Masip, W. Frank Peacock, M. Birhan Yilmaz, Piotr Ponikowski, Veli-Pekka Harjola, Christopher DeFilippi, Christian Mueller, Petar M. Seferovic, Frank Ruschitzka, Λαμπρινού, Αικατερίνη, [Mebazaa, Alexandre] Univ Paris Diderot, Sorbonne Paris Cite, INSERM, U942,Hop Lariboisiere,St Louis Univ Hosp, Paris, France -- [Yilmaz, M. Birhan] Cumhuriyet Univ, Fac Med, Dept Cardiol, TR-58140 Sivas, Turkey -- [Levy, Phillip] Wayne State Univ, Sch Med, Dept Emergency Med, Detroit, MI USA -- [Levy, Phillip] Wayne State Univ, Sch Med, Cardiovasc Res Inst, Detroit, MI USA -- [Ponikowski, Piotr] Wroclaw Med Univ, Mil Hosp 4, PL-50981 Wroclaw, Poland -- [Peacock, W. Frank] Baylor Coll Med, Ben Taub Gen Hosp, Houston, TX 77030 USA -- [Laribi, Said] Grp Hosp St Louis Lariboisiere, AP HP, INSERM, U942, Paris, France -- [Ristic, Arsen D.] Clin Ctr Serbia, Dept Cardiol, Belgrade, Serbia -- [Ristic, Arsen D.] Univ Belgrade, Sch Med, Belgrade, Serbia -- [Lambrinou, Ekaterini] Cyprus Univ Technol, Sch Hlth Sci, Dept Nursing, Limassol, Cyprus -- [Masip, Josep] Univ Barcelona, Hosp St Joan Despi Moises Broggi, Consorci Sanitari Integral, Barcelona, Spain -- [Masip, Josep] Univ Barcelona, Hosp Gen Hosp, Barcelona, Spain -- [Riley, Jillian P.] Univ London Imperial Coll Sci Technol & Med, London, England -- [McDonagh, Theresa] Kings Coll Hosp London, London, England -- [Mueller, Christian] Univ Basel Hosp, Dept Cardiol, CH-4031 Basel, Switzerland -- [deFilippi, Christopher] Univ Maryland, Sch Med, Div Cardiovasc Med, Baltimore, MD 21201 USA -- [Harjola, Veli-Pekka] Univ Helsinki, Helsinki Univ Hosp, Emergency Med, Helsinki, Finland -- [Thiele, Holger] Med Univ Lubeck, Univ Hosp Schleswig Holstein, Med Clin 2, D-23538 Lubeck, Germany -- [Piepoli, Massimo F.] AUSL Piacenza, Guglielmo da Saliceto Hosp, Dept Cardiac, Heart Failure Unit, Piacenza, Italy -- [Metra, Marco] Univ Brescia, Dept Med & Surg Specialties Radiol Sci & Publ Hlt, Cardiol, Brescia, Italy -- [Maggioni, Aldo] ANMCO Resarch Ctr, Florence, Italy -- [McMurray, John J. V.] Univ Glasgow, BHF Cardiovasc Res Ctr, Glasgow, Lanark, Scotland -- [Dickstein, Kenneth] Univ Bergen, Stavanger Univ Hosp, Bergen, Norway -- [Damman, Kevin] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands -- [Seferovic, Petar M.] Univ Belgrade, Fac Med, Belgrade, Serbia -- [Seferovic, Petar M.] Univ Med Ctr, Dept Cardiol, Belgrade, Serbia -- [Ruschitzka, Frank] Univ Heart Ctr, Dept Cardiol, CH-8091 Zurich, Switzerland -- [Leite-Moreira, Adelino F.] Univ Porto, Fac Med, Dept Physiol & Cardiothorac Surg, P-4100 Oporto, Portugal -- [Leite-Moreira, Adelino F.] Ctr Hosp Sao Joao, Dept Cardiothorac Surg, Oporto, Portugal -- [Bellou, Abdelouahab] Harvard Univ, Sch Med, Boston, MA USA -- [Bellou, Abdelouahab] Beth Israel Deaconess Med Ctr, Dept Emergency Med, Boston, MA 02215 USA -- [Bellou, Abdelouahab] Univ Rennes 1, Fac Med, Rennes, France -- [Anker, Stefan D.] Charite, Dept Cardiol, Div Appl Cachexia Res, Berlin, Germany -- [Anker, Stefan D.] Univ Med Ctr Gottingen UMG, Dept Cardiol, Div Innovat Clin Trials, Gottingen, Germany -- [Filippatos, Gerasimos] Univ Athens, Sch Med, Attikon Univ Hosp, Dept Cardiol, GR-11527 Athens, Greece, YILMAZ, MEHMET BIRHAN -- 0000-0002-8169-8628, YILMAZ, Mehmet Birhan -- 0000-0002-8169-8628, Leite-Moreira, Adelino -- 0000-0001-7808-3596, piepoli, massimo francesco -- 0000-0003-1124-234X, Ponikowski, Piotr -- 0000-0002-3391-7064, Mebazaa, Alexandre -- 0000-0001-8715-7753, mcmurray, john -- 0000-0002-6317-3975, Bellou, Abdelouahab -- 0000-0003-3457-5585, University of Zurich, Mebazaa, Alexandre, Cardiovascular Centre (CVC), and [Mebazaa, Alexandre] Univ Paris Diderot, Lariboisiere St Louis Univ Hosp, AP HP, Sorbonne Paris Cite, Paris, France -- [Yilmaz, M. Birhan] Cumhuriyet Univ, Fac Med, Dept Cardiol, TR-58140 Sivas, Turkey -- [Levy, Phillip] Wayne State Univ, Sch Med, Dept Emergency Med, Detroit, MI USA -- [Levy, Phillip] Wayne State Univ, Sch Med, Cardiovasc Res Inst, Detroit, MI USA -- [Ponikowski, Piotr] Wroclaw Med Univ, Mil Hosp 4, PL-50981 Wroclaw, Poland -- [Peacock, W. Frank] Ben Taub Gen Hosp, Baylor Coll Med, Houston, TX 77030 USA -- [Laribi, Said] INSERM, UMRS 942, Paris, France -- [Ristic, Arsen D.] Clin Ctr Serbia, Dept Cardiol, Belgrade, Serbia -- [Ristic, Arsen D.] Univ Belgrade, Sch Med, Belgrade, Serbia -- [Lambrinou, Ekaterini] Cyprus Univ Technol, Sch Hlth Sci, Dept Nursing, Limassol, Cyprus -- [Masip, Josep] Univ Barcelona, Hosp St Joan DespiMoises Broggi, Consorci Sanitari Integral, Barcelona, Spain -- [Masip, Josep] Univ Barcelona, Hosp Gen Hosp, Barcelona, Spain -- [Riley, Jillian P.] Univ London Imperial Coll Sci Technol & Med, London, England -- [McDonagh, Theresa] Kings Coll Hosp London, London, England -- [Mueller, Christian] Univ Basel Hosp, Dept Cardiol, CH-4031 Basel, Switzerland -- [deFilippi, Christopher] Univ Maryland, Sch Med, Div Cardiovasc Med, Baltimore, MD 21201 USA -- [Harjola, Veli-Pekka] Univ Helsinki, Helsinki Univ Hosp, Emergency Med, Helsinki, Finland -- [Thiele, Holger] Med Univ Lubeck, Univ Hosp Schleswig Holstein, Med Clin 2, D-23538 Lubeck, Germany -- [Piepoli, Massimo F.] AUSL Piacenza, Guglielmo da Saliceto Hosp, Dept Cardiac, Heart Failure Unit, Piacenza, Italy -- [Metra, Marco] Univ Brescia, Dept Med & Surg Specialties Radiol Sci & Publ Hlt, Cardiol, Brescia, Italy -- [Maggioni, Aldo] ANMCO Resarch Ctr, Fireze, Italy -- [McMurray, John] Univ Glasgow, BHF Cardiovasc Res Ctr, Glasgow, Lanark, Scotland -- [Dickstein, Kenneth] Univ Bergen, Stavanger Univ Hosp, Bergen, Norway -- [Damman, Kevin] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands -- [Seferovic, Petar M.] Univ Belgrade, Fac Med, Belgrade, Serbia -- [Seferovic, Petar M.] Univ Med Ctr, Dept Cardiol, Belgrade, Serbia -- [Ruschitzka, Frank] Univ Heart Ctr, Dept Cardiol, CH-8091 Zurich, Switzerland -- [Leite-Moreira, Adelino F.] Univ Porto, Fac Med, Dept Physiol & Cardiothorac Surg, P-4100 Oporto, Portugal -- [Leite-Moreira, Adelino F.] Ctr Hosp Sao Joao, Dept Cardiothorac Surg, Oporto, Portugal -- [Bellou, Abdelouahab] Harvard Univ, Sch Med, Boston, MA USA -- [Bellou, Abdelouahab] Beth Israel Deaconess Med Ctr, Dept Emergency Med, Boston, MA 02215 USA -- [Bellou, Abdelouahab] Univ Rennes 1, Fac Med, Rennes, France -- [Anker, Stefan D.] Charite, Dept Cardiol, Div Appl Cachexia Res, Berlin, Germany -- [Anker, Stefan D.] Univ Med Ctr Groningen, Dept Cardiol, Div Innovat Clin Trials, Gottingen, Germany -- [Filippatos, Gerasimos] Univ Athens, Sch Med, Attikon Univ Hosp, Dept Cardiol, GR-11527 Athens, Greece
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Male ,Cardiac Care Facilities ,vasodilators ,Vasodilator Agents ,law.invention ,0302 clinical medicine ,DESIGN ,CLINICAL CHARACTERISTICS ,Health care ,Myocardial infarction ,Diuretics ,Societies, Medical ,Emergency Service ,OUTCOMES ,Evidence-Based Medicine ,Respiration ,cardiogenic shock ,3. Good health ,Administration ,Artificial ,Acute Disease ,10209 Clinic for Cardiology ,Emergency medicine ,TRIAL ,Emergency Service, Hospital ,Cardiology and Cardiovascular Medicine ,Oral ,medicine.medical_specialty ,Infusions ,ACUTE MYOCARDIAL-INFARCTION ,Shock, Cardiogenic ,Heart failure ,Acute ,2705 Cardiology and Cardiovascular Medicine ,03 medical and health sciences ,Hospital ,Intensive care ,Medical ,Humans ,Intensive care medicine ,Aged ,Heart Failure ,Clinical Laboratory Techniques ,NATRIURETIC PEPTIDE ,Oxygen Inhalation Therapy ,Administration, Oral ,Algorithms ,Consensus ,Critical Care ,Emergency Medical Services ,Female ,Heart-Assist Devices ,Hospitalization ,Infusions, Intravenous ,Nurse's Role ,Oxygen ,Patient Discharge ,Respiration, Artificial ,Evidence-based medicine ,medicine.disease ,Coronary care unit ,Coronary care units ,Treatment decision making ,Clinical Medicine ,TASK-FORCE ,Hospital setting ,RATIONALE ,030204 cardiovascular system & hematology ,Medical and Health Sciences ,Health administration ,law ,030212 general & internal medicine ,Cardiogenic shock ,ISOSORBIDE-DINITRATE ,Vasodilators ,Shock ,Intensive care unit ,Europe ,Practice Guidelines as Topic ,Emergency Medicine ,Noninvasive ventilation ,Medical emergency ,Intravenous ,Cardiology ,Context (language use) ,610 Medicine & health ,NONINVASIVE VENTILATION ,CARDIOGENIC PULMONARY-EDEMA ,medicine ,Task force ,business.industry ,Acute heart failure ,diuretics ,Emergency department ,Cardiogenic ,SCIENTIFIC STATEMENT ,Hospital administration ,RELAX-AHF ,Societies ,business - Abstract
WOS: 000356799600005, PubMed ID: 25999021, Acute heart failure is a fatal syndrome. Emergency physicians, cardiologists, intensivists, nurses and other health care providers have to cooperate to provide optimal benefit. However, many treatment decisions are opinion-based and few are evidenced-based. This consensus paper provides guidance to practicing physicians and nurses to manage acute heart failure in the pre-hospital and hospital setting. Criteria of hospitalization and of discharge are described. Gaps in knowledge and perspectives in the management of acute heart failure are also detailed. This consensus paper on acute heart failure might help enable contiguous practice., Bayer; Cardiorentis; Medicine Company; Critical Diagnostics; Novartis; Steering Committee member of Cardiorentis; TUBITAK; Medicines Company; Cornerstone Therapeutics; Otsuka; Janssen; Apex Innovations; Inte-Section Medical; Trevena; Vifor Pharma Ltd; Amgen; Servier; Abbott Vascular; Coridea; Respicardia; Swiss National Science Foundation; Swiss Heart Foundation; Cardiovascular Research Foundation Basel; 8sense; Abbott; ALERE; Brahms; Nanosphere; Roche; Siemens; University Hospital Basel; Astra Zeneca; BG medicine; Biomerieux; Lilly; Orion; Resmed; Roche Diagnostics; Ratiopharm; BMS; Boehringer-Ingelheim; Pfizer; Daiichi Sankyo; Boehinger Ingelheim; AstraZeneca; European Union, A.M. received speaker's honoraria from Alere, Bayer, Edwards Life Sciences, The Medicines Company, Novartis, Orion, Servier, Thermofisher, Vifor Pharma and also received fee as member of advisory board and/or Steering Committee from Bayer, Cardiorentis, The Medicine Company, Critical Diagnostics.; M.B.Y. received speaker's honoraria and research fee from Novartis and received fee as Steering Committee member of Cardiorentis, and is supported by TUBITAK.; P.L. received speaker's honoraria from Beckman Coulter and Novartis and also received fees as a member of advisory board and/or Steering Committee from Bayer, Cardiorentis, The Medicines Company, Cornerstone Therapeutics, Novartis, Otsuka, Janssen, Apex Innovations, Inte-Section Medical, and Trevena.; P.P. received speaker's honoraria from Bayer, Novartis, Servier, Vifor Pharma, Amgen, Pfizer, Cardiorentis, Merck-Serono, Abbott Vascular and Respicardia and also received fee as member of advisory board and/or Steering Committee from Bayer, Cardiorentis, Novartis, Vifor Pharma Ltd, Amgen, Servier, Abbott Vascular, Coridea and Respicardia.; E.L. received consultancy fee from Novartis.; J.M. received honoraria for speaker or advisor from Abbott, Novartis, Orion, Otsuka, and Sanofi and fee as a member of Steering Committee from Corthera, Novartis, and Cardiorentis.; C.M. received research grants from the Swiss National Science Foundation and the Swiss Heart Foundation, the Cardiovascular Research Foundation Basel, 8sense, Abbott, ALERE, Brahms, Critical Diagnostics, Nanosphere, Roche, Siemens, and the University Hospital Basel, as well as speaker/consulting honoraria from Astra Zeneca, Abbott, ALERE, BG medicine, Biomerieux, Brahms, Cardiorentis, Lilly, Novartis, Pfizer, Roche, and Siemens.; V.P.H. received speaker's fee: Bayer, Orion, Resmed, Roche Diagnostics, Ratiopharm; consultation fees: Bayer, BMS, Boehringer-Ingelheim, Novartis, Pfizer, Roche Diagnostics, Servier. H.A.T. received speaker's honoraria from Daiichi Sankyo, Lilly, Medicines Company, AstraZeneca, Boehinger Ingelheim. Advisory board for Maquet Cardiovascular. Institutional research support by Maquet Cardiovascular, Teleflex, Terumo, Lilly, The Medicine Company.; G.F. has received research grants and/or has served as Committee member or Cochair of studies sponsored by Bayer, Novartis, Cardiorentis, Vifor Pharma, and the European Union.
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- 2014
41. PROGNOSTIC VALUE OF CIRCULATING SECRETONEURIN CONCENTRATIONS IN PATIENTS WITH CARDIOGENIC SHOCK: THE CARDSHOCK STUDY.
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Omland, Torbjorn, Azibani, Feriel, Kimmmoun, Antoine, Harjola, Veli-Pekka, Lassus, Johan P.E., and Mebazaa, Alexandre
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CARDIOGENIC shock , *PROGNOSIS - Published
- 2023
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42. Combined Measurement of Soluble ST2 and Amino-Terminal Pro-B-Type Natriuretic Peptide Provides Early Assessment of Severity in Cardiogenic Shock Complicating Acute Coronary Syndrome.
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Sadoune, Malha, Tolppanen, Heli, Rivas-Lasarte, Mercedes, Gayat, Etienne, Mebazaa, Alexandre, Arrigo, Mattia, Krastinova, Evguenia, Parissis, John, Spinar, Jindrich, Januzzi, James, Harjola, Veli-Pekka, Lassus, Johan, Sionis, Alessandro, Pulkki, Kari, and CardShock Investigators
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ACUTE coronary syndrome , *CARDIOGENIC shock , *SEVERITY of illness index , *NATRIURETIC peptides , *MORTALITY , *BIOMARKERS , *PATIENTS , *THERAPEUTICS , *ACADEMIC medical centers , *COMPARATIVE studies , *INTENSIVE care units , *LONGITUDINAL method , *RESEARCH methodology , *MEDICAL cooperation , *PEPTIDE hormones , *PEPTIDES , *PROGNOSIS , *RESEARCH , *RISK assessment , *EVALUATION research , *DISEASE complications - Abstract
Objectives: Mortality in cardiogenic shock complicating acute coronary syndrome is high, and objective risk stratification is needed for rational use of advanced therapies such as mechanical circulatory support. Traditionally, clinical variables have been used to judge risk in cardiogenic shock. The aim of this study was to assess the added value of serial measurement of soluble ST2 and amino-terminal pro-B-type natriuretic peptide to clinical parameters for risk stratification in cardiogenic shock.Design: CardShock (www.clinicaltrials.gov NCT01374867) is a prospective European multinational study of cardiogenic shock. The main study introduced CardShock risk score, which is calculated from seven clinical variables at baseline, and was associated with short-term mortality.Setting: Nine tertiary care university hospitals.Patients: Patients with cardiogenic shock caused by acute coronary syndrome (n=145).Interventions: In this substudy, plasma samples from the study patients were analyzed at eight time points during the ICU or cardiac care unit stay. Additional prognostic value of the biomarkers was assessed with incremental discrimination improvement.Measurements and Main Results: The combination of soluble ST2 and amino-terminal pro-B-type natriuretic peptide showed excellent discrimination for 30-day mortality (area under the curve, 0.77 at 12 hr up to 0.93 at 5-10 d after cardiogenic shock onset). At 12 hours, patients with both biomarkers elevated (soluble ST2, ≥ 500 ng/mL and amino-terminal pro-B-type natriuretic peptide, ≥ 4,500 ng/L) had higher 30-day mortality (79%) compared to those with one or neither biomarkers elevated (31% or 10%, respectively; p < 0.001). Combined measurement of soluble ST2 and amino-terminal pro-B-type natriuretic peptide at 12 hours added value to CardShock risk score, correctly reclassifying 11% of patients.Conclusions: The combination of results for soluble ST2 and amino-terminal pro-B-type natriuretic peptide provides early risk assessment beyond clinical variables in patients with acute coronary syndrome-related cardiogenic shock and may help therapeutic decision making in these patients. [ABSTRACT FROM AUTHOR]- Published
- 2017
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43. Risk Stratification for Patients in Cardiogenic Shock After Acute Myocardial Infarction.
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Pöss, Janine, Köster, Jelena, Fuernau, Georg, Eitel, Ingo, de Waha, Suzanne, Thiele, Holger, Desch, Steffen, Ouarrak, Taoufik, Zeymer, Uwe, Lassus, Johan, and Harjola, Veli-Pekka
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CARDIOGENIC shock , *MYOCARDIAL infarction complications , *MYOCARDIAL infarction risk factors , *PATIENTS , *CARDIOVASCULAR system , *COMPARATIVE studies , *EXPERIMENTAL design , *INTRA-aortic balloon counterpulsation , *RESEARCH methodology , *MEDICAL care , *EVALUATION of medical care , *MEDICAL cooperation , *MORTALITY , *RESEARCH , *RISK assessment , *THROMBOLYTIC therapy , *EVALUATION research , *RANDOMIZED controlled trials , *KAPLAN-Meier estimator , *THERAPEUTICS ,MYOCARDIAL infarction-related mortality - Abstract
Background: Mortality in cardiogenic shock (CS) remains high. Early risk stratification is crucial to make adequate treatment decisions.Objectives: This study sought to develop an easy-to-use, readily available risk prediction score for short-term mortality in patients with CS, derived from the IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock) trial.Methods: The score was developed using a stepwise multivariable regression analysis.Results: Six variables emerged as independent predictors for 30-day mortality and were used as score parameters: age >73 years, prior stroke, glucose at admission >10.6 mmol/l (191 mg/dl), creatinine at admission >132.6 μmol/l (1.5 mg/dl), Thrombolysis In Myocardial Infarction flow grade <3 after percutaneous coronary intervention, and arterial blood lactate at admission >5 mmol/l. Either 1 or 2 points were attributed to each variable, leading to a score in 3 risk categories: low (0 to 2), intermediate (3 or 4), and high (5 to 9). The observed 30-day mortality rates were 23.8%, 49.2%, and 76.6%, respectively (p < 0.0001). Validation in the IABP-SHOCK II registry population showed good discrimination with an area under the curve of 0.79. External validation in the CardShock trial population (n = 137) showed short-term mortality rates of 28.0% (score 0 to 2), 42.9% (score 3 to 4), and 77.3% (score 5 to 9; p < 0.001) and an area under the curve of 0.73. Kaplan-Meier analysis revealed a stepwise increase in mortality between the different score categories (0 to 2 vs. 3 to 4: p = 0.04; 0 to 2 vs. 5 to 9: p = 0.008).Conclusions: The IABP-SHOCK II risk score can be easily calculated in daily clinical practice and strongly correlated with mortality in patients with infarct-related CS. It may help stratify patient risk for short-term mortality and might, thus, facilitate clinical decision making. (Intraaortic Balloon Pump in Cardiogenic Shock II [IABP-SHOCK II]; NCT00491036). [ABSTRACT FROM AUTHOR]- Published
- 2017
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44. Use of noninvasive and invasive mechanical ventilation in cardiogenic shock: A prospective multicenter study.
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Hongisto, Mari, Lassus, Johan, Tarvasmaki, Tuukka, Sionis, Alessandro, Tolppanen, Heli, Lindholm, Matias Greve, Banaszewski, Marek, Parissis, John, Spinar, Jindrich, Silva-Cardoso, Jose, Carubelli, Valentina, Di Somma, Salvatore, Masip, Josep, and Harjola, Veli-Pekka
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ACIDOSIS , *NONINVASIVE diagnostic tests , *CARDIOGENIC shock , *MYOCARDIAL infarction , *HEMODYNAMICS - Abstract
Background Despite scarce data, invasive mechanical ventilation (MV) is widely recommended over non-invasive ventilation (NIV) for ventilatory support in cardiogenic shock (CS). We assessed the real-life use of different ventilation strategies in CS and their influence on outcome focusing on the use of NIV and MV. Methods 219 CS patients were categorized by the maximum intensity of ventilatory support they needed during the first 24 h into MV ( n = 137; 63%) , NIV ( n = 26; 12%), and supplementary oxygen ( n = 56; 26%) groups. We compared the clinical characteristics and 90-day outcome between the MV and the NIV groups. Results Mean age was 67 years, 74% were men. The MV and NIV groups did not differ in age, medical history, etiology of CS, PaO 2 /FiO 2 ratio, baseline hemodynamics or LVEF. MV patients predominantly presented with hypoperfusion, with more severe metabolic acidosis, higher lactate levels and greater need for vasoactive drugs, whereas NIV patients tended to be more often congestive. 90-day outcome was significantly worse in the MV group (50% vs. 27%), but after propensity score adjustment, mortality was equal in both groups. Confusion, prior CABG, ACS etiology, higher lactate level, and lower baseline PaO 2 were independent predictors of mortality, whereas ventilation strategy did not have any influence on outcome. Conclusions Although MV is generally recommended mode of ventilatory support in CS, a fair number of patients were successfully treated with NIV. Moreover, ventilation strategy was not associated with outcome. Thus, NIV seems a safe option for properly chosen CS patients. [ABSTRACT FROM AUTHOR]
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- 2017
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45. The association of admission blood glucose level with the clinical picture and prognosis in cardiogenic shock – Results from the CardShock Study.
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Kataja, Anu, Tarvasmäki, Tuukka, Lassus, Johan, Cardoso, Jose, Mebazaa, Alexandre, Køber, Lars, Sionis, Alessandro, Spinar, Jindrich, Carubelli, Valentina, Banaszewski, Marek, Marino, Rossella, Parissis, John, Nieminen, Markku S., and Harjola, Veli-Pekka
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CARDIOGENIC shock , *BLOOD sugar measurement , *HYPERGLYCEMIA , *BIOMARKERS , *MORTALITY , *PATIENTS , *THERAPEUTICS - Abstract
Background Critically ill patients often present with hyperglycemia, regardless of previous history of diabetes mellitus (DM). Hyperglycemia has been associated with adverse outcome in acute myocardial infarction and acute heart failure. We investigated the association of admission blood glucose level with the clinical picture and short-term mortality in cardiogenic shock (CS). Methods Consecutively enrolled CS patients were divided into five categories according to plasma glucose level at the time of enrolment: hypoglycemia (glucose < 4.0 mmol/L), normoglycemia (4.0–7.9 mmol/L), mild (8.0–11.9 mmol/L), moderate (12.0–15.9 mmol/L), and severe (≥ 16.0 mmol/L) hyperglycemia. Clinical presentation, biochemistry, and short-term mortality were compared between the groups. Results Plasma glucose level of 211 CS patients was recorded. Glucose levels were distributed equally between normoglycemia (26% of patients), mild (27%), moderate (19%) and severe (25%) hyperglycemia, while hypoglycemia (2%) was rare. Severe hyperglycemia was associated with higher blood leukocyte count (17.3 (5.8) E9/L), higher lactate level (4.4 (3.3–8.4) mmol/L) and lower arterial pH (7.23 (0.14)) compared with normoglycemia or mild to moderate hyperglycemia (p < 0.001 for all). In-hospital mortality was highest among hypoglycemic (60%) and severely hyperglycemic (56%) patients, compared with 22% in normoglycemic group (p < 0.01). Severe hyperglycemia was an independent predictor of in-hospital mortality (OR 3.7, 95% CI 1.19–11.7, p = 0.02), when adjusted for age, gender, LVEF, lactate, and DM. Conclusions Admission blood glucose level has prognostic significance in CS. Mortality is highest among patients with severe hyperglycemia or hypoglycemia. Severe hyperglycemia is independently associated with high in-hospital mortality in CS. It is also associated with biomarkers of systemic hypoperfusion and stress response. [ABSTRACT FROM AUTHOR]
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- 2017
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46. The role of levosimendan in acute heart failure complicating acute coronary syndrome: A review and expert consensus opinion.
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Nieminen, Markku S., Buerke, Michael, Cohen-Solál, Alain, Costa, Susana, Édes, István, Erlikh, Alexey, Franco, Fatima, Gibson, Charles, Gorjup, Vojka, Guarracino, Fabio, Gustafsson, Finn, Harjola, Veli-Pekka, Husebye, Trygve, Karason, Kristjan, Katsytadze, Igor, Kaul, Sundeep, Kivikko, Matti, Marenzi, Giancarlo, Masip, Josep, and Matskeplishvili, Simon
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LEVOSIMENDAN , *ACUTE coronary syndrome , *CARDIOGENIC shock , *CLINICAL trials , *CARDIOLOGY - Abstract
Acute heart failure and/or cardiogenic shock are frequently triggered by ischemic coronary events. Yet, there is a paucity of randomized data on the management of patients with heart failure complicating acute coronary syndrome, as acute coronary syndrome and cardiogenic shock have frequently been defined as exclusion criteria in trials and registries. As a consequence, guideline recommendations are mostly driven by observational studies, even though these patients have a particularly poor prognosis compared to heart failure patients without signs of coronary artery disease. In acute heart failure, and especially in cardiogenic shock related to ischemic conditions, vasopressors and inotropes are used. However, both pathophysiological considerations and available clinical data suggest that these treatments may have disadvantageous effects. The inodilator levosimendan offers potential benefits due to a range of distinct effects including positive inotropy, restoration of ventriculo-arterial coupling, increases in tissue perfusion, and anti-stunning and anti-inflammatory effects. In clinical trials levosimendan improves symptoms, cardiac function, hemodynamics, and end-organ function. Adverse effects are generally less common than with other inotropic and vasoactive therapies, with the notable exception of hypotension. The decision to use levosimendan, in terms of timing and dosing, is influenced by the presence of pulmonary congestion, and blood pressure measurements. Levosimendan should be preferred over adrenergic inotropes as a first line therapy for all ACS-AHF patients who are under beta-blockade and/or when urinary output is insufficient after diuretics. Levosimendan can be used alone or in combination with other inotropic or vasopressor agents, but requires monitoring due to the risk of hypotension. [ABSTRACT FROM AUTHOR]
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- 2016
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47. Treatments targeting inotropy
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Dietmar J. Manstein, Jean-Luc Balligand, Joseph M. Metzger, Veli-Pekka Harjola, Christoph Maack, Frank Ruschitzka, Marco Metra, Stefan Chlopicki, Nazha Hamdani, Alexander Dietl, Denise Hilfiker-Kleiner, M. Birhan Yilmaz, Johannes Holzmeister, Alexander R. Lyon, Christian Mueller, Petar M. Seferovic, Stefan D. Anker, Johann Bauersachs, Gilles W. De Keulenaer, Giuseppe Limongelli, Alexandre Mebazaa, Dirk L. Brutsaert, Rodolphe Fischmeister, Lucie Carrier, Rudolf A. de Boer, Josep Masip, Burkert Pieske, John G.F. Cleland, Wolfram H. Zimmermann, Zoltán Papp, Frank R. Heinzel, Carlo G. Tocchetti, Piotr Ponikowski, Lars H. Lund, Stephane Heymans, Thomas Eschenhagen, Wolfgang A. Linke, Arsen D. Ristić, Hadi Skouri, Maack, Christoph, Eschenhagen, Thoma, Hamdani, Nazha, Heinzel, Frank R, Lyon, Alexander R, Manstein, Dietmar J, Metzger, Joseph, Papp, Zoltán, Tocchetti, Carlo G, Yilmaz, M Birhan, Anker, Stefan D, Balligand, Jean-Luc, Bauersachs, Johann, Brutsaert, Dirk, Carrier, Lucie, Chlopicki, Stefan, Cleland, John G, de Boer, Rudolf A, Dietl, Alexander, Fischmeister, Rodolphe, Harjola, Veli-Pekka, Heymans, Stephane, Hilfiker-Kleiner, Denise, Holzmeister, Johanne, de Keulenaer, Gille, Limongelli, Giuseppe, Linke, Wolfgang A, Lund, Lars H, Masip, Josep, Metra, Marco, Mueller, Christian, Pieske, Burkert, Ponikowski, Piotr, Ristic, Arsen, Ruschitzka, Frank, Seferovic, Petar M, Skouri, Hadi, Zimmermann, Wolfram H, Mebazaa, Alexandre, HUS Emergency Medicine and Services, University of Helsinki, Department of Diagnostics and Therapeutics, Cardiologie, MUMC+: MA Med Staf Spec Cardiologie (9), RS: Carim - H02 Cardiomyopathy, RS: CARIM - R2.02 - Cardiomyopathy, Maack, C, Eschenhagen, T, Hamdani, N, Heinzel, Fr, Lyon, Ar, Manstein, Dj, Metzger, J, Papp, Z, Tocchetti, Cg, Yilmaz, Mb, Anker, Sd, Balligand, Jl, Bauersachs, J, Brutsaert, D, Carrier, L, Chlopicki, S, Cleland, Jg, de Boer, Ra, Dietl, A, Fischmeister, R, Harjola, Vp, Heymans, S, Hilfiker-Kleiner, D, Holzmeister, J, de Keulenaer, G, Limongelli, G, Linke, Wa, Lund, Lh, Masip, J, Metra, M, Mueller, C, Pieske, B, Ponikowski, P, Ristic, A, Ruschitzka, F, Seferovic, Pm, Skouri, H, Zimmermann, Wh, Mebazaa, A, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, and UCL - (SLuc) Service de médecine interne générale
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Inotrope ,Acute decompensated heart failure ,Phosphodiesterase Inhibitors ,Swine ,Levosimendan ,030204 cardiovascular system & hematology ,Omecamtiv mecarbil ,Contractility ,Antioxidants ,Placebos ,0302 clinical medicine ,Catecholamines ,Diastole ,Dobutamine ,Inotropes ,Urea ,Adrenergic receptors ,1102 Cardiorespiratory Medicine and Haematology ,Excitation Contraction Coupling ,Clinical Trials as Topic ,Cardiogenic shock ,3. Good health ,Receptors, Adrenergic ,Mitochondria ,Acute Disease ,Models, Animal ,Cardiology ,Nitrogen Oxides ,Cardiology and Cardiovascular Medicine ,Oxidation-Reduction ,medicine.drug ,Cardiac function curve ,Sarcomeres ,medicine.medical_specialty ,Cardiotonic Agents ,Systole ,Shock, Cardiogenic ,Heart failure ,03 medical and health sciences ,Special Article ,Dogs ,Internal medicine ,Energetics ,medicine ,Animals ,Humans ,Simendan ,business.industry ,030229 sport sciences ,medicine.disease ,Myocardial Contraction ,Excitation-contraction coupling ,Cardiovascular System & Hematology ,3121 General medicine, internal medicine and other clinical medicine ,Case-Control Studies ,Nitroxyl ,Calcium ,Human medicine ,business ,Energy Metabolism - Abstract
Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation–contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term.
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- 2019
48. Management of cardiogenic shock complicating myocardial infarction
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Demetris Yannopolos, Alexa Hollinger, Holger Thiele, Bruno Levy, Ludhmila Abrahão Hajjar, Alexandre Mebazaa, Guillaume Lebreton, Sean van Diepen, Susanna Price, Jaon N. Katz, Jin Joo Park, Alain Combes, Johan Lassus, Alessandro Sionis, Gilles Montalescot, Giovanni Landoni, Veli-Pekka Harjola, Université Paris Diderot - Paris 7 (UPD7), Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Biomarqueurs CArdioNeuroVASCulaires (BioCANVAS), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cardiovascular and Renal Clinical Trialists [Vandoeuvre-les-Nancy] (INI-CRCT), Institut Lorrain du Coeur et des Vaisseaux Louis Mathieu [Nancy], Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), University of Alberta, University Hospital Basel [Basel], University of North Carolina [Chapel Hill] (UNC), University of North Carolina System (UNC), Vita-Salute San Raffaele University and Center for Translational Genomics and Bioinformatics, San Raffaele Scientific Institute, Universidade de São Paulo (USP), University of Helsinki, CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Sorbonne Université - Faculté de Médecine (SU FM), Sorbonne Université (SU), Seoul National University [Seoul] (SNU), Department of Imaging Royal Brompton Hospital, Royal Brompton Hospital, lnstitut d’Investigacions Biomèdica San Pau (IIB Sant Pau), Interventional Cardiology, Minneapolis, Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Heart Center Leipzig, Mebazaa, Alexandre, Combes, Alain, van Diepen, Sean, Hollinger, Alexa, Katz, Jaon N., Landoni, Giovanni, Hajjar, Ludhmila Abrahao, Lassus, Johan, Lebreton, Guillaume, Montalescot, Gille, Park, Jin Joo, Price, Susanna, Sionis, Alessandro, Yannopolos, Demetri, Harjola, Veli-Pekka, Levy, Bruno, Thiele, Holger, HAL-SU, Gestionnaire, Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut de Cardiométabolisme et Nutrition = Institute of Cardiometabolism and Nutrition [CHU Pitié Salpêtrière] (IHU ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Universidade de São Paulo = University of São Paulo (USP), and Helsingin yliopisto = Helsingfors universitet = University of Helsinki
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Adult ,Male ,medicine.medical_specialty ,Critical Care ,medicine.medical_treatment ,Myocardial Infarction ,Shock, Cardiogenic ,Acute myocardial infarction ,030204 cardiovascular system & hematology ,Revascularization ,Critical Care and Intensive Care Medicine ,03 medical and health sciences ,0302 clinical medicine ,Percutaneous Coronary Intervention ,Catecholamines ,Mechanical circulatory support ,Intensive care ,Anesthesiology ,Extracorporeal membrane oxygenation ,Medicine ,Humans ,Myocardial infarction ,Acute Coronary Syndrome ,Intensive care medicine ,Cardiogenic shock ,ComputingMilieux_MISCELLANEOUS ,Aged ,Aged, 80 and over ,[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology ,business.industry ,Percutaneous coronary intervention ,030208 emergency & critical care medicine ,Middle Aged ,medicine.disease ,Triage ,3. Good health ,ANGIOPLASTIA TRANSLUMINAL PERCUTÂNEA CORONÁRIA ,Catecholamine ,Female ,business ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology - Abstract
Up to 10% of acute coronary syndromes are complicated by cardiogenic shock (CS) with contemporary mortality rates of 40–50%. The extent of ischemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis in this patient population. Individualized patient risk assessment plays an important role in determining appropriate revascularization, drug treatment with inotropes and vasopressors, mechanical circulatory support, intensive care support of other organ systems, hospital level of care triage, and allocation of clinical resources. This review will outline the underlying causes and diagnostic criteria, pathophysiology, and treatment of CS complicating acute coronary syndromes with a focus on (a) potential therapeutic issues from the perspective an interventional cardiologist, an emergency physician, and an intensive care physician, (b) the type of revascularization, and (c) new therapeutic advancements in pharmacologic and mechanical percutaneous circulatory support.
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- 2018
49. COMBINED NT-PROBNP AND ST2 MEASUREMENT HAS POWERFUL PROGNOSTIC VALUE IN CARDIOGENIC SHOCK CAUSED BY ACUTE CORONARY SYNDROME.
- Author
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Tolppanen, Heli, Lasarte, Mercedes Rivas, Lassus, Johan, Green, Alessandro Sionis, Harjola, Veli-Pekka, and Mebazaa, Alexandre
- Subjects
- *
TREATMENT of acute coronary syndrome , *CARDIOGENIC shock , *ETIOLOGY of diseases , *HEALTH outcome assessment , *CLINICAL trials - Published
- 2016
- Full Text
- View/download PDF
50. BIOACTIVE ADRENOMEDULLIN: A NOVEL PROGNOSTIC MARKER IN CARDIOGENIC SHOCK.
- Author
-
Lasarte, Mercedes Rivas, Tolppanen, Heli, Lassus, Johan, Green, Alessandro Sionis, Harjola, Veli-Pekka, and Mebazaa, Alexandre
- Subjects
- *
CARDIOGENIC shock , *BIOACTIVE compounds , *ADRENOMEDULLIN , *BIOMARKERS , *CARDIOLOGY , *PROGNOSIS , *THERAPEUTICS - Published
- 2016
- Full Text
- View/download PDF
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