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6. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM)

Author

Habib, G, Lancellotti, P, Antunes, Mj, Bongiorni, Mg, Casalta, Jp, Del Zotti, F, Dulgheru, R, El Khoury, G, Erba, Pa, Iung, B, Miro, Jm, Mulder, Bj, Plonska-Gosciniak, E, Price, S, Roos-Hesselink, J, Snygg-Martin, U, Thuny, F, Tornos Mas, P, Vilacosta, I, Zamorano, Jl, Document, Reviewers., Erol, Ç, Nihoyannopoulos, P, Aboyans, V, Agewall, S, Athanassopoulos, G, Aytekin, S, Benzer, W, Bueno, H, Broekhuizen, L, Carerj, S, Cosyns, B, De Backer, J, De Bonis, M, Dimopoulos, K, Donal, E, Drexel, H, Flachskampf, Fa, Hall, R, Halvorsen, S, Hoen, B, Kirchhof, P, Lainscak, M, Leite-Moreira, Af, Lip, Gy, Mestres, Ca, Piepoli, Mf, Punjabi, Pp, Rapezzi, C, Rosenhek, R, Siebens, K, Tamargo, J, Walker, Dm, Habib G, Lancellotti P, Antunes MJ, Bongiorni MG, Casalta JP, Del Zotti F, Dulgheru R, El Khoury G, Erba PA, Iung B, Miro JM, Mulder BJ, Plonska-Gosciniak E, Price S, Roos-Hesselink J, Snygg-Martin U, Thuny F, Tornos Mas P, Vilacosta I, Zamorano JL, Document Reviewers., Erol Ç, Nihoyannopoulos P, Aboyans V, Agewall S, Athanassopoulos G, Aytekin S, Benzer W, Bueno H, Broekhuizen L, Carerj S, Cosyns B, De Backer J, De Bonis M, Dimopoulos K, Donal E, Drexel H, Flachskampf FA, Hall R, Halvorsen S, Hoen B, Kirchhof P, Lainscak M, Leite-Moreira AF, Lip GY, Mestres CA, Piepoli MF, Punjabi PP, Rapezzi C, Rosenhek R, Siebens K, Tamargo J, Walker DM, DIPARTIMENTO DI MEDICINA SPECIALISTICA, DIAGNOSTICA E SPERIMENTALE, Facolta' di MEDICINA e CHIRURGIA, AREA MIN. 06 - Scienze mediche, Habib, G, Lancellotti, P, Antunes, Mj, Bongiorni, Mg, Casalta, Jp, Del Zotti, F, Dulgheru, R, El Khoury, G, Erba, Pa, Iung, B, Miro, Jm, Mulder, Bj, Plonska gosciniak, E, Price, S, Roos hesselink, J, Snygg martin, U, Thuny, F, Mas, Pt, Vilacosta, I, Zamorano, Jl, Erol, Ç, Nihoyannopoulos, P, Aboyans, V, Agewall, S, Athanassopoulos, G, Aytekin, S, Benzer, W, Bueno, H, Broekhuizen, L, Carerj, S, Cosyns, B, De Backer, J, DE BONIS, Michele, Dimopoulos, K, Donal, E, Drexel, H, Flachskampf, Fa, Hall, R, Halvorsen, S, Hoen, B, Kirchhof, P, Lainscak, M, Leite moreira, Af, Lip, Gy, Mestres, Ca, Piepoli, Mf, Punjabi, Pp, Rapezzi, C, Rosenhek, R, Siebens, K, Tamargo, J, and Walker, Dm

Subjects
Microbiological Techniques, Heart disease, Embolism, Heart Valve Diseases, Cardiac device, Cardiac imaging, Cardiac surgery, Congenital heart disease, Echocardiography, Endocarditis, Guidelines, Infection, Nuclear imaging, Pregnancy, Prevention, Prognosis, Prophylaxis, Prosthetic heart valves, Valve disease, Guideline, Arrhythmias, Cardiovascular, Congenital, Postoperative Complications, Recurrence, Risk Factors, Neoplasms, Ambulatory Care, Non-Infective, Pericarditis, Endocarditi, Musculoskeletal Diseases, Prophylaxi, Heart Defects, Cross Infection, Acute Kidney Injury, Operative, Anti-Bacterial Agents, Myocarditis, Prosthetic heart valve, Endocarditis, Non-Infective, Infective endocarditis, Cardiology, Female, Cardiology and Cardiovascular Medicine, Infected, Cardiac, Heart Defects, Congenital, Diagnostic Imaging, medicine.medical_specialty, Prosthesis-Related Infections, Critical Care, Prognosi, Pregnancy Complications, Cardiovascular, Risk Assessment, NO, Aneurysm, Infected, Antibiotic Prophylaxis, Arrhythmias, Cardiac, Clinical Laboratory Techniques, Dentistry, Operative, Fibrinolytic Agents, Heart Failure, Humans, Long-Term Care, Nervous System Diseases, Patient Care Team, Splenic Diseases, Thoracic Surgical Procedures, Internal medicine, medicine, business.industry, medicine.disease, Aneurysm, Pregnancy Complications, Heart failure, Dentistry, business, Fibrinolytic agent
Abstract

none 53 si The disclosure forms of all experts involved in the development of these guidelines are available on the ESC website http://www.escardio.org/guidelines. Representing the European Association of Nuclear Medicine (EANM); Representing the European Society of Clinical Microbiology and Infectious Diseases (ESCMID); and Representing the European Association for Cardio-Thoracic Surgery (EACTS). Guidelines for the management of infective endocarditis Habib G; Lancellotti P; Antunes MJ; Bongiorni MG; Casalta JP; Del Zotti F; Dulgheru R; El Khoury G; Erba PA; Iung B; Miro JM; Mulder BJ; Plonska-Gosciniak E; Price S; Roos-Hesselink J; Snygg-Martin U; Thuny F; Tornos Mas P; Vilacosta I; Zamorano JL; Document Reviewers.; Erol Ç; Nihoyannopoulos P; Aboyans V; Agewall S; Athanassopoulos G; Aytekin S; Benzer W; Bueno H; Broekhuizen L; Carerj S; Cosyns B; De Backer J; De Bonis M; Dimopoulos K; Donal E; Drexel H; Flachskampf FA; Hall R; Halvorsen S; Hoen B; Kirchhof P; Lainscak M; Leite-Moreira AF; Lip GY; Mestres CA; Piepoli MF; Punjabi PP; Rapezzi C; Rosenhek R; Siebens K; Tamargo J; Walker DM Habib G; Lancellotti P; Antunes MJ; Bongiorni MG; Casalta JP; Del Zotti F; Dulgheru R; El Khoury G; Erba PA; Iung B; Miro JM; Mulder BJ; Plonska-Gosciniak E; Price S; Roos-Hesselink J; Snygg-Martin U; Thuny F; Tornos Mas P; Vilacosta I; Zamorano JL; Document Reviewers.; Erol Ç; Nihoyannopoulos P; Aboyans V; Agewall S; Athanassopoulos G; Aytekin S; Benzer W; Bueno H; Broekhuizen L; Carerj S; Cosyns B; De Backer J; De Bonis M; Dimopoulos K; Donal E; Drexel H; Flachskampf FA; Hall R; Halvorsen S; Hoen B; Kirchhof P; Lainscak M; Leite-Moreira AF; Lip GY; Mestres CA; Piepoli MF; Punjabi PP; Rapezzi C; Rosenhek R; Siebens K; Tamargo J; Walker DM

Published
2015

7. Improvement in left intraventricular pressure gradients after aortic valve replacement in aortic stenosis patients

Author

Guerra M, Mendes-Ferreira P, Adão R, Pereira E, Vieira M, Lourenço AP, Brás-Silva C, Bastos P, Vouga L, Leite-Moreira AF

Subjects
cardiovascular system, aortic stenosis, intraventricular pressure gradients, left ventricle function
Abstract

New Findings What is the central question of this study? Normal diastolic and systolic intraventricular pressure gradients are decreased when left ventricular filling and/or emptying are compromised. We hypothesized that in patients with severe aortic valve stenosis, a condition that interferes with ventricular filling and emptying, those gradients would be disturbed. What is the main finding and its importance? We showed the existence of intraventricular pressure gradients throughout the cardiac cycle in the human left ventricle. Moreover, we demonstrated, for the first time, that diastolic and systolic gradients, which are markers of normal ventricular filling and emptying, respectively, improved in patients with severe aortic valve stenosis immediately after valve replacement. The present study was conducted to characterize left intraventicular pressure gradients, which are markers of normal cardiac function, in patients with severe aortic stenosis, a condition that interferes with ventricular filling and emptying. In 10 patients (four male; mean age 71.3 ± 4.8 years old) undergoing aortic valve replacement, two high-fidelity pressure catheters were inserted inside the cavity of the left ventricle through an apical puncture and positioned in the apex and outflow tract below the aortic valve. Pressures were continuously acquired and gradients calculated as apical minus outflow tract pressure, before and immediately after aortic valve replacement. During early filling, we recorded a negative intraventricular gradient along the basal portion of the left ventricle in the apical direction (−0.82 ± 0.45 mmHg), which increased to −3.97 ± 0.42 mmHg after aortic valve replacement. In late filling, intraventricular flow was now directed towards the outflow tract, with a positive pressure gradient both before (+1.23 ± 0.37 mmHg) and after surgery (+2.12 ± 0.58 mmHg). During systole, before surgery we observed a positive pressure gradient between the apex and outflow tract during both rapid (+1.60 ± 0.21 mmHg) and slow ejection phases (+1.68 ± 0.12 mmHg), whereas after aortic valve replacement the positive gradient (+1.54 ± 0.15 mmHg) during rapid ejection was inverted (−3.92 ± 0.34 mmHg) during the slow ejection phase. We demonstrated that in patients with severe aortic stenosis both diastolic and systolic intraventricular pressure gradients are significantly attenuated but can be restored immediately after aortic valve replacement. The assessment and measurement of intraventricular pressure gradients and their modulation in pathophysiological conditions may provide novel insights into cardiac physiology.

Published
2017

8. Improvement in left intraventricular pressure gradients after aortic valve replacement in aortic stenosis patients

Author

Guerra, M, Mendes Ferreira, P, Adao, R, Pereira, E, Vieira, M, Lourenco, AP, Brás-Silva C, Bastos, P, Vouga, L, Leite Moreira, AF, and Faculdade de Medicina

Subjects
Health sciences, Medical and Health sciences, cardiovascular system, Ciências médicas e da saúde, Medical and Health sciences, Ciências da Saúde, Ciências médicas e da saúde
Abstract

New Findings: What is the central question of this study? Normal diastolic and systolic intraventricular pressure gradients are decreased when left ventricular filling and/or emptying are compromised. We hypothesized that in patients with severe aortic valve stenosis, a condition that interferes with ventricular filling and emptying, those gradients would be disturbed. What is the main finding and its importance? We showed the existence of intraventricular pressure gradients throughout the cardiac cycle in the human left ventricle. Moreover, we demonstrated, for the first time, that diastolic and systolic gradients, which are markers of normal ventricular filling and emptying, respectively, improved in patients with severe aortic valve stenosis immediately after valve replacement. The present study was conducted to characterize left intraventicular pressure gradients, which are markers of normal cardiac function, in patients with severe aortic stenosis, a condition that interferes with ventricular filling and emptying. In 10 patients (four male; mean age 71.3 ± 4.8 years old) undergoing aortic valve replacement, two high-fidelity pressure catheters were inserted inside the cavity of the left ventricle through an apical puncture and positioned in the apex and outflow tract below the aortic valve. Pressures were continuously acquired and gradients calculated as apical minus outflow tract pressure, before and immediately after aortic valve replacement. During early filling, we recorded a negative intraventricular gradient along the basal portion of the left ventricle in the apical direction (0.82 ± 0.45 mmHg), which increased to 3.97 ± 0.42 mmHg after aortic valve replacement. In late filling, intraventricular flow was now directed towards the outflow tract, with a positive pressure gradient both before (+1.23 ± 0.37 mmHg) and after surgery (+2.12 ± 0.58 mmHg). During systole, before surgery we observed a positive pressure gradient between the apex and outflow tract during both rapid (+1.60 ± 0.21 mmHg) and slow ejection phases (+1.68 ± 0.12 mmHg), whereas after aortic valve replacement the positive gradient (+1.54 ± 0.15 mmHg) during rapid ejection was inverted (3.92 ± 0.34 mmHg) during the slow ejection phase. We demonstrated that in patients with severe aortic stenosis both diastolic and systolic intraventricular pressure gradients are significantly attenuated but can be restored immediately after aortic valve replacement. The assessment and measurement of intraventricular pressure gradients and their modulation in pathophysiological conditions may provide novel insights into cardiac physiology. (c) 2017 The Authors. Experimental Physiology (c) 2017 The Physiological Society

Published
2017

9. Poster session 3Cell growth, differentiation and stem cells - Heart511The role of the endocannabinoid system in modelling muscular dystrophy cardiac disease with induced pluripotent stem cells.512An emerging role of T lymphocytes in cardiac regenerative processes in heart failure due to dilated cardiomyopathy513Canonical wnt signaling reverses the ‘aged/senescent’ human endogenous cardiac stem cell phenotype514Hippo signalling modulates survival of human induced pluripotent stem cell-derived cardiomyocytes515Biocompatibility of mesenchymal stem cells with a spider silk matrix and its potential use as scaffold for cardiac tissue regeneration516A snapshot of genome-wide transcription in human induced pluripotent stem cell-derived hepatocyte-like cells (iPSC-HLCs)517Can NOS/sGC/cGK1 pathway trigger the differentiation and maturation of mouse embryonic stem cells (ESCs)?518Introduction of external Ik1 to human-induced pluripotent stem cell-derived cardiomyocytes via Ik1-expressing HEK293519Cell therapy of the heart studied using adult myocardial slices in vitro520Enhancement of the paracrine potential of human adipose derived stem cells when cultured as spheroid bodies521Mechanosensitivity of cardiomyocyte progenitor cells: the strain response in 2D and 3D environments522The effect of the vascular-like network on the maturation of the human induced pluripotent stem cell derived cardiomyocytes.Transcriptional control and RNA species - Heart525Gene expression regulation in heart failure: from pathobiology to bioinformatics526Human transcriptome in idiopathic dilated cardiomyopathy - a novel high throughput screening527A high-throghput approach unveils putative miRNA-mediated mitochondria-targeted cardioprotective circuits activated by T3 in the post ischemia reperfusion setting528The effect of uraemia on the expression of miR-212/132 and the calcineurin pathway in the rat heartCytokines and cellular inflammation - Heart531Lack of growth differentiation factor 15 aggravates adverse cardiac remodeling upon pressure-overload in mice532Blocking heteromerization of platelet chemokines ccl5 and cxcl4 reduces inflammation and preserves heart function after myocardial infarction533Is there an association between low-dose aspirin use and clinical outcome in HFPEF? Implications of modulating monocyte function and inflammatory mediator release534N-terminal truncated intracellular matrix metalloproteinase-2 expression in diabetic heart.535Expression of CD39 and CD73 on peripheral T-cell subsets in calcific aortic stenosis536Mast cells in the atrial myocardium of patients with atrial fibrillation: a comparison with patients in sinus rhythm539Characteristics of the inflammatory response in patients with coronary artery disease and arterial hypertension540Pro-inflammatory cytokines as cardiovascular events predictors in rheumatoid arthritis and asymptomatic atherosclerosis541Characterization of FVB/N murinic bone marrow-derived macrophage polarization into M1 and M2 phenotypes542The biological expression and thoracic anterior pain syndromeSignal transduction - Heart545The association of heat shock protein 90 and TGFbeta receptor I is involved in collagen production during cardiac remodelling in aortic-banded mice546Loss of the inhibitory GalphaO protein in the rostral ventrolateral medulla of the brainstem leads to abnormalities in cardiovascular reflexes and altered ventricular excitablitiy547Selenoprotein P regulates pressure overload-induced cardiac remodeling548Study of adenylyl cyclase activity in erythrocyte membranes in patients with chronic heart failure549Direct thrombin inhibitors inhibit atrial myocardium hypertrophy in a rat model of heart failure and atrial remodeling550Tissue factor / FVIIa transactivates the IGF-1R by a Src-dependent phosphorylation of caveolin-1551Notch signaling is differently altered in endothelial and smooth muscle cells of ascending aortic aneurysm patients552Frizzled 5 expression is essential for endothelial proliferation and migration553Modulation of vascular function and ROS production by novel synthetic benzopyran analogues in diabetes mellitusExtracellular matrix and fibrosis - Heart556Cardiac fibroblasts as inflammatory supporter cells trigger cardiac inflammation in heart failure557A role for galectin-3 in calcific aortic valve stenosis558Omega-3 polyunsaturated fatty acids- can they decrease risk for ventricular fibrillation?559Serum levels of elastin derived peptides and circulating elastin-antielastin immune complexes in sera of patients with coronary artery disease560Endocardial fibroelastosis is secondary to hemodynamic alterations in the chick model of hypoplastic left heart syndrome561Dynamics of serum levels of matrix metalloproteinases in primary anterior STEMI patients564Deletion of the alpha-7 nicotinic acetylcholine receptor changes the vascular remodeling induced by transverse aortic constriction in mice.565Extracellular matrix remodelling in response to venous hypertension: proteomics of human varicose veinsIon channels, ion exchangers and cellular electrophysiology - Heart568Microtubule-associated protein RP/EB family member 1 modulates sodium channel trafficking and cardiac conduction569Investigation of electrophysiological abnormalities in a rabbit athlete's heart model570Upregulation of expression of multiple genes in the atrioventricular node of streptozotocin-induced diabetic rat571miR-1 as a regulator of sinoatrial rhythm in endurance training adaptation572Selective sodium-calcium exchanger inhibition reduces myocardial dysfunction associated with hypokalaemia and ventricular fibrillation573Effect of racemic and levo-methadone on action potential of human ventricular cardiomyocytes574Acute temperature effects on the chick embryonic heart functionVasculogenesis, angiogenesis and arteriogenesis577Clinical improvement and enhanced collateral vessel growth after monocyte transplantation in mice578The role of HIF-1 alpha, VEGF and obstructive sleep apnoea in the development of coronary collateral circulation579Initiating cardiac repair with a trans-coronary sinus catheter intervention in an ischemia/reperfusion porcine animal model580Early adaptation of pre-existing collaterals after acute arteriolar and venular microocclusion: an in vivo study in chick chorioallantoic membraneEndothelium583EDH-type responses to the activator of potassium KCa2.3 and KCa3.1 channels SKA-31 in the small mesenteric artery from spontaneously hypertensive rats584The peculiarities of endothelial dysfunction in patients with chronic renocardial syndrome585Endothelial dysfunction, atherosclerosis of the carotid arteries and level of leptin in patient with coronary heart disease in combination with hepatic steatosis depend from body mass index.586Role of non-coding RNAs in thoracic aortic aneurysm associated with bicuspid aortic valve587Cigarette smoke extract abrogates atheroprotective effects of high laminar flow on endothelial function588The prognostic value of anti-connective tissue antibodies in coronary heart disease and asymptomatic atherosclerosis589Novel potential properties of bioactive peptides from spanish dry-cured ham on the endothelium.Lipids592Intermediate density lipoprotein is associated with monocyte subset distribution in patients with stable atherosclerosis593The characteristics of dyslipidemia in rheumatoid arthritisAtherosclerosis596Macrophages differentiated in vitro are heterogeneous: morphological and functional profile in patients with coronary artery disease597Palmitoylethanolamide promotes anti-inflammatory phenotype of macrophages and attenuates plaque formation in ApoE-/- mice598Amiodarone versus esmolol in the perioperative period: an in vitro study of coronary artery bypass grafts599BMPRII signaling of fibrocytes, a mesenchymal progenitor cell population, is increased in STEMI and dyslipidemia600The characteristics of atherogenesis and systemic inflammation in rheumatoid arthritis601Role of adenosine-to-inosine RNA editing in human atherosclerosis602Presence of bacterial DNA in thrombus aspirates of patients with myocardial infarction603Novel E-selectin binding polymers reduce atherosclerotic lesions in ApoE(-/-) mice604Differential expression of the plasminogen receptor Plg-RKT in monocyte and macrophage subsets - possible functional consequences in atherogenesis605Apelin-13 treatment enhances the stability of atherosclerotic plaques606Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and favor atherosclerotic plaque instability607Association of neutrophil to lymphocyte ratio with presence of isolated coronary artery ectasiaCalcium fluxes and excitation-contraction coupling610The coxsackie- and adenovirus receptor (CAR) regulates calcium homeostasis in the developing heart611HMW-AGEs application acutely reduces ICaL in adult cardiomyocytes612Measuring electrical conductibility of cardiac T-tubular systems613Postnatal development of cardiac excitation-contraction coupling in rats614Role of altered Ca2+ homeostasis during adverse cardiac remodeling after ischemia/reperfusion615Experimental study of sarcoplasmic reticulum dysfunction and energetic metabolism in failing myocardium associated with diabetes mellitusHibernation, stunning and preconditioning618Volatile anesthetic preconditioning attenuates ischemic-reperfusion injury in type II diabetic patients undergoing on-pump heart surgery619The effect of early and delayed phase of remote ischemic preconditioning on ischemia-reperfusion injury in the isolated hearts of healthy and diabetic rats620Post-conditioning with 1668-thioate leads to attenuation of the inflammatory response and remodeling with less fibrosis and better left ventricular function in a murine model of myocardial infarction621Maturation-related changes in response to ischemia-reperfusion injury and in effects of classical ischemic preconditioning and remote preconditioningMitochondria and energetics624Phase changes in myocardial mitochondrial respiration caused by hypoxic preconditioning or periodic hypoxic training625Desmin mutations depress mitochondrial metabolism626Methylene blue modulates mitochondrial function and monoamine oxidases-related ROS production in diabetic rat hearts627Doxorubicin modulates the real-time oxygen consumption rate of freshly isolated adult rat and human ventricular cardiomyocytesCardiomyopathies and fibrosis630Effects of genetic or pharmacologic inhibition of the ubiquitin/proteasome system on myocardial proteostasis and cardiac function631Suppression of Wnt signalling in a desmoglein-2 transgenic mouse model for arrhythmogenic cardiomyopathy632Cold-induced cardiac hypertrophy is reversed after thermo-neutral deacclimatization633CD45 is a sensitive marker to diagnose lymphocytic myocarditis in endomyocardial biopsies of living patients and in autopsies634Atrial epicardial adipose tissue derives from epicardial progenitors635Caloric restriction ameliorates cardiac function, sympathetic cardiac innervation and beta-adrenergic receptor signaling in an experimental model of post-ischemic heart failure636High fat diet improves cardiac remodelling and function after extensive myocardial infarction in mice637Epigenetic therapy reduces cardiac hypertrophy in murine models of heart failure638Imbalance of the VHL/HIF signaling in WT1+ Epicardial Progenitors results in coronary vascular defects, fibrosis and cardiac hypertrophy639Diastolic dysfunction is the first stage of the developing heart failure640Colchicine aggravates coxsackievirus B3 infection in miceArterial and pulmonary hypertension642Osteopontin as a marker of pulmonary hypertension in patients with coronary heart disease combined with chronic obstructive pulmonary disease643Myocardial dynamic stiffness is increased in experimental pulmonary hypertension partly due to incomplete relaxation644Hypotensive effect of quercetin is possibly mediated by down-regulation of immunotroteasome subunits in aorta of spontaneously hypertensive rats645Urocortin-2 improves right ventricular function and attenuates experimental pulmonary arterial hypertension646A preclinical evaluation of the anti-hypertensive properties of an aqueous extract of Agathosma (Buchu)Biomarkers648The adiponectin level in hypertensive females with rheumatoid arthritis and its relationship with subclinical atherosclerosis649Markers for identification of renal dysfunction in the patients with chronic heart failure650cardio-hepatic syndromes in chronic heart failure: North Africa profile651To study other biomarkers that assess during myocardial infarction652Interconnections of apelin levels with parameters of lipid metabolism in hypertension patients653Plasma proteomics in hypertension: prediction and follow-up of albuminuria during chronic renin-angiotensin system suppression654Soluble RAGE levels in plasma of patients with cerebrovascular events

Author

Gowran, A, primary, Kulikova, T, primary, Lewis, FC, primary, Foldes, G, primary, Fuentes, L, primary, Viiri, LE, primary, Spinelli, V, primary, Costa, A, primary, Perbellini, F, primary, Sid-Otmane, C, primary, Bax, NAM, primary, Pekkanen-Mattila, M, primary, Schiano, C, primary, Chaloupka, A, primary, Forini, F, primary, Sarkozy, M, primary, De Jager, SCA, primary, Vajen, T, primary, Glezeva, N, primary, Lee, H W, primary, Golovkin, A, primary, Kucera, T, primary, Musikhina, NA, primary, Korzhenkov, NP, primary, Santuchi, M DE C, primary, Munteanu, D, primary, Garcia, RG, primary, Ang, R, primary, Usui, S, primary, Kamilova, U, primary, Jumeau, C, primary, Aberg, M, primary, Kostina, DA, primary, Brandt, MM, primary, Muntean, D, primary, Lindner, D, primary, Sadaba, R, primary, Bacova, B, primary, Nikolov, A, primary, Sedmera, D, primary, Ryabov, V, primary, Neto, FP, primary, Lynch, M, primary, Portero, V, primary, Kui, P, primary, Howarth, FC, primary, Gualdoni, A, primary, Prorok, J, primary, Diolaiuti, L, primary, Vostarek, F, primary, Wagner, M, primary, Abela, MA, primary, Nebert, C, primary, Xiang, W, primary, Kloza, M, primary, Maslenko, A, primary, Grechanyk, M, primary, Bhattachariya, A, primary, Morawietz, H, primary, Babaeva, AR, primary, Martinez Sanchez, SM, primary, Krychtiuk, KA, primary, Starodubova, J, primary, Fiorelli, S, primary, Rinne, P, primary, Ozkaramanli Gur, D, primary, Hofbauer, T, primary, Stellos, K, primary, Pinon, P, primary, Tsoref, O, primary, Thaler, B, primary, Fraga-Silva, RA, primary, Fuijkschot, WW, primary, Shaaban, MNS, primary, Matthaeus, C, primary, Deluyker, D, primary, Scardigli, M, primary, Zahradnikova, A, primary, Dominguez, A, primary, Kondrat'eva, D, primary, Sosorburam, T, primary, Murarikova, M, primary, Duerr, GD, primary, Griecsova, L, primary, Portnichenko, VI, primary, Smolina, N, primary, Duicu, OANA M, primary, Elder, JM, primary, Zaglia, T, primary, Lorenzon, A, primary, Ruperez, C, primary, Woudstra, L, primary, Suffee, N, primary, De Lucia, C, primary, Russell-Hallinan, A, primary, Menendez-Montes, I, primary, Kapelko, VI, primary, Emmens, RW, primary, Hetman, O, primary, Van Der Laarse, WJ, primary, Goncharov, S, primary, Adao, R, primary, Huisamen, B, primary, Sirenko, O, primary, Nassiri, I, primary, Tserendavaa, SUMIYA, primary, Yushko, K, primary, Baldan Martin, M, primary, Falcone, C, primary, Vigorelli, V, additional, Nigro, P, additional, Pompilio, G, additional, Stepanova, O, additional, Valikhov, M, additional, Samko, A, additional, Masenko, V, additional, Tereschenko, S, additional, Teoh, T, additional, Domenjo-Vila, E, additional, Theologou, T, additional, Field, M, additional, Awad, W, additional, Yasin, M, additional, Nadal-Ginard, B, additional, Ellison-Hughes, GM, additional, Hellen, N, additional, Vittay, O, additional, Harding, SE, additional, Gomez-Cid, L, additional, Fernandez-Santos, ME, additional, Suarez-Sancho, S, additional, Plasencia, V, additional, Climent, A, additional, Sanz-Ruiz, R, additional, Hedhammar, M, additional, Atienza, F, additional, Fernandez-Aviles, F, additional, Kiamehr, M, additional, Oittinen, M, additional, Viiri, KM, additional, Kaikkonen, M, additional, Aalto-Setala, K, additional, Diolaiuti, L, additional, Laurino, A, additional, Sartiani, L, additional, Vona, A, additional, Zanardelli, M, additional, Cerbai, E, additional, Failli, P, additional, Hortigon-Vinagre, MP, additional, Van Der Heyden, M, additional, Burton, FL, additional, Smith, GL, additional, Watson, S, additional, Scigliano, M, additional, Tkach, S, additional, Alayoubi, S, additional, Terracciano, CM, additional, Ly, HQ, additional, Mauretti, A, additional, Van Marion, MH, additional, Van Turnhout, MC, additional, Van Der Schaft, DWJ, additional, Sahlgren, CM, additional, Goumans, MJ, additional, Bouten, CVC, additional, Vuorenpaa, H, additional, Penttinen, K, additional, Sarkanen, R, additional, Ylikomi, T, additional, Heinonen, T, additional, Grimaldi, V, additional, Aprile, M, additional, Esposito, R, additional, Maiello, C, additional, Soricelli, A, additional, Colantuoni, V, additional, Costa, V, additional, Ciccodicola, A, additional, Napoli, C, additional, Rowe, GC, additional, Johnson, K, additional, Arany, ZP, additional, Del Monte, F, additional, D'aurizio, R, additional, Kusmic, C, additional, Nicolini, G, additional, Baumgart, M, additional, Groth, M, additional, Ucciferri, N, additional, Iervasi, G, additional, Pitto, L, additional, Pipicz, M, additional, Gaspar, R, additional, Siska, A, additional, Foldesi, I, additional, Kiss, K, additional, Bencsik, P, additional, Thum, T, additional, Batkai, S, additional, Csont, T, additional, Haan, JJ, additional, Bosch, L, additional, Brans, MAD, additional, Van De Weg, SM, additional, Deddens, JC, additional, Lee, SJ, additional, Sluijter, JPG, additional, Pasterkamp, G, additional, Werner, I, additional, Projahn, D, additional, Staudt, M, additional, Curaj, A, additional, Soenmez, TT, additional, Simsekyilmaz, S, additional, Hackeng, TM, additional, Von Hundelshausen, P, additional, Koenen, RR, additional, Weber, C, additional, Liehn, EA, additional, Santos-Martinez, M, additional, Medina, C, additional, Watson, C, additional, Mcdonald, K, additional, Gilmer, J, additional, Ledwidge, M, additional, Song, SH, additional, Lee, MY, additional, Park, MH, additional, Choi, JC, additional, Ahn, JH, additional, Park, JS, additional, Oh, JH, additional, Choi, JH, additional, Lee, HC, additional, Cha, KS, additional, Hong, TJ, additional, Kudryavtsev, I, additional, Serebryakova, M, additional, Malashicheva, A, additional, Shishkova, A, additional, Zhiduleva, E, additional, Moiseeva, O, additional, Durisova, M, additional, Blaha, M, additional, Melenovsky, V, additional, Pirk, J, additional, Kautzner, J, additional, Petelina, TI, additional, Gapon, LI, additional, Gorbatenko, EA, additional, Potolinskaya, YV, additional, Arkhipova, EV, additional, Solodenkova, KS, additional, Osadchuk, MA, additional, Dutra, MF, additional, Oliveira, FCB, additional, Silva, MM, additional, Passos-Silva, DG, additional, Goncalves, R, additional, Santos, RAS, additional, Da Silva, RF, additional, Gavrilescu, CM, additional, Paraschiv, CM, additional, Manea, P, additional, Strat, LC, additional, Gomez, JMG, additional, Merino, D, additional, Hurle, MA, additional, Nistal, JF, additional, Aires, A, additional, Cortajarena, AL, additional, Villar, AV, additional, Abramowitz, J, additional, Birnbaumer, L, additional, Gourine, AV, additional, Tinker, A, additional, Takamura, M, additional, Takashima, S, additional, Inoue, O, additional, Misu, H, additional, Takamura, T, additional, Kaneko, S, additional, Alieva, TOHIRA, additional, Mougenot, N, additional, Dufilho, M, additional, Hatem, S, additional, Siegbahn, A, additional, Kostina, AS, additional, Uspensky, VE, additional, Moiseeva, OM, additional, Kostareva, AA, additional, Malashicheva, AB, 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2016
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10. Poster session 2Morphogenetic mechanisms290MiR-133 regulates retinoic acid pathway during early cardiac chamber specification291Bmp2 regulates atrial differentiation through miR-130 during early heart looping formationDevelopmental genetics294Association of deletion allele of insertion/deletion polymorphism in alpha 2B adrenoceptor gene and hypertension with or without type 2 diabetes mellitus295Association of G1359A polymorphism of the endocannabinoid type 1 receptor (CNR1) with coronary artery disease (CAD) with type 2 diabetes mellitusCell growth, differentiation and stem cells - Vascular298Gamma-secretase inhibitor prevents proliferation and migration of ductus arteriosus smooth muscle cells: a role of Notch signaling in postnatal closure of ductus arteriosus299Mesenchymal stromal-like cells (MLCs) derived from induced pluripotent stem (iPS) cells: a promising therapeutic option to promote neovascularization300Sonic Hedgehog promotes mesenchymal stem cell differentiation to vascular smooth muscle cells in cardiovacsular disease301Proinflammatory cytokine secretion and epigenetic modification in endothelial cells treated LPS-GinfivalisCell death and apoptosis - Vascular304Mitophagy acts as a safeguard mechanism against human vascular smooth muscle cell apoptosis induced by atherogenic lipidsTranscriptional control and RNA species - Vascular307MicroRNA-34a role in vascular calcification308Local delivery of a miR-146a inhibitor utilizing a clinically applicable approach attenuates neointima formation after vascular injury309Long noncoding RNA landscape of hypoxic endothelial cells310Specific circulating microRNAs levels associate with hypertension, hyperglycemia and dysfunctional HDL in acute coronary syndrome patientsCytokines and cellular inflammation - Vascular313Phosphodiesterase5A up-regulation in vascular endothelium under pro-inflammatory conditions: a newly disclosed anti-inflammatory activity for the omega-3polyunsaturated aatty acid docosahexaenoic acid314Cardiovascular risk modifying with extra-low dose anticytokine drugs in rhematoid arthritis315Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation316Lymphocytic myocarditis coincides with increased plaque inflammation and plaque hemorrhage in coronary arteries, facilitating myocardial infarction317Serum osteoprotegerin level predictsdeclined numerous of circulating endothelial- derived and mononuclear-derived progenitor cells in patients with metabolic syndromeGrowth factors and neurohormones - Vascular320Effect of gastrin-releasing peptide (GRP) on vascular inflammationSignal transduction - Heart323A new synthetic peptide regulates hypertrophy in vitro through means of the inhibition of nfkb324Inducible fibroblast-specific knockout of p38 alpha map kinase is cardioprotective in a mouse model of isoproterenol-induced cardiac hypertrophy325Regulation of beta-adrenoceptor-evoked inotropic responses by inhibitory G protein, adenylyl cyclase isoforms 5 and 6 and phosphodiesterases326Binding to RGS3 and stimulation of M2 muscarinic acetylcholine receptors modulates the substrate specificity of p190RhoGAP in cardiac myocytes327Cardiac regulation of post-translational modifications, parylation and deacetylation in LMNA dilated cardiomyopathy mouse model328Beta-adrenergic regulation of the b56delta/pp2a holoenzyme in cardiac myocytes through b56delta phosphorylation at serine 573Nitric oxide and reactive oxygen species - Vascular331Oxidative stress-induced miR-200c disrupts the regulatory loop among SIRT1, FOXO1 and eNOS332Antioxidant therapy prevents oxidative stress-induced endothelial dysfunction and Enhances Wound Healing333Morphological and biochemical characterization of red blood cell in coronary artery diseaseCytoskeleton and mechanotransduction - Heart336Novel myosin activator, JSH compounds, increased myocardial contractility without chronotropic effect in ratsExtracellular matrix and fibrosis - Vascular339Ablation of Toll-like receptor 9 causes cardiac rupture after myocardial infarction by attenuating proliferation and differentiation of cardiac fibroblasts340Altered vascular remodeling in the mouse hind limb ischemia model in Factor VII activating protease (FSAP) deficiencyVasculogenesis, angiogenesis and arteriogenesis343Pro-angiogenic effects of proly-hydroxylase inhibitors and their potential for use in a novel strategy of therapeutic angiogenesis for coronary total occlusion344Nrf2 drives angiogenesis in transcription-independent manner: new function of the master regulator of oxidative stress response345Angiogenic gene therapy, despite efficient vascular growth, is not able to improve muscle function in normoxic or chronically ischemic rabbit hindlimbs -role of capillary arterialization and shunting346Effect of PAR-1 inhibition on collateral vessel growth in the murine hind limb model347Quaking is a key regulator of endothelial cell differentiation, neovascularization and angiogenesis348"Emerging angiogenesis" in the chick chorioallantoic membrane (CAM). An in vivo study349Exosomes from cardiomyocyte progenitor cells and mesenchymal stem cells stimulate angiogenesis in vitro and in vivo via EMMPRINEndothelium352Reciprocal regulation of GRK2 and bradykinin receptor stimulation modulate Ca2+ intracellular level in endothelial cells353The roles of bone morphogenetic proteins 9 and 10 in endothelial inflammation and atherosclerosis354The contribution of GPR55 to the L-alpha-lysophosphatidylinositol-induced vasorelaxation in isolated human pulmonary arteries355The endothelial protective ACE inhibitor Zofenoprilat exerts anti-inflammatory activities through H2S production356A new class of glycomimetic drugs to prevent free fatty acid-induced endothelial dysfunction357Endothelial progenitor cells to apoptotic endothelial cell-derived microparticles ration differentiatesas preserved from reduced ejection fractionheart failure358Proosteogenic genes are activated in endothelial cells of patients with thoracic aortic aneurysm359Endothelin ETB receptors mediate relaxing responses to insulin in pericardial resistance arteries from patients with cardiovascular disease (CVD)Smooth muscle and pericytes362CX3CR1 positive myeloid cells regulate vascular smooth muscle tone by inducing calcium oscillations via activation of IP3 receptors363A novel function of PI3Kg on cAMP regulation, role in arterial wall hyperplasia through modulation of smooth muscle cells proliferation364NRP1 and NRP2 play important roles in the development of neointimal hyperplasia in vivo365Azithromycin induces autophagy in aortic smooth muscle cellsCoagulation, thrombosis and platelets368The real time in vivo evaluation of platelet-dependent aldosterone prothrombotic action in mice369Development of a method for in vivo detection of active thrombi in mice370The antiplatelet effects of structural analogs of the taurine chloramine371The influence of heparin anticoagulant drugs on functional state of human platelets372Regulation of platelet aggregation and adenosine diphosphate release by d dimer in acute coronary syndrome (in vitro study)Oxygen sensing, ischaemia and reperfusion375Sirtuin 5 mediates brain injury in a mouse model of cerebral ischemia-reperfusion376Abscisic acid: a new player in cardiomyocyte protection from ischaemia?377Protective effects of ultramicronized palmitoylethanolamide (PEA-um) in myocardial ischaemia and reperfusion injury in vivo378Identification of stem cell-derived cardiomyocytes using cardiac specific markers and additional testing of these cells in simulated ischemia/reperfusion system379Single-dose intravenous metformin treatment could afford significant protection of the injured rat kidney in an experimental model of ischemia-reperfusion380Cardiotoxicity of long acting muscarinic receptor antagonists used for chronic obstructive pulmonary disease381Dependence antioxidant potential on the concentration of amino acids382The impact of ischemia-reperfusion on physiological parameters,apoptosis and ultrastructure of rabbit myocardium with experimental aterosclerosisMitochondria and energetics385MicroRNA-1 dependent regulation of mitochondrial calcium uniporter (MCU) in normal and hypertrophied hearts386Mitochondrial homeostasis and cardioprotection: common targets for desmin and aB-crystallin387Overexpression of mitofusin-2 (Mfn2) and associated mitochondrial dysfunction in the diabetic heart388NO-dependent prevention of permeability transition pore (MPTP) opening by H2S and its regulation of Ca2+ accumulation in rat heart mitochondria389G protein coupled receptor kinase 2 (GRK2) is fundamental in recovering mitochondrial morphology and function after exposure to ionizing radiation (IR)Gender issues392Sex differences in pulmonary vascular control; focus on the nitric oxide pathwayAging395Heart failure with preserved ejection fraction develops when feeding western diet to senescence-accelerated mice396Cardiovascular markers as predictors of cognitive decline in elderly hypertensive patients397Changes in connexin43 in old rats with volume overload chronic heart failureGenetics and epigenetics400Calcium content in the aortic valve is associated with 1G>2G matrix metalloproteinase 1 polymorphism401Neuropeptide receptor gene s (NPSR1) polymorphism and sleep disturbances402Endothelin-1 gene Lys198Asn polymorphism in men with essential hypertension complicated and uncomplicated with chronic heart failure403Association of common polymorphisms of the lipoprotein lipase and pon1 genes with the metabolic syndrome in a sample of community participantsGenomics, proteomics, metabolomics, lipidomics and glycomics405Gene expression quantification using multiplexed color-coded probe pairs to determine RNA content in sporadic cardiac myxoma406Large-scale phosphorylation study of the type 2 diabetic heart subjected to ischemia / reperfusion injury407Transcriptome-based identification of new anti-inflammatory properties of the olive oil hydroxytyrosol in vascular endothelial cell under basal and proinflammatory conditions408Gene polymorphisms combinations and risk of myocardial infarctionComputer modelling, bioinformatics and big data411Comparison of the repolarization reserve in three state-of-the-art models of the human ventricular action potentialMetabolism, diabetes mellitus and obesity414Endothelial monocyte-activating polypeptide-II improves heart function in type -I Diabetes mellitus415Admission glucose level is independent predictor of impaired left ventricular function in patients with acute myocardial infarction: a two dimensional speckle-tracking echocardiography study416Association between biochemical markers of lipid profile and inflammatory reaction and stiffness of the vascular wall in hypertensive patients with abdominal obesity417Multiple common co-morbidities produce left ventricular diastolic dysfunction associated with coronary microvascular dysfunction, oxidative stress and myocardial stiffening418Investigating the cardiovascular effects of antiretroviral drugs in a lean and high fat/sucrose diet rat model of obesity419Statins in the treatment of non-alcoholic steatohepatitis (NASH). Our experience from a 2-year prospective study in Constanta County, Romania420Epicardial adipose tissue as a predictor of cardiovascular outcome in patients with ACS undergoing PCI?Arterial and pulmonary hypertension423Dependence between heart rhythm disorers and ID polymorphism of ACE gene in hypertensive patients424Molecular mechanisms underlying the beneficial effects of Urocortin 2 in pulmonary arterial hypertension425Inhibition of TGf-b axis and action of renin-angiotensin system in human ascending aorta aneurysms426Early signs of microcirculation and macrocirculation abnormalities in prehypertension427Vascular smooth muscle cell-expressed Tie-2 controls vascular tone428Cardiac and vascular remodelling in the development of chronic thrombo-embolic pulmonary hypertension in a novel swine modelBiomarkers431Arrhythmogenic cardiomyopathy: a new, non invasive biomarker432Can circulating microRNAs distinguish type 1 and type 2 myocardial infarction?433Design of a high-throughput multiplex proteomics assay to identify left ventricular diastolic dysfunction in diabetes434Monocyte-derived and P-selectin-carrying microparticles are differently modified by a low fat diet in patients with cardiovascular risk factors who will and who will not develop a cardiovascular event435Red blood cell distribution width assessment by polychromatic interference microscopy of thin films in chronic heart failure436Invasive and noninvasive evaluation of quality of radiofrequency-induced cardiac denervation in patients with atrial fibrillation437The effect of therapeutic hypothermia on the level of brain derived neurotrophic factor (BDNF) in sera following cardiopulmonary resustitation438Novel biomarkers to predict outcome in patients with heart failure and severe aortic stenosis439Biological factors linking depression and anxiety to cardiovascular disease440Troponins and myoglobin dynamic at coronary arteries graftingInvasive, non-invasive and molecular imaging443Diet composition effects on the genetic typing of the mouse ob mutation: a micro-ultrasound characterization of cardiac function, macro and micro circulation and liver steatosis444Characterization of pig coronary and rabbit aortic lesions using IV-OCT quantitative analysis: correlations with histologyGene therapy and cell therapy447Enhancing the survival and angiogenic potential of mouse atrial mesenchymal cells448VCAM-1 expression in experimental myocardial infarction and its relation to bone marrow-derived mononuclear cell retentionTissue engineering451Advanced multi layered scaffold that increases the maturity of stem cell-derived human cardiomyocytes452Response of engineered heart tissue to simulated ischemia/reperfusion in the presence of acute hyperglycemic conditions453Serum albumin hydrogels prevent de-differentiation of neonatal cardiomyocytes454A novel paintbrush technique for transfer of low viscosity ultraviolet light curable cyan methacrylate on saline immersed in-vitro sheep heart

Author

Garcia-Martinez, V, primary, Lopez Sanchez, C, primary, Hamed, W, primary, Hsu, JH, primary, Ferrer-Lorente, R, primary, Alshamrani, Maryam, primary, Pizzicannella, J, primary, Vindis, C, primary, Badi, I, primary, Korte, L, primary, Voellenkle, C, primary, Niculescu, L S, primary, Massaro, M, primary, Babaeva, AR, primary, Da Silva, F, primary, Woudstra, L, primary, Berezin, A, primary, Bae, MK, primary, Del Giudice, C, primary, Bageghni, S A, primary, Krobert, K, primary, Levay, M, primary, Vignier, N, primary, Ranieri, A, primary, Magenta, A, primary, Orlandi, A, primary, Porro, B, primary, Jeon, E-S, primary, Omori, Y, primary, Herold, J, primary, Barnett, G A, primary, Grochot-Przeczek, A, primary, Korpisalo, P, primary, Deffge, C, primary, Margariti, A, primary, Rong, W, primary, Maring, JA, primary, Gambardella, J, primary, Mitrofan, CG, primary, Karpinska, O, primary, Morbidelli, L, primary, Wilkinson, FL, primary, Kostina, AS, primary, De Mey, J G R, primary, Kumar, A, primary, Lupieri, A, primary, Pellet-Many, C, primary, Stamatiou, R, primary, Gromotowicz, A, primary, Dickhout, A, primary, Murina, M, primary, Roka-Moiia, YM, primary, Malinova, L, primary, Diaz-Canestro, C, primary, Vigliarolo, T, primary, Cuzzocrea, S, primary, Szantai, A, primary, Medic, B, primary, Cassambai, S, primary, Korda, A, primary, Revnic, C R, primary, Borile, G, primary, Diokmetzidou, A, primary, Murfitt, L, primary, Budko, A, primary, Fiordelisi, A, primary, De Wijs-Meijler, DPM, primary, Gevaert, AB, primary, Noriega De La Colina, A, primary, Benes, J, primary, Guillermo Solache Berrocal, GSB, primary, Gafarov, V, primary, Zhebel, VM, primary, Prakaschandra, R, primary, Stepien, E L, primary, Smith, LE, primary, Carluccio, MA, primary, Timasheva, Y, primary, Paci, M, primary, Dorofeyeva, N A, primary, Chimed, CH, primary, Petelina, TI, primary, Sorop, O, primary, Genis, A, primary, Parepa, I R, primary, Tscharre, M, primary, Krestjyaninov, MV, primary, Maia-Rocha, C, primary, Borges, L, primary, Sasonko, M L, primary, Kapel, SS, primary, Stam, K, primary, Sommariva, E, primary, Stojkovic, S, primary, O'reilly, J, primary, Chiva-Blanch, G, primary, Evtushenko, A, primary, Skopal, J, primary, Sunderland, N, primary, Gegenava, T, primary, Charnaia, MA, primary, Di Lascio, N, primary, Tarvainen, SJ, primary, Malandraki-Miller, S, primary, Uitterdijk, A, primary, Benzoni, P, primary, Ruivo, E, primary, Humphrey, E J, primary, Arokiaraj, MC, primary, Franco, D, additional, Garcia-Lopez, V, additional, Aranega, A, additional, Lopez-Sanchez, C, additional, Garcia-Martinez, V, additional, Tayel, S, additional, Khader, H, additional, El-Helbawy, N, additional, Alrefai, A, additional, El-Barbary, H, additional, Wu, JR, additional, Dai, ZK, additional, Yeh, JL, additional, Sanjurjo-Rodriguez, C, additional, Richaud-Patin, Y, additional, Blanco, FJ, additional, Badimon, L, additional, Raya, A, additional, Cahill, Paul A, additional, Diomede, F, additional, Merciaro, I, additional, Trubiani, O, additional, Nahapetyan, H, additional, Swiader, A, additional, Faccini, J, additional, Boya, P, additional, Elbaz, M, additional, Zeni, F, additional, Burba, I, additional, Bertolotti, M, additional, Capogrossi, MC, additional, Pompilio, G, additional, Raucci, A, additional, Widmer-Teske, R, additional, Dutzmann, J, additional, Bauersachs, J, additional, Donde, K, additional, Daniel, JM, additional, Sedding, DG, additional, Simionescu, N, additional, Sanda, GM, additional, Carnuta, MG, additional, Stancu, CS, additional, Popescu, AC, additional, Popescu, MR, additional, Vlad, A, additional, Dimulescu, DR, additional, Sima, AV, additional, Scoditti, E, additional, Pellegrino, M, additional, Calabriso, N, additional, Carluccio, MA, additional, Storelli, C, additional, De Caterina, R, additional, Solodenkova, KS, additional, Kalinina, EV, additional, Usachiova, MN, additional, Lappalainen, J, additional, Lee-Rueckert, M DE C, additional, Kovanen, PT, additional, Biesbroek, PS, additional, Emmens, RWE, additional, Van Rossum, AC, additional, Juffermans, LJM, additional, Niessen, JWM, additional, Krijnen, PAJ, additional, Kremzer, A, additional, Samura, T, additional, Berezina, T, additional, Gronenko, E, additional, Kim, MK, additional, Park, HJ, additional, Bae, SK, additional, Sorriento, D, additional, Ciccarelli, M, additional, Vernieri, E, additional, Campiglia, P, additional, Trimarco, B, additional, Iaccarino, G, additional, Hemmings, K E, additional, Porter, K E, additional, Ainscough, J F, additional, Drinkhill, M J, additional, Turner, N A, additional, Hiis, HG, additional, Cosson, MV, additional, Levy, FO, additional, Wieland, T, additional, Macquart, C, additional, Chatzifrangkeskou, M, additional, Evans, A, additional, Bonne, G, additional, Muchir, A, additional, Kemp, E, additional, Avkiran, M, additional, Carlomosti, F, additional, D'agostino, M, additional, Beji, S, additional, Zaccagnini, G, additional, Maimone, B, additional, Di Stefano, V, additional, De Santa, F, additional, Cordisco, S, additional, Antonini, A, additional, Ciarapica, R, additional, Dellambra, E, additional, Martelli, F, additional, Avitabile, D, additional, Scioli, MG, additional, Bielli, A, additional, Agostinelli, S, additional, Tarquini, C, additional, Tarallo, V, additional, De Falco, S, additional, Zaninoni, A, additional, Fiorelli, S, additional, Bianchi, P, additional, Teruzzi, G, additional, Squellerio, I, additional, Turnu, L, additional, Lualdi, A, additional, Tremoli, E, additional, Cavalca, V, additional, Lee, YJ, additional, Ju, ES, additional, Choi, JO, additional, Lee, GY, additional, Lim, BK, additional, Manickam, MANOJ, additional, Jung, S-H, additional, Omiya, S, additional, Otsu, K, additional, Deffge, C, additional, Nowak, S, additional, Wagner, M, additional, Braun-Dullaeus, RC, additional, Kostin, S, additional, Francke, A, additional, Subramaniam, S, additional, Kanse, SM, additional, Al-Lamee, K, additional, Schofield, CJ, additional, Egginton, S, additional, Gershlick, AH, additional, Kloska, D, additional, Kopacz, A, additional, Augustyniak, A, additional, Dulak, J, additional, Jozkowicz, A, additional, Hytonen, J, additional, Halonen, P, additional, Taavitsainen, J, additional, Tarvainen, S, additional, Hiltunen, T, additional, Liimatainen, T, additional, Kalliokoski, K, additional, Knuuti, J, additional, Yla-Herttuala, S, additional, Weinert, S, additional, Isermann, B, additional, Lee, J, additional, Herold, J, additional, Cochrane, A, additional, Kelaini, S, additional, Bojdo, J, additional, Vila Gonzalez, M, additional, Hu, Y, additional, Grieve, D, additional, Stitt, A W, additional, Zeng, L, additional, Xu, Q, additional, Margariti, A, additional, Reglin, B, additional, Xiang, W, additional, Nitzsche, B, additional, Maibier, M, additional, Pries, AR, additional, Vrijsen, KR, additional, Chamuleau, SAJ, additional, Verhage, V, additional, Metz, CHG, additional, Lodder, K, additional, Van Eeuwijk, ECM, additional, Van Dommelen, SM, additional, Doevendans, PA, additional, Smits, AM, additional, Goumans, MJ, additional, Sluijter, JPG, additional, Bova, M, additional, Loffredo, S, additional, Appleby, S, additional, Morrell, N, additional, Baranowska-Kuczko, M, additional, Kloza, M, additional, Ambrozewicz, E, additional, Kozlowski, M, additional, Malinowska, B, additional, Kozlowska, H, additional, Monti, M, additional, Terzuoli, E, additional, Ziche, M, additional, Mahmoud, AM, additional, Jones, AM, additional, Wilkinson, JA, additional, Romero, M, additional, Duarte, J, additional, Alexander, MY, additional, Faggian, G, additional, Kostareva, AA, additional, Malashicheva, AB, additional, Leurgans, TM, additional, Nguyen, TN, additional, Irmukhamedov, A, additional, Riber, LP, additional, Mcgeogh, R, additional, Comer, S, additional, Blanco Fernandez, A, additional, Ghigo, A, additional, Blaise, R, additional, Smirnova, NF, additional, Malet, N, additional, Vincent, P, additional, Limon, I, additional, Gayral, S, additional, Hirsch, E, additional, Laffargue, M, additional, Mehta, V, additional, Zachary, I, additional, Aidonidis, I, additional, Kramkowski, K, additional, Miltyk, W, additional, Kolodziejczyk, P, additional, Gradzka, A, additional, Szemraj, J, additional, Chabielska, E, additional, Dijkgraaf, I, additional, Bitsch, N, additional, Van Hoof, S, additional, Verhaegen, F, additional, Koenen, R, additional, Hackeng, TM, additional, Roshchupkin, D I, additional, Buravleva, K V, additional, Sergienko, VI, additional, Zhernossekov, DD, additional, Rybachuk, VM, additional, Grinenko, TV, additional, Furman, N, additional, Dolotovskaya, P, additional, Shamyunov, M, additional, Denisova, T, additional, Reiner, M, additional, Akhmedov, A, additional, Keller, S, additional, Miranda, M, additional, Briand, S, additional, Barile, L, additional, Kullak-Ublick, G, additional, Luscher, T, additional, Camici, G, additional, Guida, L, additional, Magnone, M, additional, Ameri, P, additional, Lazzarini, E, additional, Fresia, C, additional, Bruzzone, S, additional, Zocchi, E, additional, Di Paola, R, additional, Cordaro, M, additional, Crupi, R, additional, Siracusa, R, additional, Campolo, M, additional, Bruschetta, G, additional, Fusco, R, additional, Pugliatti, P, additional, Esposito, E, additional, Paloczi, J, additional, Ruivo, E, additional, Gaspar, R, additional, Dinnyes, A, additional, Kobolak, J, additional, Ferdinandy, P, additional, Gorbe, A, additional, Todorovic, Z, additional, Krstic, D, additional, Savic Vujovic, K, additional, Jovicic, D, additional, Basta Jovanovic, G, additional, Radojevic Skodric, S, additional, Prostran, M, additional, Dean, S, additional, Mee, CJ, additional, Harvey, KL, additional, Hussain, A, additional, Pena, C, additional, Paltineanu, B, additional, Voinea, S, additional, Revnic, F, additional, Ginghina, C, additional, Zaglia, T, additional, Ceriotti, P, additional, Campo, A, additional, Carullo, P, additional, Armani, A, additional, Coppini, R, additional, Vida, V, additional, Olivotto, I, additional, Stellin, G, additional, Rizzuto, R, additional, De Stefani, D, additional, Sandri, M, additional, Catalucci, D, additional, Mongillo, M, additional, Soumaka, E, additional, Kloukina, I, additional, Tsikitis, M, additional, Makridakis, M, additional, Varela, A, additional, Davos, C, additional, Vlachou, A, additional, Capetanaki, Y, additional, Iqbal, MM, additional, Bennett, H, additional, Davenport, B, additional, Pinali, C, additional, Cooper, G, additional, Cartwright, E, additional, Kitmitto, A, additional, Strutynska, NA, additional, Mys, LA, additional, Sagach, VF, additional, Franco, A, additional, Verzijl, A, additional, Stam, K, additional, Van Duin, R, additional, Reiss, IKM, additional, Duncker, DJ, additional, Merkus, D, additional, Shakeri, H, additional, Orije, M, additional, Leloup, AJ, additional, Van Hove, CE, additional, Van Craenenbroeck, EM, additional, De Meyer, GRY, additional, Vrints, CJ, additional, Lemmens, K, additional, Desjardins-Creapeau, L, additional, Wu, R, additional, Lamarre-Cliche, M, additional, Larochelle, P, additional, Bherer, L, additional, Girouard, H, additional, Melenovsky, M, additional, Kvasilova, A, additional, Benes, J, additional, Ruskova, K, additional, Sedmera, D, additional, Ana Barral, ABV, additional, Martin Fernandez, M, additional, Pablo Roman Garcia, PRG, additional, Juan Carlos Llosa, JCLL, additional, Manuel Naves Diaz, MND, additional, Cesar Moris, CM, additional, Jorge B Cannata-Andia, JBCA, additional, Isabel Rodriguez, IR, additional, Voevoda, M, additional, Gromova, E, additional, Maximov, V, additional, Panov, D, additional, Gagulin, I, additional, Gafarova, A, additional, Palahniuk, H, additional, Pashkova, IP, additional, Zhebel, NV, additional, Starzhynska, OL, additional, Naidoo, DP, additional, Rawojc, K, additional, Enguita, F J, additional, Grudzien, G, additional, Cordwell, SJ, additional, White, MY, additional, Massaro, M, additional, Martinelli, R, additional, Gatta, V, additional, Nasibullin, TR, additional, Erdman, VV, additional, Tuktarova, IA, additional, Mustafina, OE, additional, Hyttinen, J, additional, Severi, S, additional, Vorobyov, GG, additional, Batmyagmar, KH, additional, Lkhagvasuren, Z, additional, Gapon, LI, additional, Musikhina, NA, additional, Avdeeva, KS, additional, Dyachkov, SM, additional, Heinonen, I, additional, Van Kranenburg, M, additional, De Beer, VJ, additional, Octavia, Y, additional, Van Geuns, RJ, additional, Van Den Meiracker, AH, additional, Van Der Velden, J, additional, Everson, FP, additional, Ogundipe, T, additional, Grandjean, T, additional, De Boever, P, additional, Goswami, N, additional, Strijdom, H, additional, Suceveanu, A I, additional, Suceveanu, A P, additional, Mazilu, L, additional, Tofoleanu, D E, additional, Catrinoiu, D, additional, Rohla, M, additional, Hauser, C, additional, Huber, K, additional, Wojta, H, additional, Weiss, TW, additional, Melnikova, MA, additional, Olezov, NV, additional, Gimaev, RH, additional, Khalaf, H, additional, Ruzov, VI, additional, Adao, R, additional, Mendes-Ferreira, P, additional, Santos-Ribeiro, D, additional, Rademaker, M, additional, Leite-Moreira, AF, additional, Bras-Silva, C, additional, Alvarenga, LAA, additional, Falcao, RSP, additional, Dias, RR, additional, Lacchini, S, additional, Gutierrez, PS, additional, Michel, JB, additional, Gurfinkel, YU I, additional, Atkov, O YU, additional, Teichert, M, additional, Korn, C, additional, Mogler, C, additional, Hertel, S, additional, Arnold, C, additional, Korff, T, additional, Augustin, HG, additional, Van Duin, RWB, additional, De Wijs-Meijler, DPM, additional, D'alessandra, Y, additional, Farina, F M, additional, Casella, M, additional, Catto, V, additional, Carbucicchio, C, additional, Dello Russso, A, additional, Stadiotti, I, additional, Brambilla, S, additional, Chiesa, M, additional, Giacca, M, additional, Colombo, G I, additional, Tondo, C, additional, Ahlin, F, additional, Andric, T, additional, Tihanyi, D, additional, Wojta, J, additional, O'connell, E, additional, Butt, A, additional, Murphy, L, additional, Pennington, S, additional, Ledwidge, M, additional, Mcdonald, K, additional, Baugh, J, additional, Watson, C, additional, Suades, R, additional, Crespo, J, additional, Estruch, R, additional, Dyachenko, A, additional, Ryabukho, V, additional, Evtushenko, V, additional, Saushkina, YU, additional, Lishmanov, YU, additional, Smyshlyaev, K, additional, Bykov, A, additional, Popov, S, additional, Pavlyukova, E, additional, Anfinogenova, Y, additional, Szigetfu, E, additional, Kapornai, B, additional, Forizs, E, additional, Jenei, ZS, additional, Nagy, Z, additional, Merkely, B, additional, Zima, E, additional, Cai, A, additional, Dworakowski, R, additional, Gibbs, T, additional, Piper, S, additional, Jegard, N, additional, Mcdonagh, T, additional, Gegenava, M, additional, Dementieva, II, additional, Morozov, YUA, additional, Barsanti, C, additional, Stea, F, additional, Lenzarini, F, additional, Kusmic, C, additional, Faita, F, additional, Halonen, PJ, additional, Puhakka, PH, additional, Hytonen, JP, additional, Taavitsainen, JM, additional, Supit, E A, additional, Carr, C A, additional, Groenendijk, BCW, additional, Gorsse-Bakker, C, additional, Panasewicz, A, additional, Sneep, S, additional, Tempel, D, additional, Van Der Giessen, WJ, additional, Rys, J, additional, Daraio, C, additional, Dell'era, P, additional, Pigler, J, additional, Eder, A, additional, Eschenhagen, T, additional, Mazo, M M, additional, Amdursky, N, additional, Peters, N S, additional, Stevens, M M, additional, and Terracciano, C M, additional

Published
2016
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11. Condicionamento isquémico cardíaco remoto: mecanismos de cardioprotecção e aplicações clínicas

Author

Gaspar, A and Leite-Moreira, AF

Subjects
Isquemia do Miocárdio
Abstract

Despite a significant improvement in the care of acute coronary disease, mortality and morbidity remain important. One explanation for this lies in the fact that the very coronary reperfusion may paradoxically result in additional myocardial injury, through the so-called ischemia-reperfusion injury, partially mitigating the beneficial effects of myocardial reperfusion. Over the past two decades, numerous pharmacological interventions (such as the use of antioxidants, anti-inflammatory, magnesium, glucose/insulin/potassium, rapid normalization of pH) were studied in order to prevent ischemia-reperfusion injury. Despite the promising results obtained in animal experiments, attempts to transpose these results to humans, and consequently to clinical practice, have been disappointing. On the other hand, cardiac ischemic conditioning is an intervention that has produced positive results. Ischemic conditioning refers to the protection induced by short periods of ischemia followed by reperfusion, prior to a major ischemic event. Ischemic stimulus can be applied before (pre-conditioning), during (per-conditioning) or after (post-conditioning) the major ischemic event. An important finding regarding cardiac ischemic conditioning, was that protection could be induced remotely, introducing the concept of remote ischemic conditioning. In this paper, we proposed to review the mechanisms underlying remote ischemic cardiac conditioning and the possible clinical applications, considering more specifically pre and per-conditioning

Published
2012

12. Modulation of Myocardial Stiffness by beta-Adrenergic Stimulation Its Role in Normal and Failing Heart

Author

Falcao Pires, I, Fontes Sousa, AP, Lopes Conceicao, L, Bras Silva, C, Leite Moreira, AF, Instituto de Ciências Biomédicas Abel Salazar, and Faculdade de Medicina

Subjects
Health sciences, Basic medicine, Basic medicine [Medical and Health sciences], Ciências da Saúde, Medicina básica, Medicina básica [Ciências médicas e da saúde]
Abstract

The acute effects of ß-adrenergic stimulation on myocardial stiffness were evaluated. New-Zealand white rabbits were treated with saline (control group) or doxorubicin to induce heart failure (HF) (DOXO-HF group). Effects of isoprenaline (10 -10-1 -5 M), a non-selective ß-adrenergic agonist, were tested in papillary muscles from both groups. In the control group, the effects of isoprenaline were also evaluated in the presence of a damaged endocardial endothelium, atenolol (ßi-adrenoceptor antagonist), ICI-118551 (ßz-adrenoceptor antagonist), KT-5720 (PKA inhibitor), L-NNA (NO-synthase inhibitor), or indomethacin (cyclooxygenase inhibitor). Passive length-tension relations were constructed before and after adding isoprenaline (10 -5 M). In the control group, isoprenaline increased resting muscle length up to 1.017±0.006 L/L max. Correction of resting muscle length to its initial value resulted in a 28.5±3.1% decrease of resting tension, indicating decreased muscle stiffness, as confirmed by the isoprenaline-induced right-downward shift of the passive lengthtension relation. These effects were modulated by ßr and ß 2adrenoceptors and PKA. In DOXO-HF group, the effect on myocardial stiffness was significantly decreased. We conclude that ß-adrenergic stimulation is a relevant mechanism of acute neurohumoral modulation of the diastolic function. Furthermore, this study clarifies the mechanisms by which myocardial stiffness is decreased. (c) 2011 Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic.

Published
2011

13. ETB2 Receptor Subtype Stimulation Relaxes the Iris Sphincter Muscle

Author

Rocha-Sousa A, Saraiva J, Alves-Faria P, Falcão-Reis F, Leite-Moreira AF, and Faculdade de Medicina

Subjects
Other medical sciences, Outras ciências médicas, Other medical sciences [Medical and Health sciences], Outras ciências médicas [Ciências médicas e da saúde]
Abstract

Effects of ETB receptor stimulation and its subcellular pathways were evaluated in carbachol pre-contracted rabbit iris sphincter muscles (n=51). ETB stimulation with sarafotoxin (SRTX-c; 10(-10)-10(-6) M) was tested in the absence (n=7) or presence of 10(-5) M of: BQ-788 (ETB2 receptor antagonist; n=6), L-NA (NOS inhibitor; n=7) or indomethacin (cyclooxygenase inhibitor; n=10). Effects of ETB stimulation by endothelin-1 (ET-1; 10-(10)-10(-7) M) in the presence of an ETA receptor antagonist (BQ-123; 10(-5) M; n=7) and of ETB1 stimulation by IRL-1620 (10-(10)-10(-7) M; n=7) were also tested. Finally, the effects of SRTX-c (10(-9)-10(-7) M) in electric field stimulation (EFS) contraction were evaluated (n=7). ETB receptor stimulation by SRTX-c or ET-1 in presence of BQ-123 promoted a concentration-dependent relaxation of the rabbit iris sphincter muscle by 10.8 +/- 2.0 % and 9.4 +/- 1.8 %, respectively. This effect was blocked by BQ-788 (-2.3 +/- 2.0 %), L-NA (4.5 +/- 2.3 %) or indomethacin (2.3 +/- 2.9 %). Selective ETB1 stimulation by IRL-1620 did not relax the iris sphincter muscle (0.9 +/- 5.4 %). EFS elicited contraction was not altered by SRTX-c. In conclusion, ETB receptor stimulation relaxes the carbachol precontracted iris sphincter muscle, an effect that is mediated by the ETB2 receptor subtype, through NO and the release of prostaglandins.

Published
2009

14. Ghrelin, des-acyl ghrelin and obestatin: Three pieces of the same puzzle

Author

Soares JB, Leite-Moreira AF, and Faculdade de Medicina

Subjects
Other medical sciences, digestive, oral, and skin physiology, Outras ciências médicas, Other medical sciences [Medical and Health sciences], Outras ciências médicas [Ciências médicas e da saúde], hormones, hormone substitutes, and hormone antagonists
Published
2008

15. Effect of TNF-alpha blockade in monocrotaline-induced pulmonary hypertension

Author

Henriques-Coelho, T, Brandão-Nogueira, A, Moreira-Gonçalves, D, Correia-Pinto, J, Leite-Moreira, AF, and Faculdade de Medicina

Subjects
Ciências exactas e naturais, Natural sciences
Abstract

INTRODUCTION: TNF-alpha blockade in ischemic heart failure is still the subject of debate since clinical trials show conflicting results. However, its benefit in heart failure secondary to pulmonary hypertension has yet to be determined. It has been reported that transgenic rats overexpressing TNF-alpha develop pulmonary hypertension. The aim of this study was to assess the morphologic and hemodynamic effects of administration of an anti-TNF-alpha monoclonal antibody (etanercept) in rats with monocrotaline (MCT)-induced pulmonary hypertension. METHODS: Adult Wistar rats were injected with MCT (60 mg/Kg sc), or vehicle only (day 0). Beginning one day later, the animals were randomly treated with etanercept (ETC, 0.03 mg/Kg sc, three times a week) or with a similar volume of vehicle. The study thus had four groups: Ctrl (n = 6), Ctrl + ETC (n = 6), MCT (n = 6) and MCT + ETC (n = 6). On days 22-23, the rats were instrumented to record right ventricular systolic and end-diastolic pressures, dP/dtmax and tau. At the end of each experiment the heart and lungs were weighed. RESULTS AND CONCLUSIONS: Chronic administration of etanercept induced only a slight increase in relaxation velocity, with no effect on other hemodynamic parameters, including pulmonary hypertension, and no reduction in right ventricular hypertrophy. These results suggest that etanercept does not lead to a significant improvement in heart failure secondary to pulmonary hypertension.

Published
2008

16. Acute neurohumoral modulation of diastolic function

Author

Ladeiras-Lopes R, Ferreira-Martins J, Leite-Moreira AF, and Faculdade de Medicina

Subjects
Other medical sciences, Outras ciências médicas, Other medical sciences [Medical and Health sciences], Outras ciências médicas [Ciências médicas e da saúde]
Published
2008

18. Targeted gene transfer to the developing rodent lung interstitium by ultrasound guided intraparenchymal injection

Author

Henriques-Coelho, T, Gonzaga, S, Endo, M, Zoltick, PW, Davey, M, Leite-Moreira, AF, Correia-Pinto, J, Flake, AW, and Faculdade de Medicina

Subjects
Ciências médicas e da saúde, Medical and Health sciences, respiratory system
Abstract

In utero gene transfer to the developing lung may have clinical or research applications. In this study, we developed a new method for specifically targeting the fetal rat lung with adeno and lentiviral vectors encoding the enhanced green fluorescence protein (EGFP) marker gene at E15.5 using ultrasound biomicroscopy (UBM). Survival rate, morphometric parameters, viral biodistribution, and lung transduction efficiency were analyzed and compared to the intra-amniotic route of administration. Expression of EGFP started as early as 24 and 72 h after the injection of adenoviral and lentiviral vectors, respectively. Both vectors transduced lung parenchyma with gene expression limited to interstitial cells of the injected region, in contrast to intra-amniotic injection, which targeted the pulmonary epithelium. Expression of EGFP was most intense at E18.5 and E21.5 for adenoviral and lentiviral vectors, respectively. In contrast to lentivirus, adenoviral expression significantly declined until final analysis at 1 week of age. This study demonstrates the feasibility of targeting the fetal rat lung interstitium with viral vectors under UBM guidance during the pseudoglandular stage. This model system may facilitate in vivo studies of dynamic lung morphogenesis and could provide insight into the efficacy of prenatal gene transfer strategies for treatment of specific lung disorders.

Published
2007

19. Myocardial Dysfunction and Neurohumoral Activation Without Remodeling in the Left Ventricle of Monocrotaline-Induced Pulmonary Hypertensive Rat

Author

Lourenço, AP, Roncon-Albuquerque R, Jr., Brás-Silva, C, Faria, B, Wieland, J, Henriques-Coelho, T, Correia-Pinto, J, Leite-Moreira, AF, and Faculdade de Medicina

Subjects
Ciências médicas e da saúde, Medical and Health sciences
Abstract

In monocrotaline (MCT)-induced pulmonary hypertension (PH), only the right ventricle (RV) endures overload, but both ventricles are exposed to enhanced neuroendocrine stimulation. To assess whether in long-standing PH the left ventricular (LV) myocardium molecular/contractile phenotype can be disturbed, we evaluated myocardial function, histology, and gene expression of autocrine/paracrine systems in rats with severe PH 6 wk after subcutaneous injection of 60 mg/kg MCT. The overloaded RV underwent myocardial hypertrophy (P < 0.001) and fibrosis (P = 0.014) as well as increased expression of angiotensin-converting enzyme (ACE) (8-fold; P < 0.001), endothelin-1 (ET-1) (6-fold; P < 0.001), and type B natriuretic peptide (BNP) (15-fold; P < 0.001). Despite the similar upregulation of ET-1 (8-fold; P < 0.001) and overexpression of ACE (4-fold; P < 0.001) without BNP elevation, the nonoverloaded LV myocardium was neither hypertrophic nor fibrotic. LV indexes of contractility (P < 0.001) and relaxation (P = 0.03) were abnormal, however, and LV muscle strips from MCT-treated compared with sham rats presented negative (P = 0.003) force-frequency relationships (FFR). Despite higher ET-1 production, BQ-123 (ET(A) antagonist) did not alter LV MCT-treated muscle strip contractility distinctly (P = 0.005) from the negative inotropic effect exerted on shams. Chronic daily therapy with 250 mg/kg bosentan (dual endothelin receptor antagonist) after MCT injection not only attenuated RV hypertrophy and local neuroendocrine activation but also completely reverted FFR of LV muscle strips to positive values. In conclusion, the LV myocardium is altered in advanced MCT-induced PH, undergoing neuroendocrine activation and contractile dysfunction in the absence of hypertrophy or fibrosis. Neuroendocrine mediators, particularly ET-1, may participate in this functional deterioration.

Published
2006

20. Ghrelin reverses molecular, structural and hemodynamic alterations of the right ventricle in pulmonary hypertension

Author

Henriques-Coelho, T, Roncon-Albuquerque R, Jr., Lourenço, AP, Baptista, MJ, Oliveira, SM, Brandão-Nogueira, A, Correia-Pinto, J, Leite-Moreira, AF, and Faculdade de Medicina

Subjects
digestive, oral, and skin physiology, Ciências médicas e da saúde, Medical and Health sciences
Abstract

Ghrelin is an endogenous peptide that has a dual effect by activating specific receptors and by stimulating release of growth hormone. There is increasing evidence that ghrelin has a potent vasodilator effect. Recently, we demonstrated that exogenous administration of ghrelin modulates its endogenous levels and attenuates the majority of alterations induced by monocrotaline (MCT). In the present study, we evaluate the effects of chronic administration of ghrelin on hemodynamic and morphometric parameters of the right ventricle, as well as on myocardial levels of SERCA2a and endothelin-1. Adult Wistar rats were injected with MCT (60 mg/kg, sc) or just the vehicle (day 0). One week later, the animals treated with MCT were randomly divided into two groups and treated with ghrelin (100 microg/kg, bid, sc) or with a similar volume of vehicle. Between days 21-25 the animals were instrumented to record right ventricular (RV) pressures and samples were collected for morphological and molecular analysis. Ghrelin treatment attenuated the effects of MCT, namely: RV myocyte fiber diameter, pulmonary vascular remodeling (evaluated by % medial wall thickness of peripheral arteries), RV peak systolic pressure, RV end-diastolic pressure, time constant tau, and SERCA2a and endothelin-1 mRNA levels. Chronic ghrelin administration attenuates MCT-induced pulmonary hypertension, vascular remodeling and RV hypertrophy. These results suggest a potential therapeutic role for the ghrelin-growth hormone axis in pulmonary hypertension.

Published
2006

21. Contractile effects of Ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium

Author

Soares, JB, Rocha-Sousa, A, Castro-Chaves, P, Henriques-Coelho, T, Roncon-Albuquerque R, Jr., Leite-Moreira, AF, and Faculdade de Medicina

Subjects
Ciências médicas e da saúde, Medical and Health sciences
Abstract

INTRODUCTION: Ghrelin, isolated in 1999, is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R1a). Recent studies suggest that it may influence the function of normal and failing hearts. Nonetheless, it has been difficult to differentiate its effects on the intrinsic properties of the myocardium from the secondary effects resulting from growth hormone release and vasomotor action. This study investigated the contractile effects of ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium. METHODS: Adult Wistar rats randomly received monocrotaline (MCT; n=9; 60 mg/kg, s.c.) or vehicle (n=7; 1 ml/kg). Three weeks later, after right ventricular (RV) hemodynamic evaluation, the effects of 10(-6) M of a pentapeptide active fragment of ghrelin (fG) were tested on contractile parameters of RV papillary muscles (Normal, n=7; MCT, n=9). GHS-R1a mRNA expression was estimated in RV transmural free-wall samples (Normal, n=7; MCT, n=9), using real-time RT-PCR. RESULTS: In the Normal group, fG reduced active tension (AT), maximum velocity of tension rise (dT/dt(max)) and maximum velocity of tension decline (dT/dt(min)), by 27.9 +/- 4.0%, 28.5 +/- 6.7% and 21.4 +/- 4.2% respectively. In the MCT group, fG reduced AT, dT/dt(max) and dT/dt(min) by 24.1 +/- 6.3%, 24.3 +/- 6.5% and 24.5 +/- 6.1% respectively. GHS-R1a mRNA expression was similar in the two groups (Normal: 2.3*10(5) +/- 5.4*10(4); MCT: 3.0*10(5) +/- 1.1*10(5): p > 0.05). CONCLUSION: This study shows that ghrelin has negative inotropic and lusitropic effects. These effects and expression of its receptor are preserved in RV hypertrophy, suggesting that ghrelin may be a new target in progression to heart failure.

Published
2005

23. N-terminal-pro-B type natriuretic peptide as a useful tool to evaluate pulmonary hypertension and cardiac function in CDH infants

Author

Baptista, MJ, Rocha, G, Clemente, F, Azevedo, LF, Tibboel, Dick, Leite-Moreira, AF, Guimaraes, H, Areias, JC, Correia-Pinto, J, Baptista, MJ, Rocha, G, Clemente, F, Azevedo, LF, Tibboel, Dick, Leite-Moreira, AF, Guimaraes, H, Areias, JC, and Correia-Pinto, J

Abstract

Objective: In congenital diaphragmatic hernia (CDH) the severity of pulmonary hypertension (PH) is considered, by several authors, determinant of clinical outcome. Plasmatic N-terminal-pro- B type natriuretic peptide (NT-proBNP) might be useful in diagnosis and management of PH in newborns, although its interest in CDH infants remains to be defined. Early NT-proBNP levels were assessed in CDH infants and correlated with cardiovascular echocardiographic parameters. Patients and Methods: 28 newborns, CDH and age-matched controls were enrolled in a prospective study. Clinical condition, NT-proBNP plasmatic levels, echo parameters of PH and biventricular function were assessed at 24 h after delivery as well as survival outcome. Results: Estimated mean pulmonary pressure and NT-proBNP were significantly higher in CDH than control infants. NT-proBNP significantly correlated with estimated pulmonary artery pressure, right ventricular Tei index, and tricuspid E/A ratio. Additionally, we found that CDH infants with NT-proBNP >11,500 pg/ml experienced a worse prognosis. Conclusions: We demonstrated that PH is associated with NT-proBNP elevation and diastolic impairment in CDH infants. Early elevations in NT-proBNP levels seem to alert for a subset of CDH infants with worse prognosis. Copyright (C) 2007 S. Karger AG, Basel.

Published
2008

38. P81 Changes on right ventricle induced by a high caloric diet and a left ventricle model of pressure overload.

Author

Goncalves, N, Correia, E, Silva, AF, Moura, CM, Roncon Albuquerque, R, Falcao Pires, I, and Leite Moreira, AF

Subjects
RIGHT heart ventricle, CARDIOVASCULAR diseases risk factors, HEART cells, HYPERTROPHY, DATA analysis, GENE expression
Abstract

Purpose: Two major cardiovascular risk factors are hypertension and metabolic syndrome. This study aimed to evaluate the influence of a high-caloric diet, left ventricle (LV) chronic pressure overload, and their combination on right ventricle (RV) structure and function. Methods: Wistar rats (60-80g) were subjected to ascending aorta constriction (Ba) or sham procedure (Sh). After 2 weeks the animals were randomly divided and fed with a regular diet (Rd,2.9kcal) or with a western-type diet rich in carbohydrates, fat and salt(Hd,5.4kcal), resulting in 4 groups: Sh+Rd, Sh+Hd, Ba+Rd, Ba+Hd. After 8weeks of protocol RV function was assessed by pressure-volume catheters and samples obtained for morpho-histological and molecular analysis. Data presented as mean ±SEM. α vs. Sh+Rd, β vs. Ba+Rd, δ vs. Sh+Hd. p<0.05. Results: The administration of a western-type diet resulted in increased fat depots, visceral adipocyte hypertrophy, cardiomyocyte cross sectional area (CSA) and collagen III overexpression, in both Hd groups (Img1). These structural changes reflected in RV function by increased Pmax, dP/dtmax as well as impaired relaxation seen by the constant t. Constriction of ascending aorta for 8weeks resulted in increased heart/tibial length (TL) ratio, RV Pmax as well as RV cardiomyocyte hypertrophy together with BNP overexpression (Ba+Rd).The concomitant presence of these two cardiovascular risk factors in Ba+Hd animals led to a significant heart and RV cardiomyocyte hypertrophy as well as collagen I overexpression. Conclusions: This study demonstrates that both Western diet consumption and LV chronic pressure overload induce RV structural and functional changes and that the combination of these factors further promotes hypertrophy and extracellular matrix changes in the non-overloaded ventricle. [ABSTRACT FROM PUBLISHER]

Published
2014
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39. P505 Neuregulin-1 ameliorates right ventricular diastolic dysfunction in pulmonary arterial hypertension.

Author

Adao, R, Mendes-Ferreira, P, Hamdani, N, Maia-Rocha, C, Mendes, MJ, Falcao-Pires, I, De Keulenaer, GW, Linke, W, Leite-Moreira, AF, and Bras-Silva, C

Subjects
NEUREGULINS, RIGHT heart ventricle, DIASTOLE (Cardiac cycle), HEART disease diagnosis, CARDIOVASCULAR disease diagnosis, HYPERTENSION, LABORATORY rats
Abstract

Neuregulin (NRG)-1 is involved in the preservation of left ventricular performance. Nevertheless, the role of NRG-1 in pulmonary arterial hypertension(PAH) and right ventricular(RV) diastolic stiffness is unknown. We analysed the presence and possible underlying mechanisms of RV diastolic dysfunction in an animal model of PAH and the role of NRG-1 in this context.Wistar rats randomly received monocrotaline (MCT,60mg/Kg,sc) or vehicle. After 14 days, rats received NRG-1 (40ug/Kg/day,ip) or vehicle. The study resulted in 4 groups: control(CTRL,n=16); CTRL+NRG(n=15); MCT(n=13); MCT+NRG(n=18). RV invasive hemodynamic studies and sample collection were performed 25-28 days after MCT administration. Isolated cardiomyocytes were stretched to measure resting tension and phosphorylation of titin isoforms was analyzed (ProQ Diamond and SYPRO Ruby protein gel stains). Only significant results (p<0.05) are given.RV diastolic stiffness (β) was increased in MCT rats (MCT vs CTRL:0.016±0.002 vs 0.008±0.001). However, NRG-1 treatment attenuated this change (MCT+NRG:0.007±0.001). Histological analyses revealed increased cardiomyocyte cross-sectional areas (MCT vs CTRL:536.67±59.46 vs 375.39±47.43μm2), indicating RV hypertrophy. In addition, the amount of RV fibrosis was enhanced in PAH tissue (MCT vs CTRL:2.04±0.17 vs 0.98±0.07%). NRG-1 also attenuated both changes (MCT+NRG:409.01±19.72μm2 and 1.00±0.17%, respectively). MCT-group isolated cardiomyocytes developed higher passive force when compared to CTRL-group cells at the sarcomere lengths of 2.0 (MCT vs CTRL:1.90±0.43 vs 1.43±0.29N/m2), 2.2 (MCT vs CTRL:3.66±0.69 vs 2.68±0.24N/m2), and 2.3μm (MCT vs CTRL: 5.76±1.15 vs 3.86±0.87N/m2). NRG-1 restored passive force development to levels similar to the CTRL-group, at 2.0, 2.2, and 2.3μm (MCT+NRG:1.28±0.25, 3.04±0.55, and 3.63±0.89N/m2, respectively). CTRL+NRG-group cells developed less passive force compared to CTRL-group (CTRL+NRG:1.16±0.31, 2.27±0.38, and 3.05±0.54N/m2, at 2.0, 2.2, and 2.3μm respectively). Titin phosphorylation was reduced in RV tissue of MCT rats (MCT vs CTRL:1.06±0.38 vs 1.62±0.85,arbitrary units) and increased in MCT+NRG group (2.28±0.61).RV diastolic stiffness is increased in MCT rats, with important contributions from increased fibrosis and intrinsic stiffening of the RV cardiomyocyte sarcomeres. NRG-1 treatment decreases the passive force and thus myocardial stiffness, either in rats with RV hypertrophy or in healthy animals. These findings show that NRG-1 pathway regulates systolic and diastolic function at the cellular level, suggesting a potential therapeutic role of this pathway in PAH. [ABSTRACT FROM AUTHOR]

Published
2014
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40. P103 Impact of diabetes mellitus on myofilaments phosphorylation and calcium sensitivity is aortic stenosis patients.

Author

Falcao-Pires, I, Wijnke, P, Gavina, C, Paulus, WJ, Leite-Moreira, AF, and Van Der Velden, J

Subjects
DIABETES, CYTOPLASMIC filaments, PHOSPHORYLATION, AORTIC stenosis, DISEASE progression, HEART valve transplantation, DISEASE risk factors
Abstract

Background: Diabetes mellitus (DM) is an independent risk factor for progression of aortic valve stenosis (AS) and significantly impacts longterm outcome after valve replacement. Our aim was to clarify myofilamentary changes induced by DM on AS patients.Methods and Results: Patients with severe isolated AS (n=20) and AS plus type-II diabetes patients (AS-DM+, n=16) with preserved left ventricular (LV) ejection fraction and no clinical or angiographic signs of coronary artery disease were studied. Doppler echocardiographic data was used to compare in vivo LV function. Biopsies were used to isolate and permeabilize cardiomyocytes allowing to assess active force (Factive), resting force (Fpassive) and calcium sensitivity (pCa50) before and after incubation with PKA as well as to measure phosphorylation of myofilamentary proteins.Compared to AS patients, AS-DM+ patients presented aggravated diastolic dysfunction, increased myofilaments pCa50 and a higher PKA-induced drop of pCa50 which was correlated with higher baseline levels of PKA-induced phosphorylation of Troponin I.Conclusions: We have shown that myofilamentary changes induced by DM in AS patients are related to PKA-mediated hyperphosphorylation status of troponin I. This study highlights the need for earlier therapeutic interventions in order to prevent these myofilamentary alterations that fasten the progression of diastolic dysfunction in diabetic AS patients. [ABSTRACT FROM PUBLISHER]

Published
2014
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41. P755 Molecular mechanisms underlying the beneficial effects of neuregulin-1 in pulmonary arterial hypertension.

Author

Maia-Rocha, C, Mendes-Ferreira, P, Adao, R, Santos-Ribeiro, D, Alves, BS, De Keulenaer, GW, Leite-Moreira, AF, and Bras-Silva, C

Subjects
MOLECULAR biology, NEUREGULINS, PULMONARY hypertension, RIGHT heart ventricle, HEART failure, HOMEOSTASIS
Abstract

Pulmonary arterial hypertension (PAH) leads to right ventricular (RV) failure and death. Neuregulin (NRG)-1 has been implicated in several processes regulating cardiac development, as well as cardiac and vascular homeostasis. It was previously shown, in an experimental model of MCT-induced PAH, that NRG-1 treatment is able to restore PAH-induced severe abnormalities in cardiac function and structure. This study investigated the underlying molecular mechanisms to the beneficial effects of NRG-1 in myocardial function, in the same animal model of induced PAH.Male Wistar rats randomly received monocrotaline (MCT, 60mg/Kg,sc) or vehicle. After 14 days, animals received NRG-1 (40μg/Kg/day,ip) or vehicle, resulting in 4 groups: CTRL; CTRL+NRG-1; MCT; MCT+NRG-1. RV sample collection for were performed 21-24 days after MCT administration. Only significant results (mean±SEM, p<0.05) are given.NRG-1/ErbB system components expressions in MCT animals are changed. We observed increased levels of NRG-1 in RV (11.1±2.8 vs 1.0±0.3 AU, MCT vs CTRL), which were reversed by NRG-1 treatment (MCT+NRG-1: 0.7±0.5 AU), and decreased levels of ErbB4 in all MCT animals (MCT: 0.6±0.2 and MCT+NRG-1: 0.7±0.15 AU). We also found increased levels of ErbB2 (2.0±0.3 AU), ADAM-17 (2.1±0.3 AU) and ADAM-19 (2.7±0.3 AU), and increased eNOS expression (2.0±0.3 AU) in the RV of MCT animals that not reversed with NRG-1 treatment. MCT treatment led to altered GLUT1 expression (4.1±0.5 AU) and NRG-1 treatment attenuated this increase (1.7±0.3 AU). GLUT4 was increased in all animals treated with NRG-1 (CTRL+NRG-1: 1.4±0.1; MCT+NRG-1: 1.5±0.2 AU). Increased RV caspase 3 (MCT: 4.4±0.4 AU) and plasmatic expression of IL-6 and TNF-α (IL6: 2.7±0.7 AU; TNF-α: 1.7±0.3 AU) were attenuated by NRG-1 treatment (caspase 3: 1.7±0.3 AU; IL6: 2.0±0.4 AU; TNF-α: 1.5±0.4 AU). Moreover, we found that the increased expression of BNP (17.5±2.2 AU), ET-1 (5.0±1.2 AU) and HIF-1α (4.3±1.1 AU) observed in MCT animals was attenuated or reversed with NRG-1 therapy (MCT+NRG-1: 5.6±1.9; 1.7±0.7; 1.4±0.1 AU, respectively).In conclusion, we show that NRG-1 treatment is able to restore the changes in expression of markers of cardiac overload, hypertrophy and hypoxia induced by PAH. These beneficial effects of NRG-1 are associated with the modulation of different signaling pathways, namely apoptotic, metabolic, survival/ proliferation, and inflammation pathways. [ABSTRACT FROM PUBLISHER]

Published
2014
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42. Physiologic basis and pathophysiologic implications of the diastolic properties of the cardiac muscle.

Author

Ferreira-Martins J and Leite-Moreira AF

Abstract

Although systole was for long considered the core of cardiac function, hemodynamic performance is evenly dependent on appropriate systolic and diastolic functions. The recognition that isolated diastolic dysfunction is the major culprit for approximately fifty percent of all heart failure cases imposes a deeper understanding of its underlying mechanisms so that better diagnostic and therapeutic strategies can be designed. Risk factors leading to diastolic dysfunction affect myocardial relaxation and/or its material properties by disrupting the homeostasis of cardiomyocytes as well as their relation with surrounding matrix and vascular structures. As a consequence, slower ventricular relaxation and higher myocardial stiffness may result in higher ventricular filling pressures and in the risk of hemodynamic decompensation. Thus, determining the mechanisms of diastolic function and their implications in the pathophysiology of heart failure with normal ejection fraction has become a prominent field in basic and clinical research. [ABSTRACT FROM AUTHOR]

Published
2010
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43. Targeting myocardial remodelling to develop novel therapies for heart failure: a position paper from the Working Group on Myocardial Function of the European Society of Cardiology

Author

Guido Iaccarino, Johann Bauersachs, Jean-Luc Balligand, Manuel Mayr, Guido Tarone, Stephane Heymans, Thomas Thum, Adelino F. Leite-Moreira, Denise Hilfiker-Kleiner, Leon J. De Windt, Ralph Knöll, Carlo G. Tocchetti, Angela Clerk, André P. Lourenço, Emilio Hirsch, Tarone, G, Balligand, Jl, Bauersachs, J, Clerk, A, De Windt, L, Heymans, S, Hilfiker Kleiner, D, Hirsch, E, Iaccarino, G, Knöll, R, Leite Moreira, Af, Lourenço, Ap, Mayr, M, Thum, T, Tocchetti, CARLO GABRIELE, Cardiologie, MUMC+: MA Med Staf Spec Cardiologie (9), and RS: CARIM - R2 - Cardiac function and failure

Subjects
medicine.medical_specialty, Peripartum cardiomyopathy, Cell Survival, Heart failure, Contractility, Muscle hypertrophy, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Translational Research, Biomedical, Internal medicine, Cyclosporin a, Cardiomyocyte survival, Cardiac remodelling, Medicine, Humans, Urea, Myocytes, Cardiac, Pressure overload, Ventricular Remodeling, business.industry, Dilated cardiomyopathy, Drugs, Investigational, medicine.disease, Myocardial Contraction, Adaptive hypertrophy, Omecamtiv mecarbil, Cardiology, Cyclosporine, Hypertrophy, Left Ventricular, Cardiology and Cardiovascular Medicine, business
Abstract

The failing heart is characterized by complex tissue remodelling involving increased cardiomyocyte death, and impairment of sarcomere function, metabolic activity, endothelial and vascular function, together with increased inflammation and interstitial fibrosis. For years, therapeutic approaches for heart failure (HF) relied on vasodilators and diuretics which relieve cardiac workload and HF symptoms. The introduction in the clinic of drugs interfering with beta-adrenergic and angiotensin signalling have ameliorated survival by interfering with the intimate mechanism of cardiac compensation. Current therapy, though, still has a limited capacity to restore muscle function fully, and the development of novel therapeutic targets is still an important medical need. Recent progress in understanding the molecular basis of myocardial dysfunction in HF is paving the way for development of new treatments capable of restoring muscle function and targeting specific pathological subsets of LV dysfunction. These include potentiating cardiomyocyte contractility, increasing cardiomyocyte survival and adaptive hypertrophy, increasing oxygen and nutrition supply by sustaining vessel formation, and reducing ventricular stiffness by favourable extracellular matrix remodelling. Here, we consider drugs such as omecamtiv mecarbil, nitroxyl donors, cyclosporin A, SERCA2a (sarcoplasmic/endoplasmic Ca(2 +) ATPase 2a), neuregulin, and bromocriptine, all of which are currently in clinical trials as potential HF therapies, and discuss novel molecular targets with potential therapeutic impact that are in the pre-clinical phases of investigation. Finally, we consider conceptual changes in basic science approaches to improve their translation into successful clinical applications.

Published
2014

44. ESC Working Group on Myocardial Function Position Paper: how to study the right ventricle in experimental models

Author

Leite-Moreira, Adelino F., Lourenco, Andre P., Balligand, Jean-Luc, Bauersachs, Johann, Clerk, Angela, De Windt, Leon J., Heymans, Stephane, Hilfiker-Kleiner, Denise, Hirsch, Emilio, Iaccarino, Guido, Kaminski, Karol A., Knoell, Ralph, Mayr, Manuel, Tarone, Guido, Thum, Thomas, Tocchetti, Carlo G., Leite Moreira, Af, Lourenço, Ap, Balligand, Jl, Bauersachs, J, Clerk, A, De Windt, Lj, Heymans, S, Hilfiker Kleiner, D, Hirsch, E, Iaccarino, G, Kaminski, Ka, Knöll, R, Mayr, M, Tarone, G, Thum, T, Tocchetti, CARLO GABRIELE, Cardiologie, MUMC+: MA Med Staf Spec Cardiologie (9), and RS: CARIM - R2 - Cardiac function and failure

Subjects
Biomedical Research, Haemodynamics, Heart Ventricles, Ventricular Dysfunction, Right, Right ventricle function, Hemodynamics, Models, Cardiovascular, Prognosis, Research Design, Functional evaluation, Experimental myocardial preparations, Ventricular Function, Right, Chronic overload, Humans, Myocytes, Cardiac, Cardiac imaging, Biomarkers
Abstract

The right ventricle has become an increasing focus in cardiovascular research. In this position paper, we give a brief overview of the specific pathophysiological features of the right ventricle, with particular emphasis on functional and molecular modifications as well as therapeutic strategies in chronic overload, highlighting the differences from the left ventricle. Importantly, we put together recommendations on promising topics of research in the field, experimental study design, and functional evaluation of the right ventricle in experimental models, from non-invasive methodologies to haemodynamic evaluation and ex vivo set-ups.

Published
2014

47. Myosin-Inhibitor Mavacamten Acutely Enhances Cardiomyocyte Diastolic Compliance in Heart Failure With Preserved Ejection Fraction.

Author

Almeida-Coelho J, Leite-Moreira AM, Sequeira V, Hamdani N, Lourenço AP, Falcão-Pires I, and Leite-Moreira AF

Subjects
Animals, Diastole, Humans, Ventricular Function, Left drug effects, Male, Compliance, Uracil analogs & derivatives, Uracil therapeutic use, Uracil pharmacology, Benzylamines, Myocytes, Cardiac drug effects, Stroke Volume drug effects, Stroke Volume physiology, Heart Failure drug therapy, Heart Failure physiopathology
Abstract

Competing Interests: Dr Sequeira has received research funding from Bristol Myers Squibb unrelated to this work. The other authors report no conflicts.

Published
2024
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48. Ferritin, inflammation, and iron deficiency in acute heart failure: evidence from the EDIFICA cohort.

Author

Vasques-Nóvoa F, Pimentel MJ, Marques P, Vale C, Gomes F, Neves JS, Barroso I, Guimarães JT, Bettencourt P, Leite-Moreira AF, Roncon-Albuquerque R Jr, Almeida J, Ferreira JP, and Friões F

Abstract

Background: Ferritin is commonly used to evaluate iron stores and guide therapeutic decisions regarding intravenous iron supplementation. However, in the context of AHF, inflammation-driven upregulation of ferritin might disrupt its correlation with iron stores, restricting iron bioavailability and potentially amplifying the inflammatory response., Aim: This study aims to assess the clinical and prognostic associations of ferritin levels in an AHF cohort and to determine whether the prognostic value of ferritin is influenced by the presence of infection, inflammatory activation, and other markers of iron deficiency., Methods: The association between ferritin and clinical outcomes (180 days) in AHF was evaluated in a cohort of 526 patients from the EDIFICA registry., Results: The median ferritin plasma concentration at admission was 180 pg/mL. Patients with higher ferritin levels at admission were predominantly men, exhibiting a high prevalence of chronic kidney disease and alcohol consumption, and presenting with lower blood pressure and a higher incidence of clinical infection. Higher ferritin levels were associated with increased risk of the composite of heart failure hospitalization or cardiovascular death (Tertile 2: HR 1.75; 95% CI 1.10-2.79; p = 0.017; Tertile 3: HR 1.79; 95% CI 1.08-2.97; p = 0.025), independently of classical HF prognostic factors, inflammatory and iron-related markers. No significant associations were found between admission serum iron or transferrin saturation tertiles, iron status categories, or guideline-defined iron deficiency (ID) criteria and the primary composite outcome. However, at discharge, patients who met the criteria for defective iron utilization, low iron storage, or guideline-defined ID had a lower risk of the composite endpoint compared to those with normal iron utilization or who did not meet the guideline-defined ID criteria, respectively., Conclusions: Elevated ferritin levels are independently associated with poor prognosis in AHF. Low ferritin levels are associated with a favorable outcome and do not carry significant value in identifying ID in this population., (© 2024. The Author(s).)

Published
2024
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50. Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction.

Author

Silva ED, Pereira-Sousa D, Ribeiro-Costa F, Cerqueira R, Enguita FJ, Gomes RN, Dias-Ferreira J, Pereira C, Castanheira A, Pinto-do-Ó P, Leite-Moreira AF, and Nascimento DS

Subjects
Humans, Male, Female, Myocardium metabolism, Myocardium pathology, Middle Aged, Fibroblasts metabolism, Aged, Transforming Growth Factor beta metabolism, ST Elevation Myocardial Infarction metabolism, ST Elevation Myocardial Infarction pathology, ST Elevation Myocardial Infarction genetics, Interleukin-1 Receptor-Like 1 Protein metabolism, Interleukin-1 Receptor-Like 1 Protein genetics, MicroRNAs genetics, MicroRNAs metabolism, Fibrosis, Myocardial Infarction metabolism, Myocardial Infarction genetics, Myocardial Infarction pathology, Pericardial Fluid metabolism
Abstract

Pericardial fluid (PF) has been suggested as a reservoir of molecular targets that can be modulated for efficient repair after myocardial infarction (MI). Here, we set out to address the content of this biofluid after MI, namely in terms of microRNAs (miRs) that are important modulators of the cardiac pathological response. PF was collected during coronary artery bypass grafting (CABG) from two MI cohorts, patients with non-ST-segment elevation MI (NSTEMI) and patients with ST-segment elevation MI (STEMI), and a control group composed of patients with stable angina and without previous history of MI. The PF miR content was analyzed by small RNA sequencing, and its biological effect was assessed on human cardiac fibroblasts. PF accumulates fibrotic and inflammatory molecules in STEMI patients, namely causing the soluble suppression of tumorigenicity 2 (ST-2), which inversely correlates with the left ventricle ejection fraction. Although the PF of the three patient groups induce similar levels of fibroblast-to-myofibroblast activation in vitro, RNA sequencing revealed that PF from STEMI patients is particularly enriched not only in pro-fibrotic miRs but also anti-fibrotic miRs. Among those, miR-22-3p was herein found to inhibit TGF-β-induced human cardiac fibroblast activation in vitro. PF constitutes an attractive source for screening diagnostic/prognostic miRs and for unveiling novel therapeutic targets in cardiac fibrosis.

Published
2024
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