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8. Systemic Oxidative Stress and Endothelial Dysfunction is Associated With an Attenuated Acute Vascular Response to Inhaled Prostanoid in Pulmonary Artery Hypertension Patients

Author

Gabrielli, Luigi A., Castro, Pablo F., Godoy, Ivan, Mellado, Rosemarie, Bourge, Robert C., Alcaino, Hernan, Chiong, Mario, Greig, Douglas, Verdejo, Hugo E., Navarro, Mario, Lopez, Rafael, Toro, Barbra, Quiroga, Clara, Díaz-Araya, Guillermo, Lavandero, Sergio, and Garcia, Lorena

Published
2011
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12. Insulin stimulates mitochondrial fusion and function in cardiomyocytes via the Akt-mTOR-NFκB-Opa-1 signaling pathway

Author

Parra, Valentina, Verdejo, Hugo E., Iglewski, Myriam, del Campo, Andrea, Troncoso, Rodrigo, Jones, Deborah, Zhu, Yi, Kuzmicic, Jovan, Pennanen, Christian, Lopez-Crisosto, Camila, Jana, Fabian, Ferreira, Jorge, Noguera, Eduard, Chiong, Mario, Bernlohr, David A., Klip, Amira, Hill, Joseph A., Rothermel, Beverly A., Abel, Evan Dale, Zorzano, Antonio, and Lavandero, Sergio

Subjects
Obesity -- Physiological aspects, Cell physiology -- Research, Insulin resistance -- Physiological aspects, Heart cells -- Physiological aspects -- Health aspects, Molecular biology -- Research, Mitochondria -- Health aspects -- Physiological aspects, Insulin -- Physiological aspects -- Health aspects, Muscles -- Physiological aspects -- Health aspects, Health
Abstract

Insulin regulates heart metabolism through the regulation of insulin-stimulated glucose uptake. Studies have indicated that insulin can also regulate mitochondrial function. Relevant to this idea, mitochondrial function is impaired in diabetic individuals. Furthermore, the expression of Opa-1 and mitofusins, proteins of the mitochondrial fusion machinery, is dramatically altered in obese and insulin-resistant patients. Given the role of insulin in the control of cardiac energetics, the goal of this study was to investigate whether insulin affects mitochondrial dynamics in cardiomyocytes. Confocal microscopy and the mitochondrial dye MitoTracker Green were used to obtain three-dimensional images of the mitochondrial network in cardiomyocytes and L6 skeletal muscle cells in culture. Three hours of insulin treatment increased Opa-1 protein levels, promoted mitochondrial fusion, increased mitochondrial membrane potential, and elevated both intracellular ATP levels and oxygen consumption in cardiomyocytes in vitro and in vivo. Consequently, the silencing of Opa-1 or Mfn2 prevented all the metabolic effects triggered by insulin. We also provide evidence indicating that insulin increases mitochondrial function in cardiomyocytes through the Akt-mTOR-NFκB signaling pathway. These data demonstrate for the first time in our knowledge that insulin acutely regulates mitochondrial metabolism in cardiomyocytes through a mechanism that depends on increased mitochondrial fusion, Opa-1, and the Akt-mTOR-NFκB pathway. Diabetes 2014;63:75-88 | DOI: 10.2337/db13-0340, The heart requires a constant supply of metabolic substrates and oxygen. Although in the adult heart nearly 70% of energy requirements are met by free fatty acid oxidation, cardiomyocytes have [...]

Published
2014
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17. Moderate Exercise in Spontaneously Hypertensive Rats Is Unable to Activate the Expression of Genes Linked to Mitochondrial Dynamics and Biogenesis in Cardiomyocytes

Author

Quiroga, Clara, primary, Mancilla, Georthan, additional, Oyarzun, Ingrid, additional, Tapia, Anita, additional, Caballero, Mia, additional, Gabrielli, Luigi A., additional, Valladares-Ide, Denisse, additional, del Campo, Andrea, additional, Castro, Pablo F., additional, and Verdejo, Hugo E., additional

Published
2020
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19. Early left atrial dysfunction is associated with suboptimal cardiovascular health

Author

Ocaranza, María Paz, primary, Bambs, Claudia, additional, Salinas, Manuel, additional, Matamala, Cristian, additional, Garcia, Lorena, additional, Troncoso, Rodrigo, additional, Pedrozo, Zully, additional, Huidobro, Andrea, additional, Venegas, Pia, additional, Paredes, Fabio, additional, Giacaman, Arturo, additional, Zalaquett, Ricardo, additional, Chiong, Mario, additional, Verdejo, Hugo E., additional, Ferreccio, Catterina, additional, Lavandero, Sergio, additional, Castro, Pablo F., additional, and Gabrielli, Luigi, additional

Published
2019
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21. Early left atrial dysfunction is associated with suboptimal cardiovascular health.

Author

Ocaranza, María Paz, Bambs, Claudia, Salinas, Manuel, Matamala, Cristian, Garcia, Lorena, Troncoso, Rodrigo, Pedrozo, Zully, Huidobro, Andrea, Venegas, Pia, Paredes, Fabio, Giacaman, Arturo, Zalaquett, Ricardo, Chiong, Mario, Verdejo, Hugo E., Ferreccio, Catterina, Lavandero, Sergio, Castro, Pablo F., and Gabrielli, Luigi

Subjects
BIOMARKERS, BLOOD pressure, CARDIOVASCULAR diseases, CHOLESTEROL, CLASSIFICATION, ECHOCARDIOGRAPHY, HEALTH status indicators, HEART ventricles, INSULIN, INSULIN resistance, LONGITUDINAL method, PATIENTS, SPRAINS, TRIGLYCERIDES, BODY mass index, CROSS-sectional method, LEFT heart atrium
Abstract

Aims: Two‐dimensional speckle‐tracking echocardiography can assess left atrial (LA) function by measuring atrial volumes and deformation parameters (strain, strain rate). This cross‐sectional analysis explores the association between ideal CV health (CVH), LA function, and systemic biomarkers in healthy individuals from the Chilean MAUCO Cohort. Methods: We enrolled 95 MAUCO participants with different levels of CVH (mean age: 51 ± 8 years). We categorized participants into low or high CVH groups: A: 0‐2, or B: 3‐6 CVH risk factors. 2D echocardiography, glucose, insulin, total cholesterol, triglycerides, proBNP, hsCRP, insulin resistance index (HOMA), and right and left atrial strain (RASs and LASs, respectively) were determined. Results: LASs was lower in Group A, while systolic and diastolic blood pressure (BP), body mass index (BMI), insulin, HOMA, total cholesterol, triglycerides, and LV and RV end‐diastolic volume were significantly higher in Group A than Group B (P <.01). Change in LASs was inversely correlated with insulin (P =.040), HOMA (P =.013), total cholesterol (P =.039), glycemia (P =.018), and BMI (P =.0.037). Conclusion: LASs during the reservoir phase was diminished in subjects with a lower level of CVH. Higher insulin, HOMA, total cholesterol, glycemia, and BMI values were associated with decreased LA deformation during the reservoir phase. Morphofunctional alterations of the LA were also identified in the group with suboptimal CVH, as well as BP values in the range of hypertension. LA dysfunction in an asymptomatic population, along with metabolic syndrome, could be an early event in the continuum of CV damage. [ABSTRACT FROM AUTHOR]

Published
2020
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24. Nanoparticles for diagnosis and therapy of atherosclerosis and myocardial infarction: evolution toward prospective theranostic approaches

Author

Bejarano, Julian, primary, Navarro-Marquez, Mario, additional, Morales-Zavala, Francisco, additional, Morales, Javier O., additional, Garcia-Carvajal, Ivonne, additional, Araya-Fuentes, Eyleen, additional, Flores, Yvo, additional, Verdejo, Hugo E., additional, Castro, Pablo F., additional, Lavandero, Sergio, additional, and Kogan, Marcelo J., additional

Published
2018
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26. Inhibition of mitochondrial fission prevents hypoxia-induced metabolic shift and cellular proliferation of pulmonary arterial smooth muscle cells

Author

Parra, Valentina, primary, Bravo-Sagua, Roberto, additional, Norambuena-Soto, Ignacio, additional, Hernández-Fuentes, Carolina P., additional, Gómez-Contreras, Andrés G., additional, Verdejo, Hugo E., additional, Mellado, Rosemarie, additional, Chiong, Mario, additional, Lavandero, Sergio, additional, and Castro, Pablo F., additional

Published
2017
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28. Acute effect of iloprost inhalation on right atrial function and ventricular dyssynchrony in patients with pulmonary artery hypertension

Author

Gabrielli, Luigi, primary, Ocaranza, María Paz, additional, Sitges, Marta, additional, Kanacri, Andrés, additional, Saavedra, Rodrigo, additional, Sepulveda, Pablo, additional, Sepulveda, Luis, additional, Rossel, Victor, additional, Zagolin, Monica, additional, Verdejo, Hugo E., additional, Baraona, Fernando, additional, Zalaquett, Ricardo, additional, Chiong, Mario, additional, Lavandero, Sergio, additional, and Castro, Pablo F., additional

Published
2016
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29. New Molecular Insights of Insulin in Diabetic Cardiomyopathy

Author

Westermeier, Francisco, primary, Riquelme, Jaime A., additional, Pavez, Mario, additional, Garrido, Valeria, additional, Díaz, Ariel, additional, Verdejo, Hugo E., additional, Castro, Pablo F., additional, García, Lorena, additional, and Lavandero, Sergio, additional

Published
2016
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30. Atrial Function Assessed by Speckle Tracking Echocardiography Is a Good Predictor of Postoperative Atrial Fibrillation in Elderly Patients

Author

Verdejo, Hugo E., primary, Becerra, Elia, additional, Zalaquet, Ricardo, additional, del Campo, Andrea, additional, Garcia, Lorena, additional, Troncoso, Rodrigo, additional, Chiong, Mario, additional, Marin, Arnaldo, additional, Castro, Pablo F., additional, Lavandero, Sergio, additional, Gabrielli, Luigi, additional, and Corbalán, Ramón, additional

Published
2015
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31. Defective insulin signaling and mitochondrial dynamics in diabetic cardiomyopathy

Author

Westermeier, Francisco, primary, Navarro-Marquez, Mario, additional, López-Crisosto, Camila, additional, Bravo-Sagua, Roberto, additional, Quiroga, Clara, additional, Bustamante, Mario, additional, Verdejo, Hugo E., additional, Zalaquett, Ricardo, additional, Ibacache, Mauricio, additional, Parra, Valentina, additional, Castro, Pablo F., additional, Rothermel, Beverly A., additional, Hill, Joseph A., additional, and Lavandero, Sergio, additional

Published
2015
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32. Predictores de síndrome coronario agudo sin supradesnivel del ST y estratificación de riesgo en la unidad de dolor torácico. Experiencia en 1.168 pacientes

Author

Gabrielli, Luigi A, Castro, Pablo F, Verdejo, Hugo E, McNab, Paul A, Llevaneras, Silvana A, Mardonez, José M, and Corbalán, Ramón L

Subjects
Risk factors, Troponin T-1, Acute coronary syndrome
Abstract

Background: Nearly 10% of patients with an actual acute coronary syndrome (ACS) are discharged with an inadequate diagnosis. Aim To select clinical and laboratory predictors to identify patients with a high likelihood of ACS in the Chest Pain Unit. Material and methods: Prospective evaluation of patients consulting in a Chest Pain Unit of a University Hospital. Initial assessment was standardized and included evaluation of pain characteristics, electrocardiogram and Troponin I. Independent predictors of ACS were identified with a multiple logistic regression. Results: In a four years period, 1,168 patients aged 62±23 years (69% males), were studied. After initial evaluation, 62% of the patients were admitted to the hospital for further testing and in 71% of them, a definite diagnosis of ACS was made. No events were reported by patients directly discharged from the Chest Pain Unit. Independent predictors associated with a higher likelihood of ACS were an abnormal electrocardiogram at the initial evaluation (Odds ratio (OR) 5.37, 95% confidence intervals (CI) 3.61-7.99), two or more cardiovascular risk factors (OR 2.16, 95% CI 1.21-2.84), cervical irradiation of the pain (OR 1.84, 95% CI 1.25-2.69), age over 65years (OR 1.73, 95% CI (1.32-2.27) and a Troponin I above the upper normal limit (OR: 5.68, 95% CI 3.72-8.29). Conclusions: Simple clinical findings allow an appropriate identification of patients with a high likelihood of ACS without specialized methods for myocardial ischemia detection

Published
2008

33. Predictores de síndrome coronario agudo sin supradesnivel del ST y estratificación de riesgo en la unidad de dolor torácico. Experiencia en 1.168 pacientes

Author

Gabrielli,Luigi A, Castro,Pablo F, Verdejo,Hugo E, McNab,Paul A, Llevaneras,Silvana A, Mardonez,José M, and Corbalán,Ramón L

Subjects
Risk factors, Troponin T-1, Acute coronary syndrome
Abstract

Background: Nearly 10% of patients with an actual acute coronary syndrome (ACS) are discharged with an inadequate diagnosis. Aim To select clinical and laboratory predictors to identify patients with a high likelihood of ACS in the Chest Pain Unit. Material and methods: Prospective evaluation of patients consulting in a Chest Pain Unit of a University Hospital. Initial assessment was standardized and included evaluation of pain characteristics, electrocardiogram and Troponin I. Independent predictors of ACS were identified with a multiple logistic regression. Results: In a four years period, 1,168 patients aged 62±23 years (69% males), were studied. After initial evaluation, 62% of the patients were admitted to the hospital for further testing and in 71% of them, a definite diagnosis of ACS was made. No events were reported by patients directly discharged from the Chest Pain Unit. Independent predictors associated with a higher likelihood of ACS were an abnormal electrocardiogram at the initial evaluation (Odds ratio (OR) 5.37, 95% confidence intervals (CI) 3.61-7.99), two or more cardiovascular risk factors (OR 2.16, 95% CI 1.21-2.84), cervical irradiation of the pain (OR 1.84, 95% CI 1.25-2.69), age over 65years (OR 1.73, 95% CI (1.32-2.27) and a Troponin I above the upper normal limit (OR: 5.68, 95% CI 3.72-8.29). Conclusions: Simple clinical findings allow an appropriate identification of patients with a high likelihood of ACS without specialized methods for myocardial ischemia detection

Published
2008

34. Mitochondrial fragmentation impairs insulin-dependent glucose uptake by modulating Akt activity through mitochondrial Ca2+ uptake

Author

del Campo, Andrea, primary, Parra, Valentina, additional, Vásquez-Trincado, César, additional, Gutiérrez, Tomás, additional, Morales, Pablo E., additional, López-Crisosto, Camila, additional, Bravo-Sagua, Roberto, additional, Navarro-Marquez, Mario F., additional, Verdejo, Hugo E., additional, Contreras-Ferrat, Ariel, additional, Troncoso, Rodrigo, additional, Chiong, Mario, additional, and Lavandero, Sergio, additional

Published
2014
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35. Insulin Stimulates Mitochondrial Fusion and Function in Cardiomyocytes via the Akt-mTOR-NFκB-Opa-1 Signaling Pathway

Author

Parra, Valentina, primary, Verdejo, Hugo E., additional, Iglewski, Myriam, additional, del Campo, Andrea, additional, Troncoso, Rodrigo, additional, Jones, Deborah, additional, Zhu, Yi, additional, Kuzmicic, Jovan, additional, Pennanen, Christian, additional, Lopez‑Crisosto, Camila, additional, Jaña, Fabián, additional, Ferreira, Jorge, additional, Noguera, Eduard, additional, Chiong, Mario, additional, Bernlohr, David A., additional, Klip, Amira, additional, Hill, Joseph A., additional, Rothermel, Beverly A., additional, Abel, Evan Dale, additional, Zorzano, Antonio, additional, and Lavandero, Sergio, additional

Published
2013
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36. Dinámica mitocondrial: un potencial nuevo blanco terapéutico para la insuficiencia cardiaca

Author

Kuzmicic, Jovan, primary, del Campo, Andrea, additional, López-Crisosto, Camila, additional, Morales, Pablo E., additional, Pennanen, Christian, additional, Bravo-Sagua, Roberto, additional, Hechenleitner, Jonathan, additional, Zepeda, Ramiro, additional, Castro, Pablo F., additional, Verdejo, Hugo E., additional, Parra, Valentina, additional, Chiong, Mario, additional, and Lavandero, Sergio, additional

Published
2011
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37. Increased ER–mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress

Author

Bravo, Roberto, primary, Vicencio, Jose Miguel, additional, Parra, Valentina, additional, Troncoso, Rodrigo, additional, Munoz, Juan Pablo, additional, Bui, Michael, additional, Quiroga, Clara, additional, Rodriguez, Andrea E., additional, Verdejo, Hugo E., additional, Ferreira, Jorge, additional, Iglewski, Myriam, additional, Chiong, Mario, additional, Simmen, Thomas, additional, Zorzano, Antonio, additional, Hill, Joseph A., additional, Rothermel, Beverly A., additional, Szabadkai, Gyorgy, additional, and Lavandero, Sergio, additional

Published
2011
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38. Xanthine-oxidase inhibitors and statins in chronic heart failure: Effects on vascular and functional parameters

Author

Greig, Douglas, primary, Alcaino, Hernan, additional, Castro, Pablo F., additional, Garcia, Lorena, additional, Verdejo, Hugo E., additional, Navarro, Mario, additional, López, Rafael, additional, Mellado, Rosemarie, additional, Tapia, Fabiola, additional, Gabrielli, Luigi A., additional, Nogerol, Camilo, additional, Chiong, Mario, additional, Godoy, Ivan, additional, and Lavandero, Sergio, additional

Published
2011
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39. Pleiotropic Effects of Atorvastatin in Heart Failure: Role in Oxidative Stress, Inflammation, Endothelial Function, and Exercise Capacity

Author

Castro, Pablo F., primary, Miranda, Rodrigo, additional, Verdejo, Hugo E., additional, Greig, Douglas, additional, Gabrielli, Luigi A., additional, Alcaino, Hernán, additional, Chiong, Mario, additional, Bustos, Carlos, additional, Garcia, Lorena, additional, Mellado, Rosemarie, additional, Vukasovic, José Luis, additional, Godoy, Ivan, additional, and Lavandero, Sergio, additional

Published
2008
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41. Mitochondrial fragmentation impairs insulin-dependent glucose uptake by modulating Akt activity through mitochondrial Ca2+ uptake.

Author

del Campo, Andrea, Parra, Valentina, Vásquez-Trincado, César, Gutiérrez, Tomás, Morales, Pablo E., López-Crisosto, Camila, Bravo-Sagua, Roberto, Navarro-Marquez, Mario F., Verdejo, Hugo E., Contreras-Ferrat, Ariel, Troncoso, Rodrigo, Chiong, Mario, and Lavandero, Sergio

Subjects
MITOFUSIN 1 protein, MITOFUSIN 2, MITOCHONDRIAL membranes, MITOCHONDRIAL proteins, MEMBRANE proteins, SKELETAL muscle, MUSCLE cells, PHOSPHORYLATION
Abstract

Insulin is a major regulator of glucose metabolism, stimulating its mitochondrial oxidation in skeletal muscle cells.Mitochondria are dynamic organelles that can undergo structural remodeling in order to cope with these ever changing metabolic demands. However, the process by which mitochondrial morphology impacts insulin signaling in the skeletal muscle cells remains uncertain. To address this question, we silenced the mitochondrial fusion proteins Mfn2 and Opa1 and assessed insulin-dependent responses in L6 rat skeletal muscle cells. We found that mitochondrial fragmentation attenuates insulin-stimulated Akt phosphorylation, glucose uptake and cell respiratory rate. Importantly, we found that insulin induces a transient rise in mitochondrial Ca2+ uptake, which was attenuated by silencing Opa1 or Mfn2. Moreover, treatment with Ruthenium red, an inhibitor of mitochondrial Ca2+ uptake, impairs Akt signaling without affecting mitochondrial dynamics. All together, these results suggest that control of mitochondrial Ca2+ uptake by mitochondrial morphology is a key event for insulin induced glucose uptake. [ABSTRACT FROM AUTHOR]

Published
2014
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42. Low-Grade Chronic Inflammation: a Shared Mechanism for Chronic Diseases.

Author

Cifuentes M, Verdejo HE, Castro PF, Corvalan AH, Ferreccio C, Quest AFG, Kogan MJ, and Lavandero S

Subjects
Humans, Chronic Disease, Animals, Neoplasms pathology, Inflammation physiopathology, Obesity physiopathology, Cardiovascular Diseases physiopathology
Abstract

Inflammation is an important physiological response of the organism to restore homeostasis upon pathogenic or damaging stimuli. However, the persistence of the harmful trigger or a deficient resolution of the process can evolve into a state of low-grade, chronic inflammation. This condition is strongly associated with the development of several increasingly prevalent and serious chronic conditions, such as obesity, cancer, and cardiovascular diseases, elevating overall morbidity and mortality worldwide. The current pandemic of chronic diseases underscores the need to address chronic inflammation, its pathogenic mechanisms, and potential preventive measures to limit its current widespread impact. The present review discusses the current knowledge and research gaps regarding the association between low-grade chronic inflammation and chronic diseases, focusing on obesity, cardiovascular diseases, digestive diseases, and cancer. We examine the state of the art in selected aspects of the topic and propose future directions and approaches for the field.

Published
2025
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43. Mitochondrial fragmentation impairs insulin-dependent glucose uptake by modulating Akt activity through mitochondrial Ca2+ uptake.

Author

del Campo A, Parra V, Vásquez-Trincado C, Gutiérrez T, Morales PE, López-Crisosto C, Bravo-Sagua R, Navarro-Marquez MF, Verdejo HE, Contreras-Ferrat A, Troncoso R, Chiong M, and Lavandero S

Subjects
Animals, Antibodies pharmacology, Cell Line, GTP Phosphohydrolases antagonists & inhibitors, GTP Phosphohydrolases physiology, Membrane Proteins antagonists & inhibitors, Membrane Proteins physiology, Mitochondria, Muscle metabolism, Mitochondrial Proteins antagonists & inhibitors, Mitochondrial Proteins physiology, Muscle, Skeletal metabolism, Phosphorylation drug effects, Proto-Oncogene Proteins c-akt drug effects, Rats, Signal Transduction physiology, Calcium metabolism, Glucose metabolism, Insulin pharmacology, Mitochondria, Muscle ultrastructure, Muscle, Skeletal ultrastructure, Proto-Oncogene Proteins c-akt metabolism
Abstract

Insulin is a major regulator of glucose metabolism, stimulating its mitochondrial oxidation in skeletal muscle cells. Mitochondria are dynamic organelles that can undergo structural remodeling in order to cope with these ever-changing metabolic demands. However, the process by which mitochondrial morphology impacts insulin signaling in the skeletal muscle cells remains uncertain. To address this question, we silenced the mitochondrial fusion proteins Mfn2 and Opa1 and assessed insulin-dependent responses in L6 rat skeletal muscle cells. We found that mitochondrial fragmentation attenuates insulin-stimulated Akt phosphorylation, glucose uptake and cell respiratory rate. Importantly, we found that insulin induces a transient rise in mitochondrial Ca(2+) uptake, which was attenuated by silencing Opa1 or Mfn2. Moreover, treatment with Ruthenium red, an inhibitor of mitochondrial Ca(2+) uptake, impairs Akt signaling without affecting mitochondrial dynamics. All together, these results suggest that control of mitochondrial Ca(2+) uptake by mitochondrial morphology is a key event for insulin-induced glucose uptake.

Published
2014
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44. [Predictors of acute coronary syndrome without ST segment elevation and risk stratification in the chest pain unit].

Author

Gabrielli LA, Castro PF, Verdejo HE, McNab PA, Llevaneras SA, Mardonez JM, and Corbalán RL

Subjects
Acute Coronary Syndrome blood, Biomarkers blood, Chest Pain blood, Electrocardiography, Emergency Service, Hospital, Female, Humans, Male, Middle Aged, Odds Ratio, Patient Discharge, Predictive Value of Tests, Prospective Studies, Risk Assessment, Troponin I blood, Acute Coronary Syndrome diagnosis, Chest Pain diagnosis
Abstract

Background: Nearly 10% of patients with an actual acute coronary syndrome (ACS) are discharged with an inadequate diagnosis., Aim: To select clinical and laboratory predictors to identify patients with a high likelihood of ACS in the Chest Pain Unit., Material and Methods: Prospective evaluation of patients consulting in a Chest Pain Unit of a University Hospital. Initial assessment was standardized and included evaluation of pain characteristics, electrocardiogram and Troponin I. Independent predictors of ACS were identified with a multiple logistic regression., Results: In a four years period, 1,168 patients aged 62+/-23 years (69% males), were studied. After initial evaluation, 62% of the patients were admitted to the hospital for further testing and in 71% of them, a definite diagnosis of ACS was made. No events were reported by patients directly discharged from the Chest Pain Unit. Independent predictors associated with a higher likelihood of ACS were an abnormal electrocardiogram at the initial evaluation (Odds ratio (OR) 5.37, 95% confidence intervals (CI) 3.61-7.99), two or more cardiovascular risk factors (OR 2.16, 95% CI 1.21-2.84), cervical irradiation of the pain (OR 1.84, 95% CI 1.25-2.69), age over 65 years (OR 1.73, 95% CI (1.32-2.27) and a Troponin I above the upper normal limit (OR: 5.68, 95% CI 3.72-8.29)., Conclusions: Simple clinical findings allow an appropriate identification of patients with a high likelihood of ACS without specialized methods for myocardial ischemia detection.

Published
2008
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