Editorial commentary: Brugada syndrome or not? That is the question
Despite its description by the Brugada brothers more than 25 years ago [1], the Brugada syndrome (BrS) remains debated in terms of its genetics, arrhythmogenic mechanisms and clinical management. This is partly because the relationships between genotype, electrocardiographic phenotype, pathoelectrophysiology, and clinical management of BrS continue to evolve, driven by findings in the clinic and in the basic laboratory. The review article by Cerrone [2] offers a timely overview of the clinical and genetic intricacies of BrS, and shines light on the controversies and major scientific and clinical milestones that have been r...
Source: Trends in Cardiovascular Medicine - December 21, 2017 Category: Cardiology Authors: Guillaume Bassil, Sami F. Noujaim Source Type: research
Editorial commentary: Malignant PVCs: Revising the ‘idiopathic’ label
Premature ventricular contractions (PVCs) are commonly seen on routine ECGs, telemetry and Holter monitoring. When PVCs cause symptoms of palpitations or fatigue, ablation or medical therapy can be very effective. However, in the absence of symptoms, PVCs are frequently dismissed by healthcare providers without further evaluation. In the past few decades, our understanding has progressed to identify that PVCs may result in significant morbidity beyond symptoms. In this issue of Trends in Cardiovascular Medicine, Drs. (Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 21, 2017 Category: Cardiology Authors: Gregory E. Supple Source Type: research
ACE inhibition to slow progression of myocardial fibrosis in muscular dystrophies
Muscular dystrophy (MD) connotes a heterogeneous group of inherited disorders affecting skeletal and cardiac muscle. MD is typically caused by a mutation in a single gene that affects striated muscle (cardiac, skeletal), leading to progressive wasting and weakness. In several forms of MD, cardiac dysfunction occurs, and cardiac disease may even be the predominant manifestation of the underlying genetic myopathy [1]. The cardiac involvement is due to progressive interstitial fibrosis and fatty replacement in both the atria and ventricles, which may lead to cardiomyopathy, conduction defects and tachyarrhythmias [2]. (Source...
Source: Trends in Cardiovascular Medicine - December 21, 2017 Category: Cardiology Authors: Vincenzo Russo, Andrea Antonio Papa, Emmanuel Ato Williams, Anna Rago, Alberto Palladino, Luisa Politano, Gerardo Nigro Source Type: research
Malignant PVCs: Revising the ‘Idiopathic’ Label
Premature ventricular contractions (PVCs) are commonly seen on routine ECGs, telemetry and Holter monitoring. When PVCs cause symptoms of palpitations or fatigue, ablation or medical therapy can be very effective. However, in the absence of symptoms, PVCs are frequently dismissed by healthcare providers without further evaluation. In the past few decades, our understanding has progressed to identify that PVCs may result in significant morbidity beyond symptoms. In this issue of Trends in Cardiovascular Medicine, Drs. (Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 21, 2017 Category: Cardiology Authors: Gregory E. Supple Source Type: research
Brugada syndrome or not? That is the question
Despite its description by the Brugada brothers more than 25 years ago[1], the Brugada syndrome (BrS) remains debated in terms of its genetics, arrhythmogenic mechanisms and clinical management. This is partly because the relationships between genotype, electrocardiographic phenotype, pathoelectrophysiology and clinical management of BrS continue to evolve, driven by findings in the clinic and in the basic laboratory. The review article by Cerrone[2] offers a timely overview of the clinical and genetic intricacies of BrS, and shines light on the controversies and major scientific and clinical milestones that have been reac...
Source: Trends in Cardiovascular Medicine - December 21, 2017 Category: Cardiology Authors: Guillaume Bassil, Sami F. Noujaim Source Type: research
Table of Contents
(Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 19, 2017 Category: Cardiology Source Type: research
Editorial Board
(Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 19, 2017 Category: Cardiology Source Type: research
Editorial commentary: Mitochondrial autophagy in cardiac aging is all fluxed up
Functional decline towards cellular senescence presents a different set of problems in cardiomyocytes relative to proliferative cells. For example, senescence of proliferative cells serves an important tumor-suppressive role by promoting cell-cycle exit [1]. However, in non-proliferative and long-lived cardiomyocytes, senescence as a consequence of years of cumulative stress from aging may play a detrimental role and contribute to functional decline due to accumulation of damaged proteins, dysfunctional organelles, and DNA damage. (Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 19, 2017 Category: Cardiology Authors: Dieter A. Kubli, Mark A. Sussman Source Type: research
Editorial comment: Mitochondrial autophagy in cardiac aging is all fluxed up
Functional decline towards cellular senescence presents a different set of problems in cardiomyocytes relative to proliferative cells. For example, senescence of proliferative cells serves an important tumor-suppressive role by promoting cell-cycle exit [1]. However, in non-proliferative and long-lived cardiomyocytes, senescence as a consequence of years of cumulative stress from aging may play a detrimental role and contribute to functional decline due to accumulation of damaged proteins, dysfunctional organelles, and DNA damage. (Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 19, 2017 Category: Cardiology Authors: Dieter A. Kubli, Mark A. Sussman Source Type: research
Obesity and heart failure with preserved ejection fraction: A growing problem
Heart Failure with Preserved Ejection Fraction (HFpEF) is increasing in prevalence due to the aging of the United States population as well as the current obesity epidemic. While obesity is very common in patients with HFpEF, obesity may represent a specific phenotype of HFpEF characterized by unique hemodynamics and structural abnormalities. Obesity induces a systemic inflammatory response that may contribute to myocardial fibrosis and endothelial dysfunction. The most obese patients continue to be excluded from HFpEF clinical trials, and thus ongoing research is needed to determine the role of pharmacologic and intervent...
Source: Trends in Cardiovascular Medicine - December 14, 2017 Category: Cardiology Authors: Stuart B. Prenner, Paul J. Mather Source Type: research
Editorial commentary: Obesity and heart failure with preserved ejection fraction: A single disease or two co-existing conditions?
Heart failure (HF) with preserved ejection fraction (HFpEF) is characterized by the presence of multiple comorbidities. In this issue of the Journal, Prenner and Mathers [1] reviewed the literature related to the role of obesity in the development and progression of HFpEF. They describe how obesity increases the risk for HFpEF, potentially as the result of excess fat mass (FM) responsible for hemodynamics and cardiac structural changes [2,3], and for the production of proinflammatory cytokines (i.e., adipokines), with cardiodepressant properties. (Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 14, 2017 Category: Cardiology Authors: Salvatore Carbone, Ambarish Pandey, Carl J. Lavie Source Type: research
Obesity and Heart Failure with Preserved Ejection Fraction: A Growing Problem
Heart Failure with Preserved Ejection Fraction (HFpEF) is increasing in prevalence due to the aging of the United States population as well as the current obesity epidemic. While obesity is very common in patients with HFpEF, obesity may represent a specific phenotype of HFpEF characterized by unique hemodynamics and structural abnormalities. Obesity induces a systemic inflammatory response that may contribute to myocardial fibrosis and endothelial dysfunction. The most obese patients continue to be excluded from HFpEF clinical trials, and thus ongoing research is needed to determine the role of pharmacologic and intervent...
Source: Trends in Cardiovascular Medicine - December 14, 2017 Category: Cardiology Authors: Stuart B. Prenner, Paul J. Mather Source Type: research
Editorial Commentary: Obesity and Heart Failure with Preserved Ejection Fraction: A Single Disease or Two Co-Existing Conditions?
Heart failure ( HF) with preserved ejection fraction (HFpEF) is characterized by the presence of multiple comorbidities. In this issue of the Journal, Prenner and Mather [1] reviewed the literature related to the role of obesity in the development and progression of HFpEF. They describe how obesity increases the risk for HFpEF, potentially as the result of excess fat mass (FM) responsible for hemodynamics and cardiac structural changes[2,3], and for the production of proinflammatory cytokines (i.e., adipokines), with cardiodepressant properties. (Source: Trends in Cardiovascular Medicine)
Source: Trends in Cardiovascular Medicine - December 14, 2017 Category: Cardiology Authors: Salvatore Carbone, Ambarish Pandey, Carl J. Lavie Source Type: research
