scholarly journals Figures of the Heart Failure Association: Professor Dr. med. Johann Bauersachs, Chair of the Clinical Science Section

2019 ◽  
Vol 21 (5) ◽  
pp. 545-548
Author(s):  
Andrew J.S. Coats
Keyword(s):  
Heart Failure ◽  
Clinical Science ◽  
Science Section

Milton Packer, MD, Director, Center for Biostatistics and Clinical Science at UT Southwestern

2004 ◽  
Vol 52 (7) ◽  
pp. 421-424
Keyword(s):  
Heart Failure ◽  
New York ◽  
Health Care Policy ◽  
Clinical Investigation ◽  
Medical Center ◽  
Heart Association ◽  
Clinical Science ◽  
Columbia University ◽  
Cardiovascular Research ◽  
Editorial Boards

Milton Packer, MD, is the director of the Center for Biostatistics and Clinical Science and holder of The Gayle and Paul Stoffel Distinguished Chair in Cardiology. He is the former chief of the Division of Circulatory Physiology at the Columbia University College of Physicians and Surgeons and the past director of the Heart Failure Center at the Columbia-Presbyterian Medical Center in New York City. One of the leading experts in the pathophysiology and treatment of heart failure, Dr. Packer has made significant contributions to heart failure research and has been instrumental in the introduction of a number of new treatments. The author of more than 200 papers, he has won numerous honors for teaching and has lectured around the world on the treatment of heart failure, having been honored with a number of prestigious named lectureships. He has served or currently serves on the editorial boards of many major medical journals, including Circulation and the Journal of the American College of Cardiology. He has also been elected to a number of societies, including the American Society for Clinical Investigation. He is currently on the executive committees of both the American Heart Association and the American College of Cardiology and is past-president of the Heart Failure Society of America. Dr. Packer is a primary consultant to the National Institutes of Health and the US Food and Drug Administration on the management of heart failure and on matters related to cardiovascular research, drug development, and health care policy.

Role of Orexin-B/Orexin 2 receptor in myocardial protection

2019 ◽  
Vol 133 (7) ◽  
pp. 853-857 ◽  
Author(s):  
Roberta Imperatore ◽  
Luigia Cristino
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Direct Effect ◽  
Myocardial Protection ◽  
Cardiovascular Responses ◽  
Clinical Science ◽  
Clinical Severity ◽  
Dependent Manner ◽  
Protective Function

Abstract Emerging evidence attributes to orexins/hypocretins (ORs) a protective function in the regulation of cardiovascular responses, heart rate, and hypertension. However, little is known about any direct effect of orexins in the heart function. This is of special relevance considering that cardiovascular diseases, including myocardial infarction and heart failure, are one of the major causes of mortality in the world. In the article published in Clinical Science (2018) (vol. 132, 2547–2564), Patel and colleagues investigated the role of orexins in myocardial protection. Intriguingly, they revealed a source of orexin-A (OR-A) and orexin-B (OR-B) in the heart and cardiomyocytes of the rat. More interestingly, these peptides exert a direct effect on the heart rate by acting in an autocrine/paracrine manner on their respective receptors (OXRs). Indeed, OR-B, but not OR-A, by acting through orexin receptor-2 (OX2R), exerts direct cardioprotective effects in heart failure models. OR-B/OX2R signalling enhances myosin light chain (MLC) and troponin-I (TnI) phosphorylation in a dose-dependent manner, leading to an increase in the strength of their twitch contraction. This effect is mediated by extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation, both in the rat myocardial tissue and human heart samples. A negative correlation between OX2R expression and clinical severity of symptoms has been found in patients with heart failure. Thus, in addition to the known central effects of orexins/OX2R, the work of Patel and colleagues (Clinical Science (2018) 132, 2547–2564) reports a direct action of OR-B on the heart rate pinpointing to OX2R as a potential therapeutic target for prevention and treatment of cardiovascular disease.

A tangled tale of microRNA and cardiac fibrosis

2019 ◽  
Vol 133 (21) ◽  
pp. 2217-2220 ◽  
Author(s):  
Mark Chandy
Keyword(s):  
Heart Failure ◽  
Extracellular Matrix ◽  
Wound Healing ◽  
Cardiac Fibrosis ◽  
Pressure Overload ◽  
Clinical Science ◽  
Therapeutic Options ◽  
Diagnostic Modalities

Abstract Cardiac fibrosis is important for wound healing, regeneration and producing the extracellular matrix (ECM) that provides the scaffold for cells. In pathological situations, fibroblasts are activated and remodel the ECM. In volume 133, issue 17 of Clinical Science, Yang et al. discovered that the miR-214-3p/NLRC5 axis is important for fibroblast-to-myofibroblast transition (FMT) and ECM remodelling in a pressure overload model of fibrosis [Clin. Sci. (2019) 133(17), 1845–1856]. This discovery helps to explain the complicated regulation of cardiac fibrosis. It also underscores the need for more investigation into the mechanisms of cardiac fibrosis to develop better diagnostic modalities and therapeutic options in heart failure.

scholarly journals Vascular biomedicine in an era of chronic disease and multimorbidity

2019 ◽  
Vol 133 (9) ◽  
pp. 1137-1143 ◽  
Author(s):  
Gemma Currie ◽  
Christian Delles
Keyword(s):  
Heart Failure ◽  
Chronic Disease ◽  
Cardiovascular Diseases ◽  
Clinical Science ◽  
Renal Diseases ◽  
Healthcare Provision ◽  
Research Papers ◽  
New Models ◽  
Complex Features

Abstract It is increasingly common that patients present with more than one disease and that diseases are chronic in nature. Cardiovascular conditions such as hypertension, heart failure and stroke, renal diseases and cardiometabolic conditions such as diabetes are prime examples of chronic diseases which pose major challenges in contemporary healthcare provision. The complex features of multimorbidity call for precision medicine approaches that take comorbidity and chronicity into account. The research basis of chronic disease and multimorbidity, however, is currently in its infancy. This applies to all domains including basic, translational and clinical science. In this article we call for development of new models, smarter use of existing models and better characterisation of vascular and cardiovascular phenotypes in studies not directly related to cardiovascular diseases. This has the potential to further improve the quality of translational research, papers in journals such as Clinical Science and ultimately translate into better patient care.

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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