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David A. Kass
Researcher at Johns Hopkins University School of Medicine
Publications - 605
Citations - 63963
David A. Kass is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Heart failure & Cardiac resynchronization therapy. The author has an hindex of 127, co-authored 580 publications receiving 58747 citations. Previous affiliations of David A. Kass include University of Pittsburgh & Johns Hopkins University.
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Journal ArticleDOI
The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model
Christopher Semsarian,Imran Ahmad,Michael Giewat,Dimitrios Georgakopoulos,Joachim P. Schmitt,Bradley K. McConnell,Steven Reiken,Ulrike Mende,Andrew R. Marks,David A. Kass,Christine E. Seidman,Christine E. Seidman,Jonathan G. Seidman,Jonathan G. Seidman +13 more
TL;DR: It is suggested that the use of Ca2+ channel blockers in advance of established clinical disease could prevent hypertrophic cardiomyopathy caused by sarcomere protein gene mutations and disruption of sarcoplasmic reticulum Ca1+ homeostasis is an important early event in the pathogenesis of this disorder.
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In vivo murine left ventricular pressure-volume relations by miniaturized conductance micromanometry
Dimitrios Georgakopoulos,Wayne A. Mitzner,Chen Huan Chen,Barry J. Byrne,Huntly Millar,Joshua M. Hare,David A. Kass +6 more
TL;DR: A miniaturized conductance-manometer system was developed to study detailed systolic and diastolic left ventricular chamber mechanics in mice in vivo, further supporting comparable chamber mechanics between species.
Journal ArticleDOI
Ventricular–Vascular Interaction in Heart Failure
Barry A. Borlaug,David A. Kass +1 more
TL;DR: The pathophysiology of abnormal ventriculoarterial stiffening and how it affects ventricular function, cardiovascular hemodynamics, reserve capacity, and symptoms is discussed.
Journal ArticleDOI
Ventricular–Vascular Interaction in Heart Failure
Barry A. Borlaug,David A. Kass +1 more
TL;DR: The pathophysiology of abnormal ventriculoarterial stiffening and how it affects ventricular function, cardiovascular hemodynamics, reserve capacity, and symptoms is discussed.
Journal ArticleDOI
Intravenous Allopurinol Decreases Myocardial Oxygen Consumption and Increases Mechanical Efficiency in Dogs With Pacing-Induced Heart Failure
Ulf Ekelund,Robert W. Harrison,Ori Shokek,Rajiv N. Thakkar,Richard S. Tunin,Hideaki Senzaki,David A. Kass,Eduardo Marbán,Joshua M. Hare +8 more
TL;DR: The data indicate that allopurinol possesses unique inotropic properties, increasing myocardial contractility while simultaneously reducing cardiac energy requirements, and may prove beneficial in the treatment of congestive heart failure.