D
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
Pathophysiology and Therapy of Cardiac Dysfunction in Duchenne Muscular Dystrophy
Daniel P. Judge,Daniel P. Judge,Daniel P. Judge,David A. Kass,W. Reid Thompson,W. Reid Thompson,Kathryn R. Wagner,Kathryn R. Wagner +7 more
TL;DR: In this article, the authors focus on the regulatory role of dystrophin in relation to neuronal nitric oxide synthase (nNOS) and transient receptor potential canonical channels (TRPC).
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Acute cardiovascular effects of OPC-18790 in patients with congestive heart failure: Time- and dose-dependence analysis based on pressure-volume relations
Marc D. Feldman,Peter H. Pak,Clarence C. Wu,Howard L. Haber,Christian M. Heesch,James D. Bergin,Eric R. Powers,T. Douglas Cowart,William C. Johnson,Arthur M. Feldman,David A. Kass +10 more
TL;DR: In this article, the authors studied the contribution and relative dose sensitivities of the inotropic, lusitropic, and vascular effects of OPC-18790 in patients with dilated cardiomyopathy.
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Ventricular systolic assessment in patients with dilated cardiomyopathy by preload-adjusted maximal power: Validation and noninvasive application
Tali Sharir,Marc D. Feldman,Howard L. Haber,Arthur M. Feldman,Alon Marmor,Lewis C. Becker,David A. Kass +6 more
TL;DR: Preload-adjusted PWRmx is a steady-state index of ventricular systolic function that is sensitive to inotropic state and minimally influenced by physiological changes in afterload impedance or volume load, and appears useful for noninvasive cardiac-specific analysis of acute drug effects.
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Comparison of ventricular pressure relaxation assessments in human heart failure: quantitative influence on load and drug sensitivity analysis.
TL;DR: In this article, the authors compared various methods for assessing ventricular pressure decay time constants to test whether sensitivity to slight data instability or disparities between model-assumed and real decay are systematically altered by cardiac failure.
Journal ArticleDOI
Sildenafil does not improve cardiomyopathy in Duchenne/Becker muscular dystrophy
Doris G. Leung,Doris G. Leung,Daniel A. Herzka,W. Reid Thompson,W. Reid Thompson,Bing He,Genila Bibat,Gihan Tennekoon,Stuart D. Russell,Karl H. Schuleri,Albert C. Lardo,David A. Kass,Richard E. Thompson,Daniel P. Judge,Daniel P. Judge,Kathryn R. Wagner,Kathryn R. Wagner +16 more
TL;DR: To determine whether the PDE5‐inhibitor sildenafil benefits human dystrophinopathy, a randomized, double‐blind, placebo‐controlled trial was conducted.