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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
Association Between Left Atrial Stiffness Index and Atrial Fibrillation Recurrence in Patients Undergoing Left Atrial Ablation
Irfan M. Khurram,Farhan Maqbool,Ronald D. Berger,Joseph E. Marine,David D. Spragg,Hiroshi Ashikaga,Vadim Zipunnikov,David A. Kass,Hugh Calkins,Saman Nazarian,Stefan L. Zimmerman +10 more
TL;DR: LA stiffness index, a novel measure to assess LA diastolic function, increases with age and is higher in persistent AF and in the setting of repeat AF ablation.
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Wall Tension Is a Potent Negative Regulator of In Vivo Thrombomodulin Expression
Jason L. Sperry,Clayton B. Deming,Ce Bian,Peter L. Walinsky,David A. Kass,Frank D. Kolodgie,Renu Virmani,Antony Y. Kim,Jeffrey J. Rade +8 more
TL;DR: It is concluded that the primary stimulus for altered TM expression in vein grafts is the exposure to arterial pressure, and strain is identified as a novel and important pathway for in vivo TM gene regulation.
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Sustained Soluble Guanylate Cyclase Stimulation Offsets Nitric-Oxide Synthase Inhibition to Restore Acute Cardiac Modulation by Sildenafil
TL;DR: PDE5 regulation of adrenergic reserve and systemic vasodilation depends upon NOS-induced cGMP/protein kinase G and can be enhanced by sustained low-level stimulation of sGC, which may prove beneficial for enhancing the efficacy of PDE5 inhibitors in conditions with chronically reduced NOS activity.
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Heart failure-associated alterations in troponin I phosphorylation impair ventricular relaxation-afterload and force-frequency responses and systolic function.
Kenneth C Bilchick,Jennifer G. Duncan,Jennifer G. Duncan,Rajashree Ravi,Eiki Takimoto,Hunter C. Champion,Wei Dong Gao,Linda B. Stull,David A. Kass,Anne M. Murphy +9 more
TL;DR: Abnormal TnI phosphorylation observed in cardiac failure may explain exacerbated relaxation delay in response to increased afterload and contribute to blunted chronotropic reserve.
Journal ArticleDOI
Cellular and molecular determinants of altered Ca2+ handling in the failing rabbit heart: primary defects in SR Ca2+ uptake and release mechanisms
Antonis A. Armoundas,Jochen Rose,Rajesh Aggarwal,Bruno D. Stuyvers,Brian O'Rourke,David A. Kass,Eduardo Marbán,Stephen R. Shorofsky,Gordon F. Tomaselli,C. William Balke +9 more
TL;DR: A prominent role for the sarcoplasmic reticulum (SR) in the pathogenesis of HF is supported, in which abnormal SR Ca(2+) uptake and release synergistically contribute to the depressed [Ca(2+)](i) and the altered AP profile phenotype.