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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
A Simple Adaptive Transfer Function for Deriving the Central Blood Pressure Waveform from a Radial Blood Pressure Waveform.
Mingwu Gao,William C. Rose,Barry J. Fetics,David A. Kass,Chen Huan Chen,Ramakrishna Mukkamala +5 more
TL;DR: The ATF was assessed using the original data that helped popularize the GTF and may permit more accurate, non-invasive central BP monitoring in elderly and hypertensive patients.
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Anti-hypertrophic and anti-oxidant effect of beta3-adrenergic stimulation in myocytes requires differential neuronal NOS phosphorylation
Vabren L. Watts,Fernando M. Sepulveda,Oscar H. Cingolani,Alice S Ho,Xiaolin Niu,Xiaolin Niu,Rosa Kim,Karen L. Miller,Koenraad Vandegaer,Djahida Bedja,Kathleen L. Gabrielson,Gerald A. Rameau,Brian O'Rourke,David A. Kass,Lili A. Barouch +14 more
TL;DR: The data identify a novel and potent anti-oxidant and anti-hypertrophic pathway due to nNOS post-translational modification that is coupled to β3-AR receptor stimulation.
Journal ArticleDOI
Novel Model of Constrictive Pericarditis Associated With Autoimmune Heart Disease in Interferon-γ–Knockout Mice
Marina Afanasyeva,Marina Afanasyeva,Dimitrios Georgakopoulos,Dimitrios Georgakopoulos,De Lisa Fairweather,Patrizio Caturegli,David A. Kass,Noel R. Rose +7 more
TL;DR: It was found that the acute phase of experimental autoimmune myocarditis in IFN-γ–KO mice was characterized by reduced left ventricular volumes compared with wild-type mice, and pericarditis was responsible for smaller LV volumes, reduced cardiac output, increased cardiac stiffness, and increased peak filling rate adjusted for end-diastolic volumes in KO mice.
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Lack of nitric oxide synthase depresses ion transporting enzyme function in cardiac muscle.
Lan Zhou,Arthur L. Burnett,Paul L. Huang,Lewis C. Becker,Periannan Kuppusamy,David A. Kass,J. Kevin Donahue,David Proud,James S.K. Sham,Ted M. Dawson,Kai Y. Xu +10 more
TL;DR: The experimental results suggest that disrupted endogenous NO* production may change local redox conditions and lead to an unbalanced free radical homeostasis in cardiac muscle cells which, in turn, may affect key enzyme activities and membrane ion active transport systems in the heart.
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Imaging cardiac resynchronization therapy.
Theodore P. Abraham,David A. Kass,Giovanni Tonti,Gery Tomassoni,William T. Abraham,Jeroen J. Bax,Thomas H. Marwick +6 more
TL;DR: Nonsynchrony markers that seem promising include assessment of the location and extent of myocardial scar and imaging of the coronary venous and phrenic nerve anatomy and potential new contributors to the assessment of mechanical synchrony include echocardiographic and magnetic resonance techniques.