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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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Mechanisms, Pathophysiology, and Therapy of Arterial Stiffness

TL;DR: A number of lifestyle changes and therapies that reduce arterial stiffness are presented, including weight loss, exercise, salt reduction, alcohol consumption, and neuroendocrine-directed therapies, such as those targeting the renin-angiotensin aldosterone system, natriuretic peptides, insulin modulators, as well as novel therapies that target advanced glycation end products.
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Estimation of Central Aortic Pressure Waveform by Mathematical Transformation of Radial Tonometry Pressure Validation of Generalized Transfer Function

TL;DR: Central aortic pressures can be accurately estimated from radial tonometry with the use of a generalized TF, and the reconstructed waveform can provide arterial compliance estimates but may underestimate the augmentation index because the latter requires greater fidelity reproduction of the wave contour.
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Improved Left Ventricular Mechanics From Acute VDD Pacing in Patients With Dilated Cardiomyopathy and Ventricular Conduction Delay

TL;DR: VDD pacing acutely enhances contractile function in heart failure patients with intraventricular conduction delay and single-site pacing at the site of greatest delay achieves similar or greater benefits to biventricular pacing in such patients, to clarify pacing-effect mechanisms.
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Combined Ventricular Systolic and Arterial Stiffening in Patients With Heart Failure and Preserved Ejection Fraction. Implications for Systolic and Diastolic Reserve Limitations

TL;DR: Patients with HF-lnEF have systolic-ventricular and arterial stiffening beyond that associated with aging and/or hypertension, which may play an important pathophysiological role by exacerbating systemic load interaction with diastolic function, augmenting blood pressure lability, and elevating cardiac metabolic demand under stress.