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Scott B. Kribbs

Researcher at Medical University of South Carolina

Publications -  17
Citations -  1405

Scott B. Kribbs is an academic researcher from Medical University of South Carolina. The author has contributed to research in topics: Heart failure & Hemodynamics. The author has an hindex of 10, co-authored 17 publications receiving 1364 citations.

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Pathophysiologically relevant concentrations of tumor necrosis factor- α promote progressive left ventricular dysfunction and remodeling in rats

TL;DR: These studies suggest that pathophysiologically relevant concentrations of TNF-alpha are sufficient to mimic certain aspects of the phenotype observed in experimental and clinical models of heart failure.
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Matrix Metalloproteinase Inhibition During the Development of Congestive Heart Failure Effects on Left Ventricular Dimensions and Function

TL;DR: Concomitant MMPi with developing CHF limited LV dilation and reduced wall stress, and it is suggested that increased myocardial MMP activity contributes to LV myocardian remodeling in developingCHF.
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Effects of Growth Hormone Supplementation on Left Ventricular Morphology and Myocyte Function With the Development of Congestive Heart Failure

TL;DR: Short-term GH supplementation improved LV pump function in pacing CHF as a result of favorable effects on LV remodeling and contractile processes, and GH supplementation may serve as a novel therapeutic modality in developing CHF.
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Tranexamic acid reduces bleeding after cardiopulmonary bypass when compared to epsilon aminocaproic acid and placebo.

TL;DR: TA was more effective in reducing blood loss postoperatively following CABG, suggesting that TA may be beneficial as an effective and inexpensive antifibrinolytic in first‐time CABGs patients.
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Angiotensin converting enzyme inhibition, AT1 receptor inhibition, and combination therapy with pacing induced heart failure: effects on left ventricular performance and regional blood flow patterns

TL;DR: These findings suggest that with developing CHF, combined ACE inhibition and AT1 receptor blockade improved vascular resistive properties and regional blood flow distribution to a greater degree than that of either treatment alone.