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Francis G. Spinale

Researcher at University of South Carolina

Publications -  469
Citations -  24683

Francis G. Spinale is an academic researcher from University of South Carolina. The author has contributed to research in topics: Heart failure & Ventricular remodeling. The author has an hindex of 84, co-authored 451 publications receiving 23239 citations. Previous affiliations of Francis G. Spinale include Biogen Idec & Veterans Health Administration.

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Relationship between bioimpedance, thermodilution, and ventriculographic measurements in experimental congestive heart failure

TL;DR: In a tachycardia induced model of heart failure, bioimpedance was significantly correlated with thermodilution stroke volume and the peak first derivative of the bioimPedance signal dZ/dtmax may provide a non-invasive index of ventricular pump performance.
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The effects of endothelin-A receptor blockade during the progression of pacing-induced congestive heart failure

TL;DR: ET(A) receptor activation may contribute to the progression of LV dysfunction with CHF and be a factor in the development of congestive heart failure.
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Myocyte Contractile Responsiveness after Hypothermic, Hyperkalemic Cardioplegic ArrestDisparity between Exogenous Calcium and β-Adrenergic Stimulation

TL;DR: The minimal improvement in myocyte contractile function after HHCA with increased extracellular Calcium2+ suggests that Cal calcium2+ depletion is not the primary mechanism for depressed myocytes contractility after HH CA.
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Release of matrix metalloproteinases following alcohol septal ablation in hypertrophic obstructive cardiomyopathy.

TL;DR: Induction of a controlled myocardial injury in humans, specifically through alcohol-induced MI, caused species- and time-dependent perturbations of MMP/TIMP stoichiometry that would facilitate myocardIAL remodeling in the early post-MI setting.
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Dual Angiotensin Receptor-Neprilysin Inhibition With Sacubitril/Valsartan Attenuates Systolic Dysfunction in Experimental Doxorubicin-Induced Cardiotoxicity

TL;DR: Sac/Val offers greater protection against left ventricular remodeling and dysfunction compared with standard angiotensin receptor blocker therapy in a rodent model of progressive DOX-induced cardiotoxicity.