R
Robert A. Kloner
Researcher at Huntington Medical Research Institutes
Publications - 801
Citations - 56448
Robert A. Kloner is an academic researcher from Huntington Medical Research Institutes. The author has contributed to research in topics: Myocardial infarction & Ischemia. The author has an hindex of 111, co-authored 780 publications receiving 53767 citations. Previous affiliations of Robert A. Kloner include Case Western Reserve University & Harvard University.
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Journal ArticleDOI
The stunned myocardium: prolonged, postischemic ventricular dysfunction.
TL;DR: If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardia perfusion by surgical treatment.
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The “No-Reflow” Phenomenon after Temporary Coronary Occlusion in the Dog
TL;DR: Results suggest that 40 minutes of ischemia were tolerated by the capillary bed of the dog heart without serious capillary damage or perfusion defects, but that 90 min of ischemic injury was associated with the "no-reflow" phenomenon, i.e., failure to achieve uniform reperfusion.
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Reperfusion injury induces apoptosis in rabbit cardiomyocytes.
Roberta A. Gottlieb,Katharine O. Burleson,Robert A. Kloner,Bernard M. Babior,Robert L. Engler +4 more
TL;DR: Parts of apoptosis (programmed cell death) in myocytes are identified as a response to reperfusion but not ischemia, which indicates that apoptosis may be a specific feature of reperfusions injury in cardiac myocytes, leading to late cell death.
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Myocardial infarct size and ventricular function in rats.
Marc A. Pfeffer,Janice M. Pfeffer,Michael C. Fishbein,P J Fletcher,J Spadaro,Robert A. Kloner,Eugene Braunwald +6 more
TL;DR: In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium, and the entire spectrum of postinfarction ventricularfunction was observed, from no detectable impairment to congestive failure.
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Regional ischemic 'preconditioning' protects remote virgin myocardium from subsequent sustained coronary occlusion.
TL;DR: Brief episodes of ischemia in one vascular bed protect remote, virgin myocardium from subsequent sustained coronary artery occlusion in this canine model, and implies that preconditioning may be mediated by factor(s) activated, produced, or transported throughout the heart during brief ischemic/reperfusion.