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Kenneth M. Kent

Researcher at Georgetown University

Publications -  64
Citations -  5645

Kenneth M. Kent is an academic researcher from Georgetown University. The author has contributed to research in topics: Myocardial infarction & Angioplasty. The author has an hindex of 27, co-authored 64 publications receiving 5602 citations. Previous affiliations of Kenneth M. Kent include Georgetown University Medical Center & MedStar Washington Hospital Center.

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Impaired left ventricular diastolic filling in patients with coronary artery disease: assessment with radionuclide angiography.

TL;DR: LV diastolic filling, evaluated noninvasively by radionuclide angiography, is abnormal in a high percentage of patients with CAD at rest independent of LV systolic function or previous myocardial infarction.
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Percutaneous transluminal coronary angioplasty: report of complications from the National Heart, Lung, and Blood Institute PTCA Registry.

TL;DR: The results support the relative safety of PTCA as a method of nonsurgical myocardial revascularization in carefully selected patients and nonfatal complications were significantly influenced by the presence of unstable angina and initial lesion severity > 90% diameter stenosis.
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Incidence and consequences of periprocedural occlusion. The 1985-1986 National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry.

TL;DR: Baseline patient factors independently associated with increased occlusion rates included triple-vessel disease, high risk status for surgery, and acute coronary insufficiency, while Lesion characteristics showing significant positive association included severe stenosis before PTCA, diffuse or multiple discrete morphology, thrombus, and collateral flow from the lesion.
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Effects of verapamil on left ventricular systolic function and diastolic filling in patients with hypertrophic cardiomyopathy.

TL;DR: LV diastolic filling is abnormal in a high percentage of patients with HCM, and verapamil normalizes or improves these abnormalities without altering systolic function, and this mechanism may contribute to the clinical improvement of many HCM patients during verAPamil therapy.