E
Edward G. Lakatta
Researcher at National Institutes of Health
Publications - 902
Citations - 95504
Edward G. Lakatta is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Blood pressure & Population. The author has an hindex of 146, co-authored 858 publications receiving 88637 citations. Previous affiliations of Edward G. Lakatta include University of Pittsburgh & University College London.
Papers
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Journal ArticleDOI
Uremic Cardiomyopathy—An Endogenous Digitalis Intoxication?: Central Role for the Cardiotonic Steroid Marinobufagenin in the Pathogenesis of Experimental Uremic Cardiomyopathy. Hypertension 47: 488–495, 2006
David J. Kennedy,Sandeep Vetteth,Sankaridrug M. Periyasamy,M Kanj,L Fedorova,S Khouri,MB Kahaleh,Zijian Xie,Deepak Malhotra,NI Kolodkin,Edward G. Lakatta,Olga V. Fedorova,Alexei Y. Bagrov,Joseph I. Shapiro +13 more
TL;DR: The heart is a target organ in uremia, and by the beginning of the 20th century it had been recognized that heart failure and cardiac death were frequent in renal patients.
Journal ArticleDOI
Ischemic preconditioning increases the bioavailability of cardiac enkephalins
TL;DR: IPC appears to increase available bioactive enkephalins (MEAP + ME) within the heart by enhancing synthesis of precursors and their subsequent processing from the larger proenkephalin precursor (PEP) pool.
Journal ArticleDOI
Early contribution of arterial wave reflection to left ventricular relaxation abnormalities in a community-dwelling population of normotensive and untreated hypertensive men and women
Marco Canepa,Majd AlGhatrif,James B. Strait,Hao Min Cheng,Shao Yuan Chuang,Chen Huan Chen,Chen Huan Chen,Claudio Brunelli,Luigi Ferrucci,Edward G. Lakatta +9 more
TL;DR: The contribution of wave reflection to left ventricular diastolic dysfunction was independent of arterial stiffness, more pronounced in normotensive individuals and explained a significant portion of the gender difference in diastolics function.
Book ChapterDOI
Spontaneous sarcoplasmic reticulum Ca2+ release leads to heterogeneity of contractile and electrical properties of the heart.
TL;DR: S-CaOs may be implicated in diverse manifestations of heart failure--impaired systolic performance, increased diastolic tonus and an increased probability for the occurrence of arrhythmias.
Journal ArticleDOI
Dilated cardiomyopathy with increased SR Ca2+ loading preceded by a hypercontractile state and diastolic failure in the α1CTG mouse
Su Wang,Bruce D. Ziman,Ilona Bodi,Marta Rubio,Ying Ying Zhou,Karen M. D'Souza,Nanette H. Bishopric,Arnold Schwartz,Edward G. Lakatta +8 more
TL;DR: It is demonstrated that older NFTG myocytes exhibit a hypercontractile state over a wide range of stimulation frequencies, but maintain a normal SR Ca2+ load compared to age matched non-transgenic (NTG) myocytes, but at high stimulation rates signs of diastolic contractile failure appear in N FTG cells.