title: Left ventricular systolic dysfunction precedes diastolic dysfunction during myocardial ischemia in conscious dogs.
abstract: We studied the initial effects of regional and global left ventricular (LV) ischemia induced by left circumflex and left main coronary artery occlusion (CAO), respectively, on indexes of systolic and diastolic LV function in conscious dogs to determine whether diastolic abnormalities precede systolic dysfunction or vice versa during the onset of either regional or global myocardial ischemia. With regional myocardial ischemia, within four beats after left circumflex CAO, there was a significant decrease in end-systolic wall thickness in the ischemic zone followed by significantly enhanced postsystolic wall thickening in the nonischemic zone at beat 6. Both peak negative first derivative of left ventricular pressure (LV dP/dt) and the isovolumic relaxation half-time (T 1/2) were prolonged, but later (i.e., by the 9th beat). During sustained CAO T1/2 was normalized shortly after postsystolic thickening in the nonischemic zone had disappeared despite persistent regional systolic asynchrony and shortened ejection time. Thus postsystolic thickening in the nonischemic zone played a major role in the early, transient changes in isovolumic relaxation after acute induction of regional ischemia. With global myocardial ischemia, induced by left main coronary occlusion, indexes of systolic function (e.g., LV dP/dt, ejection fraction, and velocity of circumferential endocardial fiber shortening) were also depressed significantly before (by 5-15 beats) indexes of LV diastolic function [e.g., time constant of isovolumic relaxation and LV myocardial and chamber stiffness (by 35-45 beats)]. Similar results were observed in the presence of autonomic blockade, when heart rate did not change with CAO. Thus, during the induction of either acute regional or acute global LV ischemia in conscious dogs, LV systolic dysfunction occurs before diastolic dysfunction.
authors.affiliation: Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston 02115.
authors.forename: T
authors.initials: T
authors.lastname: Ihara
authors.forename: K
authors.initials: K
authors.lastname: Komamura
authors.forename: Y T
authors.initials: YT
authors.lastname: Shen
authors.forename: T A
authors.initials: TA
authors.lastname: Patrick
authors.forename: I
authors.initials: I
authors.lastname: Mirsky
authors.forename: R P
authors.initials: RP
authors.lastname: Shannon
authors.forename: S F
authors.initials: SF
authors.lastname: Vatner
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D003971:Diastole; D004285:Dogs; D006439:Hemodynamics; D017202:Myocardial Ischemia / Q000503:physiopathology*; D013599:Systole; D013997:Time Factors; D016277:Ventricular Function, Left