Impaired early and intact late diastolic function in stunned myocardium induced by demand ischemia.
Changes in left ventricular diastolic properties of pacing-induced stunned myocardium were examined in 10 anesthetized dogs instrumented with a micromanometer for left ventricular pressure and sonomicrometers for left ventricular short axis, anterior and posterior segment lengths, and posterior wall thickness. After the creation of a critical stenosis on a carotid-circumflex coronary artery bypass, left ventricular pressure and dimensions were recorded simultaneously during temporary superior and inferior vena caval occlusion to allow for the construction of end-diastolic pressure-segment length curves. After 15 min of high-frequency pacing (190-220 beats/min), measurements were repeated and compared with those before pacing. The mean lengthening rate of each dimension during the first half of diastole was calculated as an index of early diastolic function. Three minutes after the end of pacing, coronary blood flow and perfusion pressure were unchanged, whereas systolic function of the posterior wall was depressed, indicating stunning of the posterior myocardium. The time constant of left ventricular pressure decay was prolonged by 14%. The mean lengthening rate during the first half of diastole decreased by 50% in the left ventricular internal short axis and by 119% in the posterior segment. Despite the significant impairment of early diastolic function, the regional end-diastolic pressure-segment length relation of the posterior wall was unchanged. Thus, in contrast to the results reported for pacing-induced ischemia that were measured immediately after pacing, the distensibility of the left ventricular wall in stunned myocardium induced by pacing was unchanged despite depressed early diastolic function.
Miyazaki
S
S
Department of Internal Medicine, National Cardiovascular Center, Suita, Japan.
Goto
Y
Y
Nonogi
H
H
Kawase
Y
Y
Haze
K
K
Hiramori
K
K
D000818:Animals; D001783:Blood Flow Velocity; D009202:Cardiomyopathies / Q000209:etiology / Q000503:physiopathology*; D003326:Coronary Circulation / Q000502:physiology; D003971:Diastole / Q000502:physiology*; D004285:Dogs; D006439:Hemodynamics; D017202:Myocardial Ischemia / Q000150:complications*; D011312:Pressure; D016277:Ventricular Function, Left