Transient myocardial ischemia: experimental echocardiographic demonstration and evaluation of myocardial contraction abnormalities.

A continuing theme in our laboratory has been the use of echocardiographically-measured systolic myocardial wall thickening to demonstrate and evaluate the consequences of regional myocardial ischemia. This presentation focuses on two areas: the immediate mechanical consequences of induced myocardial ischemia in two experimental models: canine and human; the correlation between persistent regional myocardial dysfunction and morphologic infarction after sequences of coronary artery occlusion and reperfusion. Many experiments using animal models have demonstrated that acute myocardial ischemia produces almost immediate replacement of normal systolic myocardial wall thickening by systolic thinning. Less is known about the immediate mechanical response of human myocardium to acute ischemia. This was studied in 5 open-chest humans undergoing various cardiac operations. Wall thickening was continuously displayed by a 7 MHz M-mode echocardiographic transducer coupled to the epicardium by suction to maintain constant position. Coronary flow velocity was displayed by a pulsed Doppler device coupled to an epicardial coronary artery by suction. Ischemia was induced by the surgeon who manually occluded the coronary artery with a soft-tipped Kitner dissector or vascular forceps for 30 seconds. It was found that cessation of coronary flow was accompanied by reductions in normal systolic thickening but systolic thinning or expansion only rarely occurred. In contrast, when the identical techniques were used in 5 dogs, systolic thinning always occurred immediately after coronary arterial occlusion. This suggests that there are important species differences between canine and human myocardium in the immediate mechanical response to myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)