Acute effects of delayed reperfusion on myocardial infarct shape and left ventricular volume: a potential mechanism of additional benefits from thrombolytic therapy.
The purpose of this study was to characterize the effects of late reperfusion on myocardial infarct shape and to quantitate associated changes in left ventricular volume. Reperfusion was delayed until there was no salvage of ischemic myocardium. Dogs underwent 6.5 h of left anterior descending coronary artery occlusion (n = 5) or 5.5 h of occlusion and 1 h of reperfusion (n = 5). Infarct shape was measured with pairs of ultrasonic crystals implanted circumferentially in the mid myocardium. Infarct stiffness was determined from end-diastolic pressure-segment length curves produced by aortic clamping. Left ventricular volume was measured with three pairs of endocardial ultrasonic crystals and the effect of infarct shape change on left ventricular volume was determined. Infarct size, expressed as a percent of the area at risk, was similar in reperfused (97 +/- 1%) and nonreperfused (98 +/- 1%) hearts. After coronary artery occlusion, infarct segments became akinetic and functional dilation, measured as end-diastolic ultrasonic crystal separation, increased to a similar extent in reperfused (24 +/- 7%) and nonreperfused (19 +/- 3%) hearts. In 13 additional dogs that underwent reperfusion and instrumentation with endocardial ultrasonic crystals for volume measurement, left ventricular volume increased 42 +/- 6% over the preocclusion level (p less than 0.001). Within minutes of reperfusion, the infarct stiffened, infarct dilation decreased to 1 +/- 4% over the baseline preocclusion level (p less than 0.05 vs. prereperfusion) and left ventricular volume decreased to 16 +/- 11% over the baseline level (p less than 0.01 vs. postocclusion). Thus, coronary artery reperfusion reverses initial infarct dilation. Changes in infarct dilation occur immediately after reperfusion and are accompanied by infarct stiffening and a decrease in left ventricular volume. Reperfusion can affect infarct shape and stiffness at a point in time when myocardial salvage is no longer possible.
Brown
E J
EJ
Department of Medicine, State University of New York, Health Sciences Center, Stony Brook 1794-8171.
Swinford
R D
RD
Gadde
P
P
Lillis
O
O
D000818:Animals; D004285:Dogs; D005260:Female; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology / Q000628:therapy*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology*; D015912:Thrombolytic Therapy; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*