MYOCARDIAL SEGMENT SHRINKAGE DURING CORONARY REPERFUSION IN-SITU - RELATION TO HYPERCONTRACTURE AND MYOCARDIAL NECROSIS

We have investigated the changes in myocardial segment length induced by reperfusion, and their relation to myocyte hypercontracture and con traction band necrosis. Regional wall function was monitored by ultras onic gauges in 39 pigs submitted to 48-min occlusion of the left anter ior descending coronary artery (LAD) and 6 h of reperfusion. Infarct s ize (triphenyltetrazolium reaction), the extent of contraction band ne crosis (quantitative histology) and myocardial water content (desiccat ion) were measured. Reperfusion induced a marked reduction in end-dias tolic length of the LAD segment in all animals, maximal within 15 min after reflow. After 30 min of reperfusion, end-diastolic length of the LAD segment remained below the basal value in 15 animals. The 15 anim als that showed shrinkage of the reperfused segment did not differ fro m the remaining animals in heart rate, aortic pressure, or control seg ment variables, but had larger infarcts (mean +/- SEM: 32.1 +/- 5.4 vs 12.1 +/- 3.2% of the area at risk, P = 0.003). There was an inverse c orrelation between end-diastolic length of the LAD segment after 30 mi n of reperfusion and infarct percentage (r = -0.72) or the extent of c ontraction band necrosis (r = -0.71). End-diastolic length reduction w as more pronounced in larger infarcts despite a more severe myocardial oedema. Neither systolic shortening of the LAD segment nor end-diasto lic length or systolic shortening of the control segment, or haemodyna mic variables after 30 min of reperfusion correlated to infarct percen tage or to the extent of contraction band necrosis. It is concluded th at myocardial segment shrinkage during reperfusion reflects myocyte hy percontracture leading to contraction band necrosis.