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 contraction band necrosis. Regional wall function was monitored by ultrasonic gauges in 39 pigs submitted to 48-min occlusion of the left anterior descending coronary artery (LAD) and 6h of reperfusion. Infarct size (triphenyltetrazolium reaction), the extent of contraction band necrosis (quantitative histology) and myocardial water content (desiccation) were measured. Reperfusion induced a marked reduction in end-diastolic 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 animals that showed shrinkage of the reperfused segment did not differ from the remaining animals in heart rate, aortic pressure, or control segment 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 correlation between end-diastolic length of the LAD segment after 30 min of reperfusion and infarct percentage (r = -0.72) or the extent of contraction band necrosis (r = -0.71). End-diastolic length reduction was more pronounced in larger infarcts despite a more severe myocardial oedema. Neither systolic shortening of the LAD segment nor end-diastolic length or systolic shortening of the control segment, or haemodynamic variables after 30 min of reperfusion correlated to infarct percentage or to the extent of contraction band necrosis. It is concluded that myocardial segment shrinkage during reperfusion reflects myocyte hypercontracture leading to contraction band necrosis.

Clinical outcome of severe asymptomatic chronic aortic regurgitation: a long-term prospective follow-up study.

One hundred one patients with asymptomatic chronic severe aortic regurgitation and normal ejection fraction were monitored for up to 10 years (mean 55.4 +/- 33.5 months). Predefined surgical indications were the development of cardiac symptoms or the documentation of impaired basal left ventricular function. During the follow-up period there were no cardiac deaths; 14 patients needed surgery, 8 because of development of symptoms and 6 because of left ventricular impairment. The risk of surgery was 12% at 5 years and 24% at 10 years. Baseline end-systolic diameter > 50 mm and radionuclide ejection fraction < 60% were independent predictors or either cardiac symptoms or left ventricular dysfunction. In patients needing surgery, a pattern of progressive left ventricular dilatation was demonstrated. There were no deaths during surgery, and echocardiographic and radionuclide parameters normalized in the first year of follow-up. Our data confirm that the prognosis of severe aortic regurgitation in patients with no symptoms is good and that the occurrence of asymptomatic left ventricular dysfunction is an uncommon event. Surgery can be safely postponed until the appearance of cardiac symptoms or the documentation of left ventricular dysfunction at rest.