Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis.

Abstract

To assess the importance of contraction band necrosis (CBN) in patients with acute myocardial infarction (AMI) treated with selective intracoronary thrombolysis, CBN, coagulation necrosis, and infarct size (expressed as CBN + coagulation necrosis) were analyzed quantitatively in 16 autopsied hearts. Intracoronary thrombolysis was performed from 2 to 6 hr after the onset of AMI, and the time from the onset of AMI to death was 7 to 168 hr. Cineangiography revealed no evidence of good collateral circulation in any of the patients. The 16 patients were classified into three groups: six patients with successful thrombolysis (100% to 99% stenosis, group I), five patients with unsuccessful thrombolysis (100% to 100%, group II), and five patients with 99% stenosis before thrombolysis (group III). Among the three groups, there were no significant differences in the time from the onset of AMI to thrombolysis, the time from the onset of AMI to death, the cause of death, or the degree of collateral circulation. The percentage of the risk area involved by the infarct in group 1 (82 6%) was similar to that in group 11 (80 + 1 1 %). Infarct size was not reduced in group I because collateral circulation was not good and because the degree of recanalization after thrombolysis was 1%. However, the percentage of the infarct area with CBN was significantly higher in group 1 (20 + 9%) then in group 11 (3 + 3%). This finding shows that diffuse CBN occurred after reperfusion in patients with AMI treated with thrombolysis. In group III, three hearts had a smaller infarct area than that in group I or II and a larger area-of CBN than that in group II. In the other two hearts, the infarct area was similar to that in groups I and II and the CBN area was as small as in group II. We believe that in the former three cases, spontaneous recanalization occurred before thrombolysis and a considerable portion of the risk area was salvaged. In all three groups, the distribution of CBN was mainly in the peripheral zone of the infarct area. Most of the noninfarct tissue areas in the risk area were in the outer third of the left ventricular wall. These findings reflect the transmural gradient of ischemic cellular damage in human AMI. The degree of ischemia immediately before reperfusion is milder in the areas of CBN than in the areas of coagulation necrosis in human AMI. In conclusion, a method should be developed to protect the heart against CBN to reduce infarct size. Circulation 76, No. 5, 981-989, 1987. SINCE Rentrop et al.' first described selective intracoronary thrombolysis in patients with acute myocardial infarction (AMI) in 1979, the technique has been used more and more widely. An

Early Reperfusion During Acute Myocardial Infarction Affects Ventricular Tachycardia Characteristics and the Chronic Electroanatomic and Histological Substrate

“…5 Similar results were found in human autopsied hearts with acute MI after treatment with thrombolysis. 13 These findings from the acute phase of AMI are supported and extended by our data because biopsies were taken in the chronic healing phase 13Ϯ9 years after the index MI in 10 studied patients (28%). Likely as a result of transmural necrosis, the core infarct consisted of transmural fibrosis in nonreperfused patients, whereas the majority of early reperfused patients showed no transmural fibrosis at all with thick layers of viable myocardium even in the core infarct region.…”

Early Reperfusion Therapy Affects Inducibility, Cycle Length, and Occurrence of Ventricular Tachycardia Late After Myocardial Infarction

“…3 Histological studies in patients and animal models of acute MI have shown that the duration of coronary artery occlusion is proportionally correlated to the size and transmural extent of myocardial scar. 4,5,26 Scar size and geometry are important determinants for the reentrant circuit geometry and may contribute to occurrence and CL of VT. 9,27 We recently demonstrated that reperfused patients referred for ablation of recurrent VT late after MI appeared to have smaller and less confluent electroanatomic scars with thick layers of surviving myocardium found at histology. Interestingly, the CL of spontaneous and induced VTs was shorter in reperfused than in nonreperfused patients, probably because of the observed differences in scar geometry after reperfusion therapy.…”

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

“…The section (3 μm thick) was stained with phosphotungstic acid hematoxylin (PTAH). CBN was identified from the appearance of a deep blue color, multiple granulations, and hypercontraction bands, as described by Matsuda et al 9 The whole area of the section was divided into 25-27 regions and photographed with a microscope (Eclipse E400, Nikon, Tokyo, Japan) at ×40 magnification. CBN-positive cells were marked using digital image editing software Photoshop ® 6.0 (Adobe Systems, San Jose, CA, USA).…”

“…CBN is thought to spread during the first minutes of reperfusion and to contribute to development of infarct in the later phase. 5,9,10 Temporary inhibition of contraction at the onset of reperfusion results in infarct limitation. 36 Consistent with those observations, infusion of CBX for only 1 min before onset of reperfusion not only prevented CBN in the early phase, but also delayed infarct development in the late phase of reperfusion.…”