Coronary Artery Reperfusion

Abstract

A B S T R A C T The question of whether or not the size of an area of myocardial infarction, measured at 1 wk after coronary occlusion, can be influenced by coronary artery reperfusion was examined in dogs. In seven control experiments the anterior descending coronary artery was ligated, while in seven other studies the occlusion was released after 3 hr. In all animals calibrated photographs were used to assess the zone of hypoperfusion and the acutely injured area of epicardial ST segment elevation, as well as the extent of damage at postmortem 1 wk later. In control dogs, the gross infarct size at postmortem averaged 63.8±7.3% of that predicted from the acutely injured zone. However, in reperfused hearts the average gross infarct size at 1 wk was only 10.2+4.4% of that predicted. Transmural specimens were obtained at autopsy for histology and measurement of myocardial creatine phosphokinase (CPK) activity from sites initially used for epicardial electrocardiography. In control animals, there was a direct relationship between the degree of ST segment elevation and the degree of cell necrosis in transmural histologic sections. ST segment elevation also predicted myocardial CPK (international units per milligram protein): log CPK = -0.0613 ST + 1.17 (r = 0.66, n = 56 sites). In the reperfused animals, log CPK =-0.166 ST + 1.36 (r = 0.69, n = 46 sites) showing almost complete preservation of CPK activity at 1 wk, sparing being most prominent in the epicardial zone. Similarly, there was a good correlation between myocardial CPK activity and the histological assessment of cell destruction, the degree of cell damage = -0.152 CPK + 3.86 (r = 0.86; n = 102 sites). Thus, control dogs showed severe myocardial CPK depletion

Prolonged derangements of canine myocardial purine metabolism after a brief coronary artery occlusion not associated with anatomic evidence of necrosis

“…Reperfusion has been shown to protect ischemic myocardium from necrosis even when it is delayed for 6 hr (16,17). However, with prolonged myocardial ischemia, hemorrhagic infarcts may occur (18) and postreperfusion mechanical dysfunction, which may persist for prolonged periods, occurs (19).…”

The Coronary Circulation as a Target of Cardioprotection

“…Although today it is unequivocally clear that timely reperfusion of an occluded coronary artery is the only way to rescue myocardium from impending infarction, this notion is a little more than 40 years old and goes back to the study by Ross and collaborators 39,40 who first reported that reperfusion after 180-minute coronary occlusion reduced infarct size in dogs. These findings were quickly translated to humans with acute myocardial infarction who were reperfused by thrombolysis or percutaneous coronary interventions (PCIs).…”

Coronary thrombolysis and infarct size reduction after intravenous infusion of recombinant tissue-type plasminogen activator in nonhuman primates.

“…The preservation of ischemic myocardium by early revascularization in animal models is a controversial issue (10)(11)(12)(13)(14)(15)(16)(17). Variability in experimental results may be due to many factors, including differences in collateral flow within (18) and between…”

“…The duration of coronary occlusion, after which reperfusion results in salvage of ischemic myocardium, seems to be species related. In dogs, reperfusion as early as 3 h resulted in a decrease of ultimate infarction in the majority of reports (10)(11)(12)(13)(14), but revascularization after 5 h or later produced either extension of infarction by hemorrhage (15) or no significant change in infarct size (13)(14)(15). Collateral circulation in pigs is less extensive than in dogs (19), and an equivalent coronary occlusion producing primarily a subendocardial infarction in the dog, results in a transmural infarct in the pig (20).…”