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Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second-or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery. Our data indicate that early atrial fibrillation in acute myocardial infarction occurs when there is coexistent occlusion of the left circumflex artery proximal to the origin of its left atrial circumflex branch and impaired perfusion of the atrioventricular nodal artery. Since these two arteries both contribute to left atrial perfusion, our data suggest that acute left atrial ischemia is the pathophysiologic mechanism of early atrial fibrillation.Circulation 75, No. 1, 146-150, 1987. ATRIAL FIBRILLATION complicates acute myocardial infarction in about 20% of patients. It usually occurs later than 24 hr after the onset of infarction as a consequence of either pericarditis or heart failure.1 In contrast, atrial fibrillation during the early hours of myocardial infarction is rare`and its pathogenesis is poorly understood. The purpose of this study was to investigate the pathogenesis of atrial fibrillation in the early hours of an acute myocardial infarction in a population of patients who were admitted within 3 hr of the

SUMMARY We investigated the effects of brief intermittent periods of ischemia on myocardial viability. Brief periodic coronary occlusions were produced up to 18 times by inflating and deflating the balloon of an intracoronary #2F catheter for periods of 15, 10 or 5 minutes, followed by 15-minute periods of reperfusion. Creatine kinase (CK) release, triphenyl tetrazolium chloride staining, and light and electron microscopy were used to detect the presence of myocardial necrosis. For the study of CK release, blood was taken from the great cardiac vein and the aorta before and at 5-minute intervals during each left anterior descending coronary occlusion, as well as during and 1, 5, 10 and 15 minutes after balloon deflation. In seven of 24 dogs with 15-minute occlusions, in five of 21 dogs with 10-minute occlusions, and in three of 32 dogs with 5-minute occlusions, small but distinct areas of subendocardial necrosis were present. In all dogs with morphologic proof of necrosis, there was periodic release of CK into the great cardiac vein, which peaked immediately after reperfusion, reflecting CK washout. Thus, brief periods of ischenia, which when single do not cause necrosis, have a cumulative effect and may cause myocardial necrosis. This mechanism of necrosis may be relevant clinically in patients with frequent anginal episodes. Since many dogs of this study did not have any myocardial necrosis, the findings also suggest that intermittent repefdusion has a beneficial effect and may prevent necrosis, even when total occlusion time exceeds 200 minutes.EXPERIMENTAL STUDIES have established that to cause myocardial necrosis, an ischemic injury must be of sufficient duration and severity. Even with the severest ischemia in dogs, the injury must be present for at least 20-30 minutes before necrosis will occur.1 For example, if flow is restored after 15 minutes of ischemia, no myocardial necrosis will be present. ' However, even when ischemia is brief and myocardial necrosis does not occur, there is usually a lengthy delay in return of normal function and metabolism in the injured myocardium.2-Therefore, we evaluated the possibility that brief periods of ischemia before the myocardium has fully recovered from the effects of preceding episodes of ischemia may gradually increase the degree of injury to the point of nonreversibility and necrosis. Methods PreparationThe study was with room air was instituted with a Harvard respirator. Systemic blood pressure was measured through a catheter inserted into the femoral artery. A #5F catheter was inserted through the external jugular vein under fluoroscopic control into the coronary sinus and advanced into the great cardiac vein. The position was verified by injection of contrast material. A #7F Judkins catheter was inserted through the left carotid artery into the ostium of the left anterior descending coronary artery (LAD). A #2F Fogarty catheter was then passed through the lumen of the Judkins catheter and advanced 2-3 cm into the LAD. The Judkins catheter was withdrawn into...

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