Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.

Abstract

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

Atrial Fibrillation in Acute Myocardial Infarction

“…The higher incidence of AF during the first 24 hours could be explained by the fact that during the process of cell death there will be an increase in the release of catecholamine with electrolytes disturbances especially hypokalemia and hypomagnesaemia; this process ceases with the maturation of infarction. [19][20][21][22][23][24] Hod et al investigated the pathogenesis of AF in the early hours of an AMI in a population of patients who were admitted within three hours of the onset AMI. They suggested that acute left atrial ischemia is the patho-physiological mechanism of early AF.…”

The Prognostic Value of Atrial Fibrillation on 30-Day Clinical Outcome in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

“…[1][2][3][4] The causal etiologies of AF in the setting of AMI that have been fully established include atrial ischemia or infarction, pericardial inflammation, acute hypoxia or electrolytemetabolic imbalance, and hemodynamic impairment secondary to left ventricular dysfunction. [18][19][20][21] Additionally, endogenous or exogenous catecholamines may also contribute to AF. 22) Moreover, an association between AF and an increased incidence of severe ischemia and CHF and pump failure has also been identified.…”

Myocardial Infarction and Atrial Fibrillation

“…Figure 7A shows the number of AF events by group. The AF incidence rate ratio (IRR) was significantly higher in LCX compared with LAD (LCX versus LAD, IRR, 6 [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]; P=0.001) or control group (LCX versus control, IRR, 12 [3.26-44.14]; P<0.001, negative binomial model). In contrast, there was no significant differences in IRR between the LAD and control groups (IRR, 2 [0.47-8.5]; P=0.4).…”