Acute ischemia induced by thrombotic coronary occlusion resulted in a significantly higher incidence of malignant ventricular arrhythmias compared to nonthrombotic balloon occlusion (58% vs 7%).
Does intracoronary thrombosis increase the incidence of malignant ventricular arrhythmias compared to nonthrombotic balloon occlusion during acute myocardial ischemia in dogs?
Intracoronary thrombosis exerts arrhythmogenic effects beyond the impact of ischemia alone, leading to a significantly higher incidence of malignant ventricular arrhythmias compared to nonthrombotic occlusion.
Absolute Event Rate: 58% vs 7%
BACKGROUND: Patients with acute coronary artery thrombosis often develop primary malignant ventricular arrhythmias (MVA) early after coronary occlusion. In contrast, acute ischemia induced by nonthrombotic balloon occlusion during routine coronary angioplasty rarely elicits such arrhythmias. This study was designed to assess the role of intracoronary thrombosis in arrhythmogenesis during acute ischemia. METHODS AND RESULTS: We compared the incidence of MVA associated with acute left anterior descending coronary artery (LAD) thrombosis elicited in open-chest anesthetized dogs by electrical injury (n = 10) or intracoronary stent (n = 9) versus LAD balloon occlusion (n = 15). Compared with animals subjected to balloon occlusion, those with thrombotic occlusion had a significantly greater incidence of MVA, defined as nonsustained ventricular tachycardia (total duration > 10 seconds), sustained ventricular tachycardia, or ventricular fibrillation developing within the first 30 minutes of occlusion. In the combined thrombosis groups, MVA developed in 11 of 19 animals (58%) (6 of 10 dogs with electrical injury and 5 of 9 stent animals). In contrast, MVA occurred in only 1 of 15 animals (7%) subjected to balloon occlusion. This striking and significant difference in arrhythmias occurred despite the fact that radioactive microsphere perfusion analysis documented that the extent of left ventricular myocardium rendered ischemic was equal in all groups (percent of left ventricular myocardium with occlusion flow < or = 50% of baseline: electrical injury, 25.2 +/- 5.3%; stent, 27.1 +/- 3.6%; balloon, 34.3 +/- 11.6%; P = NS). Furthermore, there were no differences between the animals with thrombosis or balloon occlusion with respect to changes in echocardiographic parameters of left ventricular function, aortic pressure, or heart rate after occlusion. CONCLUSIONS: These data provide evidence that despite equal magnitudes of jeopardized myocardial mass, acute ischemia induced by thrombotic coronary occlusion results in a greater incidence of MVA than does nonthrombotic balloon occlusion. These findings suggest that the process of intracoronary thrombosis itself exerts arrhythmogenic effects above and beyond the impact of ischemia on myocardium induced by coronary occlusion.
Goldstein et al. (Fri,) conducted a other in Acute myocardial ischemia (n=34). Intracoronary thrombosis (electrical injury or stent) vs. Nonthrombotic balloon occlusion was evaluated on Incidence of malignant ventricular arrhythmias (MVA) within the first 30 minutes of occlusion. Acute ischemia induced by thrombotic coronary occlusion resulted in a significantly higher incidence of malignant ventricular arrhythmias compared to nonthrombotic balloon occlusion (58% vs 7%).