Myocardial stunning induced and detected by adenosine stress perfusion imaging

Abstract

Adenosine is a potent vasodilator that is thought to induce perfusion defects by causing heterogeneity in blood flow that consists of a large increase in flow through normal arteries and a smaller increase or no increase in flow through stenotic arteries.1 As such, it is not supposed to induce true myocardial ischemia. However, vasodilator stress agents, such as adenosine and dipyridamole, can also cause “coronary steal,” in which the increased blood flow in a normal artery can actually siphon flow away from the bed distal to a highly stenotic lesion through collateral channels.1 This might result in myocardial ischemia with secondary electrocardiographic changes and wall motion abnormalities. Exercise-induced myocardial stunning has been well recognized in the past.2 However, vasodilator stress-induced myocardial stunning has only recently been reported with dipyridamole.3 Our case provides direct evidence that adenosine can induce true myocardial ischemia with secondary stunning, as illustrated by the persistent wall motion abnormality and the significant drop in ejection fraction detected 1 hour after the adenosine infusion. Thus the perfusion defects induced by adenosine are probably the result of a combination of heterogeneity in flow and true myocardial ischemia, presumably secondary to coronary steal.