Abstract
The restoration of oxygenated blood to ischaemic myocardium—reperfusion—halts the process leading to infarction. Early reperfusion is the only way to prevent progression to myocardial necrosis and thus to limit the size of the infarct. It may also, however, injure the heart. This paradox has become clinically important with the advent of thrombolytic treatment and primary coronary angioplasty for acute myocardial infarction. Several studies have shown that there are three main components of reperfusion injury: reperfusion arrhythmias, myocardial stunning, and lethal myocyte injury. Sixty years ago Tennant and Wiggers recognised that the reintroduction of blood flow could cause arrhythmias.1 In animal experiments arrhythmias may occur within seconds of the onset of reflow.2 In humans reperfusion arrhythmias are commonly associated with intracoronary thrombolytic treatment3 and primary coronary angioplasty.4 5 They may be less common after intravenous thrombolytic treatment,6 and in these circumstances it has been proposed that they pose no additional threat to life.7 The disparity may, however, be related to the rate of recanalisation. Yamazaki et al showed that in dogs sudden reperfusion was more likely to be associated with a high frequency of arrhythmias than was staged reperfusion.8 In a randomised clinical study comparing intravenous thrombolytic treatment with primary coronary angioplasty, ventricular fibrillation was significantly more common in the angioplasty group (6.7% v 2.0%).4 These studies provided angiographic …
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