Cardiovascular reflexes stimulated by reperfusion of ischemic myocardium in acute myocardial infarction.

Acute myocardial infarction (AMI), especially of the inferior left ventricular wall, where most cardiac receptors with vagal afferents that are stimulated during coronary occlusion are located, is commonly associated with reflex hypotension and sinus bradycardia. To determine whether reperfusion of an acutely ischemic area can activate cardiac reflexes, changes in the heart rate, arterial pressure and rhythm were correlated with the time course and location of intracoronary thrombolytic therapy in 41 patients with AMI. Of the 27 patients with successful reperfusion, 17 developed significant transient bradycardia and hypotension and one became tachycardic and hypertensive at the time of recanalization. Spontaneous reversion of the bradycardia and hypotension occurred definitely in six patients and possibly in more (nine reverted after atropine and two after fluids). A positive correlation existed between the changes in heart rate and blood pressure, in contrast to the usual inverse relationship when baroreceptors are stimulated. Two of the three patients in whom reperfusion was transient also developed hypotension and bradycardia. In contrast, all 11 patients with persistent occlusion demonstrated no reflex cardiovascular changes during intracoronary thrombolytic therapy. Thus, successful reperfusion in AMI stimulates cardioinhibitory and vasodepressor (Bezold-Jarisch) reflexes. These findings raise the possibility that the transient hypotension and bradycardia observed during AMI, particularly inferior MI, may sometimes reflect the occurrence of spontaneous reperfusion of the acutely ischemic myocardium.