No abstract

Adenosine produces a receptor mediated shortening of monophasic action potential duration and refractoriness which increases vulnerability to transient atrial arrhythmias. During sustained atrial flutter, these effects may also contribute to destabilisation and termination of the arrhythmia.

SUMMARY Experimental and clinical cases have been described in which bradycardia, i.e., heart rates below 60 beats/min or slowing of the heart rate, resulted in lethal ventricular arrhythmias during various stages of myocardial ischemia and infarction. The present study was designed to determine the relationship of lethal ventricular arrhythmias and slow heart rates. In 18 dogs anesthetized with sodium pentobarbital, the left anterior descending (LAD) coronary artery was ligated. Standard ECGs, His bundle electrograms and composite electrograms from intramural and epicardial areas in ischemic and normal zones were recorded during the first 3 hours of ischemia. Vagosympathetic trunk stimulation caused varying degrees of slowing and bradycardia. Of the 18 dogs, slowing of the heart rate or marked bradycardia induced ventricular ectopic beats coupled to the sinus beats in two, sustained ventricular tachycardia in two, and ventricular fibrillation in two. In another group of six dogs studied 17-25 days after LAD ligation, one dog showed sustained ventricular tachycardia in response to vagal-induced bradycardia. In all acute or chronic cases of arrhythmias after LAD ligation, continuous electrical activity was recorded on one or more of the electrograms within or overlying the ischemic or infarcted zones. This bridging electrical activation, which is indicative of slow conduction, provided strong presumptive evidence for reentry as the mechanism of lethal or potentially lethal ventricular arrhythmias triggered by bradycardia in the setting of myocardial infarction.THE ARRHYTHMOGENIC effects of increasing the heart rate during acute myocardial infarction in experimental'-" and clinical studies" 6have been reported. Bradycardia has also been associated with the onset of malignant ventricular arrhythmias reported in several experimental7' 8 and clinical'"' studies.However, some reports have indicated significant beneficial effects, such as a decrease of ventricular arrhythmias or abolition of arrhythmias, due to slowing of the heart rate in acute myocardial infarction.2' 4 12, 1 Han et al."4 proposed that in the ischemic heart, both tachycardia and bradycardia could lead to reentrant arrhythmias as a result of dispersion of refractoriness, i.e., nonuniform recovery of excitability.Direct evidence for a reentrant mechanism is lack- dogs were studied 17-25 days after the onset of myocardial ischemia and infarction (group 2).Acute Studies -Group 1In group 1, a left thoracotomy was performed through the fourth intercostal space. The left anterior descending coronary artery (LAD) was dissected within 1.0-1.5 cm of its orign and two ligatures were placed around the vessel. A standard lead II ECG was monitored, as were direct electrogram recordings from the heart. The His bundle electrogram was recorded from a bipolar catheter introduced through a carotid artery and positioned in the noncoronary cusp at the aortic root.'6 An electrogram was recorded from the epicardial surface at the center of the area perfused by the LAD usin...