Ventricular arrhythmias in rapid pacing induced heart failure with and without prior myocardial infarction

Investigations of arrhythmias in heart failure are hampered by a lack of good animal models. This study assesses the usefulness of dogs with chronic rapid pacing induced heart failure for studying arrhythmias both with and without prior myocardial infarction. Group I animals received ventricular pacemakers and electrodes for extrastimulus testing. Group II animals were similarly instrumented, and also underwent coronary ligation/reperfusion. After surgical recovery, both groups were paced (250 beats/min) and studied biweekly for arrhythmia inducibility. In addition to clinical signs of failure, changes in left ventricular dimensions/function were monitored using M-mode echocardiography (Grouop I) or ultrasonisc dimensiobn crystals (Group II). In Group I (noninfarcted), four of six dogs became inducible following variable periods of rapid pacing, and an additional animal died suddenly without demonstrating prior inducibility. Ventricular effective refractory periods shortened from 158 ± 12 ms to 137 ± 15 ms (P<0.05). In Group II, two dogs fibrillated at the initial study following infarction. Of the remaining 4, following onset rapid pacing, three developed new inducible arrhythmias. Ventricular effective refactory periods were unchanged. Rapid pacing induced dysfunction developed in both groups, with arrhythmia induction occuring earlier following onset of rapid pacing in the post infarct group. Thus, these models appear promising for investigating arrhythmias associated with heart failure. Particularly unique are the progressive nature of myocardial dysfunction, potential for recovery, and the fact that these models mimic many features present in human cardiomyopathy.