Ischemic myocardial injury in rapidly paced dogs: Contribution to ventricular dysfunction

Chronic rapid ventricular pacing in the dog has been shown to provide a predictable and stable model of heart failure for which the operative pathomechanism remains in question. In a group of 20 dogs with congestive failure induced by rapid ventricular pacing for a mean duration of 29.5 ± 13.1 days (range 7 to 55 days), mean left ventricular end diastolic pressure (LVEDP) was elevated as compared with unpaced controls (23.2 ± 2.7 mmHg vs. 2.0 ± 0 mmHg, p < 0.001). Gross myocardial hemorrhage was present at autopsy in 9 of 20 (45%) paced animals, and necrosis was present in 5 of 20 (25%). Histologic findings included acute ischemic myocardial injury with contraction band necrosis, wavy myofibers, and coagulation necrosis ranging from 0 to 4 lesions per paced animal (1.4 ± 1.4, mean ± SD), compared with none in unpaced animals (p < 0.03). Healed ischemic lesions ranged from 0 to 10 per animal (mean 3.2 ± 2.9) versus none in control animals (p < 0.0001). Total injury score (acute plus healed) for each paced animal ranged from 0 to 12 (mean 4.6 ± 2.9), compared with no injury in nonpaced controls (p < 0.0001). Thus ischemic injury reflected by multiple foci of acute and healed myocardial injury is a prominent and common feature in the canine rapid ventricular pacing model of heart failure.