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To determine whether chronic bradycardial pacing could change myoeardial capillary density and heart performance, we used transvenous right atrial pacing to reduce the heart rate of rabbits to about 66% of normal for up to 52 days. We compared control animals, animals which had been chronically paced, and sham-operated animals. The chronically paced animals showed no cardiac hypertrophy [heart;body weight ratio (H:BR) was unchanged]. All animals paced for longer than 10 days showed increased myoeardial capillary density (CD) when compared with controls of similar heart weight. The increase in CD was correlated with the duration of pacing (r = 0.830) and reached levels up to 70% greater than those of controls. The increase In stroke volume seen during acute bradycardial pacing was more than twice as great in animals which had been chronically paced as in the controls, which had not previously been paced (84% vs. 38%). Resting minute work and stroke work were similar in all groups, but maximum values achieved after norepinephrine administration were much greater in animals that had been chronically paced. Minute work increased by 59.1 ± 9.6% in controls, by 82.1 ± 18.3% in sham-operated animals, and by 107.1 ± 8% (means ± SE) in paced animals. Stroke work increased by 84.9 ± 9.8% in controls, by 75.4 ± 19.5% in sham-operated animals, and by 121.8 ± 7.8% in paced animals. Although the greater CD of most of the chronically paced hearts may be partly responsible for their improved performance, this cannot be the only factor, since animals paced for short periods showed improved performance but normal CD.

Capillary growth and changes in heart performance induced by chronic bradycardial pacing in the rabbit.