The effect of long-term bradycardia on heart microvascular supply and performance

Bradycardia has been shown to be beneficial for the normal and ischaemic heart because it improves diastolic perfusion and oxygen supply demand balance. Experimentally, a chronically induced decrease in heart rate, either by electrical pacing or pharmacological means, was found previously to increase myocardial capillary supply in normal rabbit and rat hearts. These studies have been extended to a larger mammal, the pig, in which a direct bradycardia (approximately 30% decrease in heart rate) was induced by electrical pacing for 4-5 weeks. There was no evidence of heart hypertrophy and capillary density was found to be significantly increased in the left, but not right, ventricle. Cardiac function during dobutamine inotropic challenge was better in pig hearts which had been paced bradycardially. They performed greater stroke work-higher stroke flow output at lower heart rate--for similar coronary blood flow, thus demonstrating an improved economy of flow utilisation. Heart rate reduction may facilitate capillary growth in the absence of cardiac hypertrophy by prolonging diastolic perfusion, and/or mechanical stretch of vessels due to increased stroke volume capacity. In either case, capillaries would be exposed to increased wall tension which could trigger angiogenesis.