Myocardial morphology and blood flow distribution in chronic volume-overload hypertrophy in dogs.

In this study we investigated myocardial structural alterations and regional myocardial blood flow in chronic volume-overload induced left ventricular hypertrophy in the dog. Moderate hypertrophy (28%) was produced by inserting a shunt between the left subclavian artery and the left atrial appendage in 7 dogs (LVH), while a sham operation was performed on 5 control dogs (C). At a paced heart rate of 100 beats/min there were no differences in blood-flow distribution to the subendocardium (ENDO) mid-myocardium (MYO) or subepicardium (EPI) or in ENDO/EPI ratios between the two groups of dogs. Following adenosine-induced coronary vasodilatation (1 mg/kg/min), there was a relative shift in blood flow away from the ENDO in the LVH dogs so that the ENDO/EPI ratio was reduced. Analysis of the microvascular bed and myocyte cross-sectional area in the same three regions of interest revealed a significant reduction in capillary density in the ENDO region of the hypertrophied hearts when compared to controls (LVH = 2463 +/- 10, C = 2773 +/- 75 caps/mm2) and a corresponding increase in myocardial cell cross-sectional area (LVH = 262 +/- 10, C = 233 +/- 36 microns 2). The reduction in capillary density in LVH may be explained on the basis of increased muscle growth without appropriate capillary proliferation indicating an inadequate neovascular response to this form of overload. The results also indicate that blood-flow distribution abnormalities may not be detected at resting flow with moderate LVH produced by volume overload.