Coronary, collateral, and perfusion territory responses to aortic banding.

The objectives of this study were 1) to separate anatomic from functional variables causing the increased minimal coronary resistance seen with hypertrophy; 2) to investigate whether increased intraluminal pressure and tangential wall stress lead to collateral proliferation; 3) to define changes in vascular perfusion territories resulting from hypertrophy. Coronary and collateral resistances of the four coronary arteries were determined in empty, beating hearts from 10 control dogs and 11 dogs with myocardial hypertrophy produced by 4 wk of aortic banding. In hypertrophied hearts the coronary flow per gram at 100 mmHg and the slope of the pressure-flow line were significantly decreased. Coronary flow-to-body weight ratios were not different; thus the decreased flow per gram tissue with hypertrophy was due to increased tissue mass rather than changes in vascular resistance. Collateral flows were similar for both groups, indicating that increased pressure and wall stress did not cause significant collateral growth. Both ventricles hypertrophied and all vascular beds were equally affected, but distribution of the increased mass varied for different vascular beds.