Abstract
In order to describe the mechanisms and significance of coronary flow velocity and increased stenosis severity during coronary vasodilation, stenosis geometry was determined by quantitative coronary arteriography in conscious dogs at resting and high coronary flows. The circumflex coronary artery was instrumented with a Doppler flow velocity transducer, periarterial balloon constrictor and small implanted arterial catheters proximal and distal to the constrictor for contrast injection and pressure measurements. Biplane, orthogonal X-rays of coronary stenosis were taken in mid-diastole at resting and high coronary blood flow after intracoronary papaverine. Arterial borders on X-ray prints were outlined on a digitizing tablet and stenoses reconstructed in 3 dimensions by computer. Dimensions for each of 51 stenoses ranging from 45%-78% diameter narrowing were compared before and after papaverine with 3 important findings. There was no significant change in the minimum cross-sectional area or in exit outflow angle of the stenosis from resting to high coronary flow. Cross-sectional area of the normal artery proximal and distal to the stenosis increased significantly during high flow by 16% and 12%, respectively (P < 0.001), thereby causing diameter stenosis to increase from 68% to 71% (P < 0.001) associated with a 16% increase in the pressure gradient across the stenosis due solely to changes in stenosis geometry. These observations raise basic questions about how stenosis severity should be defined. The cross-sectional area of the artery within the chronically implanted Doppler transducer increased by 32% with vasodilation despite perivascular scarring within the transducer observed at postmortem. Consequently, relative changes in coronary flow velocity were 30-40% less than changes in volume flow, thereby introducing a significant error in measuring relative coronary flow responses unless changes in arterial diameter were also determined. Proximal, large, epicardial coronary arteries vasodilated in response to distal arteriolar vasodilation, probably by an ascending wave of vasodilation from the arteriolar bed.