Coronary hemodynamics during percutaneous transluminal coronary angioplasty

Abstract

The hemodynamic consequences of multiple transient occlusions (9.8 ± 3.7 seconds) of the left anterior descending coronary artery were assessed in 15 conscious patients during percutaneous transluminal coronary angioplasty. Thermodilution coronary venous blood flow, measured in the great cardiac vein, decreased from control values of 75.9 ± 24 ml/min to 50.9 ± 21.9 with coronary occlusion (probability [p] < 0.00001) and increased to 101.6 ± 34.3 after release of occlusion (p < 0.00001). Changes in coronary sinus blood flow, measured simultaneously, reflected the alterations in the great cardiac vein. Restoration of postocclusion blood flow to control values occurred in 18.2 ± 6.7 seconds, and is compatible with reactive hyperemia rather than sustained improvement in resting coronary blood flow. Flow repayment during reactive hyperemia exceeded flow debt incurred during coronary occlusion by 288.4 ± 106 percent (p < 0.05). The increase in reactive hyperemic flow after initial coronary occlusion (24.2 ± 15.7 ml/min) was less than that after final occlusion (42.2 ± 10.1, p < 0.05). This suggests an initial limitation of reactive hyperemia by persistent coronary stenosis. In all patients, reactive hyperemia accentuated the trans-stenotic coronary ostial to distal coronary arterial pressure gradient. Compared with a control value of 53.5 ± 7.7 percent, the great cardiac vein oxygen saturation transiently decreased to 49.3 ± 7.0 percent (p < 0.001) on release of the occlusion and then increased to 62.5 ± 5.2 percent (p < 0.001) during reactive hyperemia. A small reduction in aortic pressure from 96.4 ± 10.2 mm Hg to 89.9 ± 10.9 mm Hg(p < 0.00001) was observed during occlusion. A reduction in first derivative of left ventricular pressure (dP/dt) during coronary occlusion, in three patients in whom it was measured, suggests that the decrease in systemic pressure is due to transient ischemic myocardial dysfunction rather than to peripheral arteriolar vasodilation. These observations are relevant to the performance of coronary angioplasty, and to the understanding of the physiology of transient coronary occlusion in conscious patients.