Coronary steal mechanisms in dogs with one-vessel occlusion and other arteries normal.

Abstract

Whether coronary steal can occur in 1-vessel coronary occlusion when other arteries are normally patent was studied, and the quantitative effect on the magnitude of coronary steal of a graded partial stenosis in the coronary circulation proximal to the origin of the collaterals was examined. In 10 dogs, occlusion of the left anterior descending coronary artery (LAD) was induced and perfusion of the left main coronary artery was maintained with a special servo pump at constant pressure (measured distal to the cannula tip) during intracoronary adenosine infusion. Adenosine increased left main coronary blood flow from 85 .+-. 15 to 229 .+-. 42 ml/min, while mean pressure in the left main coronary artery was held constant at 83 .+-. 3 mm Hg (mean .+-. SD). Systemic hemodynamics did not change, but 3 indexes of collateral function decreased: peripheral LAD coronary pressure, from 14.0 .+-. 2.7 to 12.5 .+-. 2.9 mm Hg (P < 0.005); retrograde LAD flow, from 3.2 .+-. 2.5 to 2.4 .+-. 2.6 ml/min (P < 0.001); and microsphere blood flow to ischemic myocardium, from 0.055 .+-. 0.029 to 0.040 .+-. 0.031 ml .cntdot. min-1 .cntdot. g-1 (P < 0.03). Next, the resistance of the Gregg cannula was added to the perfusion system, i.e., in the same dogs constant pressure was regulated in the tubing proximal to the cannula tip. This added resistance created a 4.5- mm Hg pressure gradient (multivessel occlusion) and a larger drop in retrograde LAD flow (23% vs. 36%, P < 0.05). Because a screwclamp caused graded increments in resistance of the left main coronary perfusion system and the resting pressure gradient, there was a linear increase in the magnitude of coronary steal (r = 0.71). Thus, arteriolar vasodilators increased flow velocity, which led to decreased pressure at the origin of the collaterals because there was some resistance in the native coronary circulation between the left main coronary artery and the origin of the collaterals (12% of total resting resistance). Further increments in vascular resistance proximal to the origin of the collaterals caused a linear increase in the magnitude of coronary steal.