Abstract 4566: Is Coronary Microvascular Function Impaired In Patients With Coronary Spastic Angina?
Background: Coronary spastic angina (CSA) is characterized by transient vasoconstriction of epicardial coronary arteries leading to myocardial ischemia. There have been several studies of coronary microvascular function in patients with CSA, but it is not yet clear whether coronary microvascular function is impaired. We investigated this relationship in the present study.
Methods: Thirty-four patients with CSA (28 men, mean age 58 years) were enrolled. CSA was defined as >90% narrowing of the epicardial coronary arteries on the angiogram during a spasm provocation test with ergotamine maleate, accompanied by characteristic chest pain and/or ST-segment deviation on ECG. Thirty-six patients with a negative spasm provocation test matched for age and gender were enrolled in the control group. Before the spasm provocation test, acetylcholine (ACh) at a low dose (3 μg/min) was infused into the left coronary ostium for 2 min. Coronary blood flow (CBF) was calculated from quantitative angiography and Doppler flow velocity measurements. The CBF response to ACh was expressed as percent change from the baseline value. Just after the end of the spasm provocation test, 0.2 mg nitroglycerin was administered intracoronally. Coronary flow reserve (CFR) was calculated as the ratio of coronary flow velocity after injection of adenosine triphosphate (20 μg) to the baseline value.
Results: A low dose of ACh did not cause coronary spasm. The change in epicardial coronary diameter in response to ACh at a low dose was significantly lower in the CSA group (−1.0±1.4%) than in the control group (3.1±1.3%, p<0.05), while nitroglycerin-induced dilation of the epicardial coronary arteries was not different in the two groups (CSA, 16.0±2.0%; control, 13.7±2.0%). The increase in CBF in response to ACh at a low dose (CSA, 55±9%; control, 65±8%) or CFR (CSA, 3.2±0.1; control, 3.1±0.1) did not differ significantly between the groups
Conclusions: These findings suggest that the ACh-induced change in epicardial coronary arteries, but not the ACh-induced increase in CBF or CFR, was impaired in patients with CSA compared with those without CSA. In patients with CSA, microvascular coronary function may be preserved despite endothelial dysfunction of the epicardial coronary arteries.