Myocardial ischaemia in patients with coronary endothelial dysfunction: insights from body surface ECG mapping and implications for invasive evaluation of chronic chest pain.

Abstract

Coronary endothelial dysfunction (ED), by predisposing to abnormal vasomotion, may cause chest pain in individuals with non-obstructed coronary arteries. The aim of this study was to correlate the magnitude of coronary ED with the presence and extent of inducible myocardial ischaemia using body surface electrocardiogram (ECG) mapping in symptomatic patients. In 30 patients with chest pain and angiographically normal coronary arteries or mild atherosclerosis, we studied endothelium-dependent responses with acetylcholine (ACH) and endothelium-independent function with nitroglycerin and adenosine in the left anterior descending artery. Eighty-lead body surface ECG maps were collected at baseline and after each dose of ACH. There was a significant correlation between the maximal change in epicardial diameter with ACH and the magnitude of ST-segment shift [r = -0.44 (95% CI: -0.097 to -0.69), P = 0.015]. Patients with ≥ 0.05 mV ST-segment shift/lead had greater epicardial vasoconstriction (31.6 vs. 15.6%, P = 0.019), and lower coronary flow reserve (2.9 vs. 3.6, P = 0.047) compared with those with ST-segment shift <0.05 mV. Four patients had inducible ischaemia with ACH in the absence of abnormal epicardial or global microvascular vasomotion (>20% decrease in diameter or <50% increase in blood flow). This study demonstrates that abnormal vasomotion due to coronary ED is associated with myocardial ischaemia in patients with chest pain. The magnitude of ischaemia correlates with the extent of ED. A small subset of patients develop myocardial ischaemia during ACH infusion without significant abnormalities in epicardial or global microvascular endothelium-dependent blood flow responses.