Objective: This study was designed to examine whether patients with coronary spastic angina have an impaired coronary artery dilator response to substance P, an endothelium-dependent vasodilator.
Background: Impairment of the endothelium-dependent vasodilator response has been suggested to be involved in the pathogenesis of coronary spasm.
Methods: In 11 patients with coronary spastic angina and 11 control patients, substance P was infused into the coronary artery at 20 pmol/min for 5 min. Incremental doses of acetylcholine were then injected into the coronary artery. The effects of these drugs and nitroglycerin on the coronary artery diameter were quantitatively analyzed.
Results: Heart rate, systolic blood pressure and rate-pressure product did not change after substance P infusion. In 12 coronary arteries of the patients with coronary spastic angina, spasm was induced with acetylcholine. At the site of coronary spasm documented, the lumen diameter, which was 1.6 +/- 0.5 mm at baseline, increased to 2.1 +/- 0.7 mm after substance P infusion (p less than 0.01). It decreased to 0.2 +/- 0.3 mm during acetylcholine-induced spasm (p less than 0.001) and increased to 2.3 +/- 0.8 mm after nitroglycerin administration (p less than 0.001 vs. baseline and p = NS vs. after substance P infusion). Of the 12 arteries with spasm, 5 were angiographically normal and the other 7 were minimally or moderately atherosclerotic: the diameter change after substance P was +28 +/- 20% and +30 +/- 22%, respectively (p = NS). In control patients, the diameter of the middle portion of the left anterior descending artery, which was 2.0 +/- 0.4 mm at baseline, increased to 2.5 +/- 0.4 mm after substance P infusion (p less than 0.001). The diameter changes after substance P infusion were not different between the patients with coronary spastic angina and control patients.
Conclusions: Substance P dilated the artery with spasm of the patients with coronary spastic angina to a degree similar to that in control patients, indicating the preserved endothelium-dependent dilator response at the site of coronary spasm by way of substance P receptor.