CORONARY VASOCONSTRICTION IN RESPONSE TO ACETYLCHOLINE AFTER BALLOON ANGIOPLASTY - POSSIBLE ROLE OF ENDOTHELIAL DYSFUNCTION

Background: Abnormal endothelium-dependent vasomotion has frequently b een observed early after coronary angioplasty. The aim of this study w as to investigate endothelium-mediated coronary vasomotion caused by i ncreasing intracoronary infusions of acetylcholine into epicardial cor onary arteries 3-6 months after coronary angioplasty in patients witho ut restenosis (50% luminal diameter reduction). Methods: Intracoronary acetylcholine was infused during follow-up coronary angiography follo wed by an intracoronary bolus of 250 g nitroglycerin in 18 patients wh o had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery me asurements were performed in the proximal reference segment, in the pr oximal part of the angioplasty site, at the site of previous maximal s tenosis, in the distal part of the angioplasty site, and in the distal reference segment. Results: In the segments of the coronary artery no t manipulated by balloon catheter, acetylcholine did not produce signi ficant luminal diameter changes (+2+/-23% in the proximal segment and -3+/-27% in the distal segment at 10(-4) mol/l). All the angioplasty v essel segments, excluding the proximal reference segments, showed an a bnormal dose-related reactivity to the acetylcholine. Maximal vasocons triction was observed at 10(-4) mol/l and was 4.9+/-11.1% in the proxi mal reference segment, 9.3+/-19.1% in the proximal angioplasty site (P =0.0314), 20.3+/-24.1% at the site of previous maximal stenosis (P=0.0 005), 10.7+/-16.8% at the distal angioplasty site (P=0.0098), and 9.3/-14.1% in the distal reference segment (P=0.0032). The maximal respon se of the angioplasty site to acetylcholine and to nitroglycerin did n ot correlate either with the time to follow-up or with the follow-up s tenosis. Nitroglycerin-induced vasodilation was significant in all seg ments, but was lower in the lesion-related segments. Acetylcholine evo ked the same effect on both the vessels that were manipulated and thos e that were not. Conclusions: Three to 6 months after coronary angiopl asty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injur ed by balloon inflation. In contrast, endothelium-independent vasodila tion by nitroglycerin is maintained in all segments. These observation s suggest that the endothelium is still functionally impaired in the a rea of balloon dilation.