An increased tissue endothelin-1 (ET-1) immunoreactivity has been demonstrated at the site of the culprit lesion (CL) in patients with unstable angina (UA) thus suggesting that ET-1 may be involved in the abnormal vasoreactivity of the CL in UA. The aim of this study was to establish whether an enhanced local release of ET-1 is involved in the pathogenesis of the enhanced vasoreactivity of the unstable plaque in patients with UA. We studied 9 patients with UA and 9 patients with stable angina (SA) with a single proximal lesion of the left anterior descending coronary artery. Luminal diameter of the CL and of the proximal, middle and distal normal-appearing coronary segments were measured by quantitative coronary angiography at baseline, during cold pressor test (CPT) and after intracoronary administration of nitroglycerine (NTG). ET-1 levels were measured in blood samples obtained proximally and distally to the coronary CL before and after successful stent implantation. During CPT, the CL in patients with UA constricted more than that of patients with SA (percent reduction compared with baseline -25 ± 8 vs -8 ± 10%, p = 0.0007). After NTG, the CL in patients with UA dilated more than that of patients with SA (percent increase compared with baseline 48 ± 21 vs 22 ± 7%, p = 0.0028). The uninvolved proximal, middle and distal coronary artery segments had similar changes during CPT and after NTG in patients with UA and SA. Baseline proximal and distal ET-1 levels before stenting were similar in patients with UA and SA (1.29 ± 0.08 vs 1.24 ± 0.20 pmol/L, p = 0.54 and 1.27 ± 0.20 vs 1.25 ± 0.23, p = 0.79 respectively). After stenting, proximal and distal ET-1 levels significantly increased compared to baseline values both in patients with UA and SA (1.88 ± 0.11 vs 1.40 ± 0.16 pmol/L, p = 0.0001 and 1.89 ± 0.18 vs 1.5 ± 0.30 pmol/L, p = 0.003 respectively); however, the relative increase was greater in UA than in SA patients (45 ± 6 vs 14 ± 16%, p = 0.001 and 51 ± 23 vs 22 ± 12%, p = 0.0035 respectively). The enhanced potential to release ET-1 might be responsible, at least in part, for the enhanced vasoreactivity of the CL in patients with UA.
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