Elevations in endothelin-1 (ET-1) and inflammatory cytokines may impair myocardial reperfusion through the induction of microvascular constriction or obstruction; however, the generation of these factors close to the site of lesion rupture is unknown.

Coronary sinus (CS) and aortic blood was sampled during angioplasty for acute myocardial infarction (AMI) or stable angina to assess the local release of ET-1, interleukin-1β, interleukin-6, tumor necrosis factor-⍺ and C-reactive protein following atherosclerotic plaque rupture. Transthoracic echocardiography documented left ventricular function in AMI. ET-1 levels were higher in CS than in aortic blood in AMI (3.0 ± 0.3 pmol/L vs 2.6 ± 0.3 pmol/L, P = .04), but not in stable angina (1.7 ± 0.2 pmol/L vs 1.5 ± 0.3 pmol/L, P = NS). CS ET-1 levels were also higher in AMI than in stable angina (3.0 ± 0.3 pmol/L vs 1.7 ± 0.2 pmol/L, P = .002), and correlated with left ventricular dysfunction (R² = 0.51, P = .02). In contrast, C-reactive protein levels were higher in CS than in aortic blood only in stable angina (2.3 ± 0.4 mg/L vs 1.8 ± 0.3 mg/L, P = .01). Similarly, CS tumor necrosis factor-⍺ was higher in stable angina than in AMI (6.0 ± 1.4 pg/mL vs 2.5 ± 0.9 pg/mL, P = .02).

Local myocardial release of ET-1 is highest in AMI, where it relates to the extent of myocardial dysfunction. Although local inflammation is a component of stable coronary artery disease, it does not appear acutely enhanced in AMI.