C-Terminal Provasopressin (Copeptin) is Associated With Left Ventricular Dysfunction, Remodeling, and Clinical Heart Failure in Survivors of Myocardial Infarction

Background: Acute myocardial infarction (AMI) is associated with left ventricular (LV) dysfunction and clinical heart failure. Arginine vasopressin is elevated in heart failure and the C-terminal of provasopressin (Copeptin) is associated with adverse outcome post-AMI. The aim of this study was to describe the association between Copeptin with LV dysfunction, volumes and remodeling and clinical heart failure post-AMI. Methods and Results: We studied 274 subjects with AMI. Copeptin was measured from plasma at charge and subjects underwent echocardiography at discharge and follow-up (median 155 days). Subjects were followed tor clinical heart failure for a median of 381 days. Remodeling was assessed as the change (Delta) in LV volumes between echo examinations. Copeptin correlated directly with wall motion index score (WMIS) and inversely with LV ejection fraction (LVEF) at discharge (WMIS. r = 0.276, P < .001 LVEF r = -0.188. P = .03) and follow-up (WMIS. r = 0.244. P < .001: LVEF. r = -0.270. P < .001) and with ventricular volumes at follow-up (LVEDV, r = 0.215. P = .002; LVESV, r = 0.299. P < .001). Copeptin was associated with ventricular remodeling; Delta EDV: r = 0.171, P = 0.015, Delta ESV: r = 0.186, P = .008. Subjects with increasing LVESV had higher levels of Copeptin (median 6.30 vs. 5.75 pmol/L. P = .012). Subjects with clinical heart failure (n = 30) during follow-up had higher Copeptin before discharge (median 13.55 vs. 5.80. P < .001). In a Cox proportional hazards model. Copeptin retained association with clinical heart failure. Kaplan-Meier assessment revealed increased risk in subjects With Copeptin >6.31 pmol/L. Conclusions: Copeptin is associated with I-V dysfunction, volumes, and remodeling and clinical heart failure post-AMI. Measurement of Copeptin may provide prognostic information and AVP system may be a therapeutic target in post-MI LV dysfunction. (J Cardiac Fail 2008:14:739-745)