Acute myocardial infarction (AMI) is associated with left ventricular dysfunction and clinical heart failure. Arginine vasopressin (AVP), also known as antidiuretic hormone, is a nonapeptide released from the hypothalamus, which promotes renal water conservation via the V2 receptor and hence influences osmoregulation and cardiovascular homeostasis. AVP is elevated in heart failure and post-myocardial infarction and is associated with adverse prognosis; however, its measurement in plasma is hampered by rapid clearance from the circulation and instability ex vivo. Copeptin, the C-terminal fragment of provasopressin is a 39 amino acid glycoprotein with a molecular mass of 5 kDa, which is secreted in equimolar amounts to vasopressin, is stable for several days after blood withdrawal and is hence more readily measured as a surrogate for AVP. The aim of this study was to describe the association between copeptin with left ventricular dysfunction, volumes, remodelling and clinical heart failure post-AMI.

Methods We studied 274 subjects with AMI. Copeptin was measured from plasma at discharge and subjects underwent echocardiography at discharge and follow-up (median 155 days). Subjects were followed for clinical heart failure for a median of 381 days. Remodelling was assessed as the change in left ventricular volumes between echo examinations.

Results Copeptin correlated directly with the wall motion index score (WMIS) and inversely with left ventricular ejection fraction (LVEF) at discharge (WMIS, r  =  0.276, p<0.001; LVEF, r  =  −0.188, p = 0.03) and follow-up (WMIS, r  =  0.244, p<0.001; LVEF, r  =  −0.270, p<0.001) and with ventricular volumes at follow-up (left ventricular end-diastolic volume, r  =  0.215, p = 0.002; left ventricular end-systolic volume (LVESV), r  =  0.299, p<0.001). Copeptin was associated with ventricular remodelling: change in end-diastolic volume, r  =  0.171, p = 0.015; change in end-systolic volume, r  =  0.186, p = 0.008. Subjects with increasing LVESV had higher levels of copeptin (median 6.30 vs 5.75 pmol/l, p = 0.012). Subjects with clinical heart failure (n  =  30) during follow-up had higher copeptin before discharge (median 13.55 vs 5.80 pmol/l, p<0.001). In a Cox proportional hazards model, copeptin retained its association with clinical heart failure (p = 0.032). Kaplan–Meier assessment revealed increased risk in subjects with copeptin greater than 6.31 pmol/l (odds ratio 5.26; 95% CI 2.07 to 13.3, log rank, p<0.001).

Conclusion Copeptin is associated with left ventricular dysfunction, volumes, remodelling and clinical heart failure post-AMI. Measurement of copeptin may provide prognostic information and the AVP system may be a therapeutic target in post-myocardial infarction left ventricular dysfunction.