• Critical Care Genomics
• Myocardial Infarction Clinical Trials

• Critical Care
• Cardiology Genomics
• Cardiology
• Myocardial Infarction
• Cardiology Clinical Trials

Acute myocardial infarction (AMI) carries a high risk of death, but diagnosis in patients with a pacemaker or a left bundle branch block (LBBB) is difficult through an electrocardiogram alone. While cardiac troponin (cTn) is essential in the diagnosis of AMI, it is possible that other biomarkers may improve diagnosis in patients who present early or may have other causes of troponin elevation [Klimczak A et al. Cardiol J. 2007]. Francisco Javier Martin-Sanchez, MD, Hospital Clínico San Carlos, Madrid, Spain, presented results of a study indicating that copeptin may be a useful biomarker to rule out NSTEMI among patients who present to the emergency department (ED) with acute chest pain but have a pacemaker and a normal troponin value at baseline.

The definition of myocardial infarction based on specific cTns has been universally accepted since 2007. A recent meta-analysis of 14 studies that assessed the incremental value of copeptin for rapid rule-out of AMI suggests that copeptin levels can identify patients at risk of all-cause mortality and that, when added to troponin, it improves the sensitivity and negative likelihood ratio for diagnosis of AMI when compared with troponin alone [Lipinski MJ et al. Am J Cardiol. 2014].

The multicenter cohort-based COPeptin in ED [COPED] was an observational longitudinal study designed to evaluate the usefulness of copeptin in ruling out NSTEMI in patients who present to the ED with non-traumatic chest pain suspected to be related to myocardial ischemia. Prof Martin-Sanchez provided results of a retrospective subanalysis from COPED that sought to assess the predictive capacity of copeptin to rule out NSTEMI in ED adult patients with acute ischemic chest pain and previous history of pacemaker or LBBB on an electrocardiogram. Patients were excluded if they arrived at the ED ≥ 12 hours after pain onset, had troponin levels first determined to be positive, or had STEMI and noncoronary chest pain according to the current European Society of Cardiology guidelines. Copeptin was determined in all patients upon arrival at the ED. The cutoff for a positive result was ≥ 14 pmol/L. The primary study outcome was diagnosis of NSTEMI by an emergency physician blinded to copeptin value.

Of the 2292 patients in COPED, 119 were eligible for the present study (81 with LBBB; 38 with pacemaker). More than 50% of the patients were men; most were aged ≥ 74 years. More than 80% were hypertensive; > 50% had a diagnosis of dyslipidemia. The time of the current episode ranged from 90 minutes in the pacemaker group to 120 minutes in those with LBBB. Fourteen patients (3 in the pacemaker group; 11 in the group with LBBB) were diagnosed as having NSTEMI. Of these, 11 (78.6%) were copeptin positive at baseline.

The capacity of copeptin to rule out NSTEMI was lower in patients with LBBB than in those with a pacemaker. Using a copeptin cutoff level ≥ 25 pmol/L (vs ≥ 14 pmol/L) improved the specificity, negative predictive value, and negative likelihood ratio.

While these data suggest that copeptin may play a role in excluding AMI in patients who present early after symptom onset (< 12 hours), the results will require further confirmation in setting of emerging higher-sensitivity troponin assays. In addition, the exploratory cut point of 25 pmol/L will require verification in other data sets.

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