DOI: 10.1161/circ.148.suppl_1.14300 ISSN: 0009-7322

Abstract 14300: Biomarkers of Myocardial Injury, but Not Systemic Inflammation, Predict the Risk of Incident Ventricular Arrhythmia

Egil Riveland, Nur Sourur, Patrycja Naesgaard, Harald Kjekshus, Alf Inge Larsen, Helge Rosjo, Torbjorn Omland, Peder L Myhre
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Background: Cardiac troponins and biomarkers of inflammation are elevated in heart failure (HF) and predict cardiovascular risk. Whether these biomarkers associate with risk of ventricular arrhythmias (VA) is unclear.

Purpose: To assess whether cardiac Troponin T (cTnT), growth differentiation factor 15 (GDF-15), interleukin-6 (IL-6), and C-reactive protein (CRP) concentrations are associated with incident VA.

Methods: In a prospective, observational study of patients treated with implantable cardioverter defibrillator (ICD), cTnT, GDF-15, IL-6, and CRP were measured at baseline and after 1.4±0.5y, and associated with ICD-detected incident VA, HF hospitalizations and mortality.

Results: We included 489 patients, aged 66±12y and 83% were men. Median (quartile 1-3) concentrations of cTnT were 15 (9-25) ng/L at inclusion, and higher concentrations were associated with higher age, male sex, diabetes mellitus, coronary artery disease (CAD), and HF. During 3.1±0.7y follow-up, 137 (28%) patients had ≥1 VA. cTnT concentrations were associated with an increased VA risk (HR 1.63 [95% CI 1.31-2.01] per log-unit, p<0.001), also after adjustment for age, sex, BMI, CAD, HF, renal function, and LVEF (p<0.001). GDF-15, IL-6, and CRP concentrations were not associated with incident VA, but all (including cTnT) were associated with HF hospitalization and mortality. Changes in cTnT, GDF-15, IL-6, and CRP from baseline to 1.4y were not associated with subsequent VA.

Conclusions: Higher concentrations of cTnT, GDF-15, IL-6, and CRP associate with HF hospitalization and death, but only cTnT predicts incident VA. These findings suggest that myocardial injury rather than inflammation may play a pathophysiological role in VA and sudden cardiac death.

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