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Published on: January 28, 2020
Associations Between Biomarkers of Myocardial Injury and Systemic Inflammation and Risk of Incident Ventricular
Nur Sourour1, Egil Riveland2, Patrycja Næsgaard3
1Department of Cardiology, Division of Medicine, Akershus University Hospital, Lørenskog, Norway; K.G. Jebsen Center for Cardiac Biomarkers, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Insights
Cardiac troponin T (cTnT) predicts ventricular arrhythmias (VA) in heart failure patients, while inflammation biomarkers do not. Myocardial injury, not inflammation, may drive VA and sudden cardiac death.
Area of Science:
- Cardiology
- Biomarkers
- Heart Failure
Background:
- Cardiac troponins (cTns) and inflammation biomarkers are elevated in heart failure (HF) and predict cardiovascular risk.
- The association between these biomarkers and the risk of ventricular arrhythmias (VAs) remains unclear.
Purpose of the Study:
- To assess if 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.
- To investigate the role of myocardial injury versus inflammation in the pathophysiology of VA.
Main Methods:
- A prospective, observational study involving 489 patients treated with implantable cardioverter-defibrillators.
- Measurements of cTnT, GDF-15, IL-6, and CRP were taken at baseline and after 1.4 years.
- Association with implantable cardioverter-defibrillator-detected incident VA, HF hospitalizations, and mortality was analyzed over a 3.1-year follow-up.
Main Results:
- Higher cTnT concentrations were significantly associated with an increased risk of incident VA (HR: 1.63; P < 0.001), even after multivariable adjustment.
- GDF-15, IL-6, and CRP were not associated with incident VA.
- All measured biomarkers, including cTnT, were associated with HF hospitalization and mortality.
Conclusions:
- Only cTnT predicts incident VA in patients with HF.
- Elevated cTnT, GDF-15, IL-6, and CRP are associated with HF hospitalization and death.
- These findings suggest myocardial injury, rather than inflammation, plays a key pathophysiological role in VA and sudden cardiac death.
Background:
Cardiac troponins (cTns) and biomarkers of inflammation are elevated in heart failure (HF) and predict cardiovascular risk. Whether these biomarkers associate with risk of ventricular arrhythmias (VAs) is unclear.
Objectives:
This study sought to assess whether 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, cTnT, GDF-15, IL-6, and CRP were measured at baseline and after 1.4 ± 0.5 years and were associated with implantable cardioverter-defibrillator-detected incident VA, HF hospitalizations, and mortality.
Results:
This study included 489 patients aged 66 ± 12 years and 83% were men. Median concentrations of cTnT were 15 (Q1-Q3: 9-25) ng/L at inclusion, and higher concentrations were associated with higher age, male sex, diabetes mellitus, coronary artery disease, and HF. During 3.1 ± 0.7 years of follow-up, 137 patients (28%) had ≥1 VA. cTnT concentrations were associated with an increased VA risk (per log-unit, HR: 1.63; 95% CI: 1.31-2.01; P < 0.001), also after adjustment for age, sex, body mass index, coronary artery disease, HF, renal function, and left ventricular ejection fraction (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 1.4 years 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 predict 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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