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Circulating heart-type fatty acid-binding protein levels predict ventricular fibrillation in Brugada syndrome
Hyuma Daidoji1, Takanori Arimoto1, Tadateru Iwayama1
1Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Insights
Heart-type fatty acid-binding protein (H-FABP) effectively predicts ventricular fibrillation in Brugada syndrome patients with implantable cardioverter-defibrillators (ICDs). Elevated H-FABP indicates higher risk for appropriate ICD shocks.
Area of Science:
- Cardiology
- Electrophysiology
- Biomarker Research
Background:
- Outcomes in Brugada syndrome patients with implantable cardioverter-defibrillators (ICDs) remain unclear regarding ongoing myocardial damage.
- The prognostic value of myocardial injury markers in this specific patient population requires further investigation.
Purpose of the Study:
- To investigate the association between myocardial damage markers and appropriate ICD shocks in Brugada syndrome patients.
- To identify predictors of ventricular arrhythmias in patients with Brugada syndrome and ICDs.
Main Methods:
- Prospective enrollment of 31 Brugada syndrome patients with ICDs.
- Defined myocardial membrane injury (H-FABP >2.4ng/mL) and myofibrillar injury (troponin T >0.005ng/mL).
- Followed patients for a median of 5 years for appropriate ICD shocks.
Main Results:
- Myocardial membrane and myofibrillar injuries were prevalent (29% and 26%, respectively).
- Appropriate ICD shocks occurred in 19% of patients.
- Elevated H-FABP (>2.4ng/mL) was an independent predictor of appropriate ICD shock (HR 25.2, p=0.03), unlike troponin T.
Conclusions:
- Heart-type fatty acid-binding protein (H-FABP) shows promise as a tool for predicting ventricular arrhythmias.
- H-FABP levels can aid in risk stratification for Brugada syndrome patients with ICDs.
- Further research into H-FABP for predicting adverse events in Brugada syndrome is warranted.
Background:
The association between ongoing myocardial damage and outcomes in patients with Brugada syndrome who had received an implantable cardioverter-defibrillator (ICD) is unclear.
Methods:
Consecutive patients with Brugada syndrome (n=31, 50±13 years) who had received an ICD were prospectively enrolled. Minor myocardial membrane injury [heart-type fatty acid-binding protein (H-FABP) >2.4ng/mL] and myofibrillar injury (troponin T >0.005ng/mL) were defined using receiver operating characteristic curves. Patients were followed for a median period of 5 years to an endpoint of appropriate ICD shock.
Results:
Myocardial membrane injury (29%) and myofibrillar injury (26%) were similarly prevalent among patients with Brugada syndrome who had received ICDs. Appropriate ICD shocks occurred in 19% of patients during the follow-up period. Multivariate Cox regression analysis showed that serum H-FABP level >2.4ng/mL, but not troponin T level, was an independent prognostic factor for appropriate ICD shock due to ventricular fibrillation [hazard ratio (HR) 25.2, 95% confidence interval (CI) 1.33-1686, p=0.03].
Conclusions:
Evaluating myocardial damage using H-FABP may be a promising tool for predicting ventricular arrhythmia in patients with Brugada syndrome who have received ICDs.
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