Elevated plasma fatty acid-binding protein 3 is related to prolonged corrected QT interval and reduced ejection
Yung-Chuan Lu1,2, Thung-Lip Lee3,2, Chin-Feng Hsuan3,4,5
1Division of Endocrinology and Metabolism, Department of Internal Medicine, E-Da Hospital, Kaohsiung, 82445 Taiwan.
Insights
Plasma fatty acid-binding protein 3 (FABP3) may indicate prolonged QTc interval and reduced ejection fraction (EF) in stable angina patients. Higher FABP3 levels correlate with abnormal QTc, worse EF, and increased mortality, suggesting FABP3 as a potential biomarker.
Area of Science:
- Cardiology
- Biomarkers
- Electrophysiology
Background:
- Elevated plasma fatty acid-binding protein 3 (FABP3) is linked to cardiovascular events and heart failure.
- The association between plasma FABP3 and prolonged QT interval or reduced ejection fraction (EF) is not well understood.
Purpose of the Study:
- To investigate the relationship between plasma FABP3 levels and prolonged corrected QT (QTc) interval and reduced EF in patients with stable angina.
- To explore associations between plasma FABP3, inflammatory cytokines, and adipocytokines.
Main Methods:
- Evaluated 249 stable angina patients.
- Measured plasma FABP3 using ELISA.
- Obtained 12-lead ECG and echocardiography for QTc interval and EF assessment.
Main Results:
- High FABP3 levels were independently associated with prolonged QTc interval and reduced EF.
- Patients with abnormal QTc intervals had higher FABP3 levels.
- Increased FABP3 tertiles correlated with higher incidence of abnormal QTc, left ventricular systolic dysfunction, all-cause mortality, and lower EF.
Conclusions:
- Plasma FABP3 may serve as a surrogate marker for prolonged QTc interval and reduced EF in stable angina.
- Inflammation and cardiomyocyte injury might mediate the effects of FABP3.
- Further research is needed to confirm FABP3's role in the pathogenesis of QTc prolongation and reduced EF.
Abstract:
Background: Higher concentrations of plasma fatty acid-binding protein 3 (FABP3) play a role in the development of cardiovascular events, cerebrovascular deaths, and acute heart failure. However, little is known about the relationship between plasma FABP3 level and prolonged QT interval and reduced ejection fraction (EF). This study aimed to investigate the relationship between plasma FABP3 level and prolonged corrected QT (QTc) interval and reduced EF in patients with stable angina. Inflammatory cytokine and adipocytokine levels were also measured to investigate their associations with plasma FABP3. Methods: We evaluated 249 consecutive patients with stable angina. Circulating levels of FABP3 were measured by ELISA. In addition, 12-lead ECG and echocardiography recordings were obtained from each patient. Results: Multiple regression analysis showed that high-density lipoprotein cholesterol, high sensitivity C-reactive protein (hs-CRP), white blood cell (WBC) count, visfatin, adiponectin, FABP4, heart rate, QTc interval, left atrial diameter, left ventricular mass index, end-systolic volume, end-systolic volume index, fractional shortening, and EF were independently associated with FABP3 (all p<0.05). Patients with an abnormal QTc interval had a higher median plasma FABP3 level than those with a borderline and normal QTc interval. With increasing FABP3 tertiles, the patients had higher frequencies of abnormal QTc interval, left ventricular systolic dysfunction, and all-cause mortality, incrementally lower EF, higher WBC count, and higher levels of hs-CRP, visfatin, adiponectin, and FABP4. Conclusion: This study indicates that plasma FABP3 may act as a surrogate parameter of prolonged QTc interval and reduced EF in patients with stable angina, partially through the effects of inflammation or cardiomyocyte injury. Further studies are required to elucidate whether plasma FABP3 plays a role in the pathogenesis of QTc prolongation and reduced EF.
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