Figure 1
Comparison of cardiac mortality between the low-EPA/AA and high-EPA/AA groups. Kaplan-Meier analysis for cardiac mortality in patients with HF (n = 577). Cardiac mortality was significantly higher in the low-EPA/AA group than in the high-EPA/AA group (P = 0.004).
Figure 2
Cardiac mortality with or without ischemic etiology. Kaplan-Meier analysis for cardiac mortality (A) with ischemic etiology (n = 152) and (B) without ischemic etiology (n = 425). Cardiac mortality was significantly higher in the low-EPA/AA group than in the high-EPA/AA groups irrespective of ischemic or non-ischemic etiologies.
Figure 3
Cardiac mortality with or without statins. Kaplan-Meier analysis for cardiac mortality (A) without statins (n = 343) and (B) with statins (n = 234). Cardiac mortality was significantly higher in the low-EPA/AA group than in the high-EPA/AA group in HF patients with statins (P = 0.003), but not in HF patients without statins (P = 0.193).
Study Limitations
The present study has several limitations. First, the present study, which was conducted as a prospective observational study in a single institution with homogenous racial mix and relatively small number of subjects, might be insufficient to accurately estimate the association between EPA/AA ratio and mortality in patients with HF. However, diagnosis of cardiac death was accurately made by our experienced cardiologists. Although we analyzed using multivariate Cox proportional hazard regression analyses and subgroup analyses under consideration of multiple confounding factors, the effects of the differences in clinical backgrounds between the two groups might not be completely adjusted. Thus, the present results should be viewed as preliminary and potentially limiting the generalizability of the findings. Therefore, further studies with a larger population are needed. Second, we did not measure and consider any changes in the EPA/AA ratio, and only the baseline EPA/AA ratio at admission was used for the analyses. Third, our study did not elucidate whether an increased EPA/AA ratio has a causal role in the adverse outcome, nor did it clarify the mechanisms underlying the association. Our data suggest that a lowered EPA/AA ratio is a potential biomarker that may be helpful in the risk-stratification of patients with HF. Future studies to determine the causal relationship and the impact of an increased EPA/AA ratio and develop treatment strategies in reducing mortality in patients with HF are required.
Conclusions and perspectives
The EPA/AA ratio was an independent predictor of cardiac mortality in patients with HF. This impact was found to be more distinct when patients with HF took statins. Although it is not well known whether EPA supplementation improves prognosis in patients with HF, taking appropriate management to control the EPA/AA balance may reduce the residual risk of patients with HF.
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