Over a median 7 years of follow-up, 597 of 39 367 men without a history of MI or diabetes at baseline developed HF (563 hospitalizations and 34 deaths with HF listed as the primary cause) corresponding to a rate of two cases/1000 person-years. Fatty-fish intake was positively associated with age, family history of MI, history of hypertension and high cholesterol, and intake of alcohol and red and processed meats (Table ).
Baseline characteristicsa of the population by fatty-fish intake
The association between fatty-fish consumption and HF was U-shaped in age-adjusted analyses (P-value for quadratic trend = 0.04) (Table ). The association was attenuated in multivariable-adjusted models (HR 1/week vs. no consumption = 0.88, 95% CI 0.68–1.13) and the quadratic trend was no longer statistically significant (P = 0.32). A potentially nonlinear pattern was observed for total fish intake. Compared with consumption <1/week, the multivariable-adjusted HR was 0.78 (95% CI 0.57–1.08) for 1/week, 0.80 (95% CI 0.58–1.11) for 2/week, 0.76 (95% CI 0.54–1.06) for 3–6/week, and 0.89 (95% CI 0.60–1.33) for ≥1/day, though the quadratic trend was not statistically significant (P = 0.26).
Fish intake and incidence of heart failure
The association between marine omega-3 fatty acids and HF was also U-shaped, with the multivariable-adjusted HR lowest among those in the middle quintile (0.32–0.40 g/day) (P-value for quadratic trend = 0.02) (Table ). Further adjustment for macronutrients did not materially change the results. A formal analysis of the shape of the association using a restricted cubic spline also suggested a U-shaped relationship (P-value for deviation from linearity = 0.04) (Figure ).
Marine omega-3 intake and incidence of heart failure
Figure 1 The solid line represents hazard ratio and the dashed line represents the 95% confidence intervals. The curve was produced from a Cox proportional hazards model where marine omega-3 intake was modelled as a restricted cubic spline with three knots, the (more ...)
Five percent of participants reported consuming ≥1 fish oil capsule/week. When fatty acids from this source were included in the calculation of marine omega-3, the multivariable-adjusted HR across quintiles were 1, 0.99 (95% CI 0.77–1.27), 0.73 (95% CI 0.54–0.97), 0.97 (95% CI 0.75–1.27), 1.05 (95% CI 0.82–1.36). Although the confidence intervals were wider, the pattern of results was similar when we excluded cases of HF occurring during the first 2 years of follow-up. Compared with the lowest quintile, HR adjusted for incident MI as a time-varying covariate in addition to lifestyle and dietary covariates were 0.94 (95% CI 0.74–1.20), 0.67 (95% CI 0.50–0.90), 0.89 (95% CI 0.68–1.16), and 1.00 (95% CI 0.77–1.29) across quintiles.
Among men with a history of MI or diabetes at baseline, multivariable-adjusted HR were 0.84 (95% 0.58–1.21) for consumption <1/week, 0.94 (95% CI 0.66–1.35) for 1/week, 1.32 (95% CI 0.89–1.96) for 2/week, and 1.20 (95% CI 0.67–2.14) for ≥3/week compared with no consumption of fatty fish. Hazard ratios across quintiles of marine omega-3 fatty acids were 1, 1.04 (95% CI 0.72–1.48), 0.87 (95% CI 0.58–1.28), 1.12 (95% CI 0.77–1.62), and 1.30 (95% CI 0.92–1.83). In the combined population of men with and without a history of MI and diabetes at baseline, HR were 0.88 (95% CI 0.72–1.09) for consumption of fatty fish <1/week, 0.89 (0.73–1.09) for 1/week 1.08 (95% CI 0.85–1.36) for 2/week, and 0.99 (95% CI 0.69–1.42) for ≥3/week compared with no consumption of fatty fish. Corresponding HR across quintiles of marine omega-3 fatty acids were 1, 0.98 (95% CI 0.60–1.58), 0.84 (95% CI 0.49–1.43), 1.27 (95% CI 0.77–2.09), and 1.19 (95% CI 0.75–1.91).