AIM: To examine the relationship between cardiorespiratory fitness (CRF) and risk of incident heart failure (HF). METHODS AND RESULTS: Cardiorespiratory fitness, as measured by maximal oxygen uptake (VO2 max), was assessed at baseline in a prospective cohort of 1873 men aged 42-61 years without HF or chronic respiratory disease. During a mean follow-up of 20.4 years, 152 incident HF events were recorded. Within-person variability was calculated using data from repeat measurements taken 11 years apart. The age-adjusted hazard ratio (HR) per unit increase (1 mL/kg/min of VO2 max) in CRF was 0.89 [95% confidence interval (CI) 0.86-0.93], which was minimally attenuated to 0.94 (95% CI 0.90-0.98) after further adjustment for established HF risk factors (body mass index, systolic blood pressure, history of cardiovascular disease, diabetes, heart rate, and LV hypertrophy) and incident coronary events as a time-varying covariate. In a comparison of extreme quartiles of CRF levels (VO2 max ≥35.4 vs. ≤25.7 mL/kg/min), the corresponding HRs were 0.27 (0.15-0.50) and 0.48 (0.25-0.92), respectively. Each 1 MET (metabolic equivalent of oxygen consumption) increment in CRF was associated with a 21% (7-33%) reduction in multivariable adjusted risk of HF. Addition of CRF to a HF risk prediction model containing established risk factors did not significantly improve risk discrimination (C-index change = 0.0164, P = 0.07). CONCLUSIONS: In this Finnish population, there is a strong, inverse, and independent association between long-term CRF and HF risk, consistent with a dose-response relationship. The protective effect of CRF on HF risk warrants further evaluation.
AIM: To examine the relationship between cardiorespiratory fitness (CRF) and risk of incident heart failure (HF). METHODS AND RESULTS:Cardiorespiratory fitness, as measured by maximal oxygen uptake (VO2 max), was assessed at baseline in a prospective cohort of 1873 men aged 42-61 years without HF or chronic respiratory disease. During a mean follow-up of 20.4 years, 152 incident HF events were recorded. Within-person variability was calculated using data from repeat measurements taken 11 years apart. The age-adjusted hazard ratio (HR) per unit increase (1 mL/kg/min of VO2 max) in CRF was 0.89 [95% confidence interval (CI) 0.86-0.93], which was minimally attenuated to 0.94 (95% CI 0.90-0.98) after further adjustment for established HF risk factors (body mass index, systolic blood pressure, history of cardiovascular disease, diabetes, heart rate, and LV hypertrophy) and incident coronary events as a time-varying covariate. In a comparison of extreme quartiles of CRF levels (VO2 max ≥35.4 vs. ≤25.7 mL/kg/min), the corresponding HRs were 0.27 (0.15-0.50) and 0.48 (0.25-0.92), respectively. Each 1 MET (metabolic equivalent of oxygen consumption) increment in CRF was associated with a 21% (7-33%) reduction in multivariable adjusted risk of HF. Addition of CRF to a HF risk prediction model containing established risk factors did not significantly improve risk discrimination (C-index change = 0.0164, P = 0.07). CONCLUSIONS: In this Finnish population, there is a strong, inverse, and independent association between long-term CRF and HF risk, consistent with a dose-response relationship. The protective effect of CRF on HF risk warrants further evaluation.
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