Cardiorespiratory fitness and risk of heart failure: a population‐based follow‐up study

Abstract

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 (VO2max), 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 VO2max) 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 (VO2max ≥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.

Exercise and heart failure: an update

“…They observed that lower physical activity, assessed with a standardized validated questionnaire, is associated with higher incidence of HF. More recently, Khan et al 12. in 2014 evaluated, in a first population‐based prospective study, 1873 men (aged 42–61) from eastern Finland to assess the prospective associations (follow‐up of 20.4 years) of cardiorespiratory fitness and the risk of HF.…”

Dose–Response Relationship Between Physical Activity and Risk of Heart Failure

“…[15][16][17] In contrast, the role of PA in reducing risk of HF has not been emphasized in existing guidelines and public health recommendations. 15 Although observational cohort studies have reported an inverse association between higher levels of PA and HF risk, [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] a comprehensive assessment of the quantitative dose-response association between PA and HF risk has not been previously reported. Understanding this relationship is important because recent studies suggest that there may be important differences in the mechanisms through which PA modifies HF risk and CHD risk, 20 and the dose of PA needed to significantly lower HF risk may differ from that currently recommended to reduce CHD risk.…”

Association of Physical Activity or Fitness With Incident Heart Failure

“…One of the studies was US based (including a multiethnic population) 25 and the other was from Finland. 26 These studies included participants from both the sexes aged ≥45 years, with a majority of white race and a follow-up period of 6.5 to 20.4 years.…”

“…Fitness was assessed through maximal oxygen uptake, VO 2 max (Table 2). 25,26 The ascertainment of HF was mostly based on hospital or death records, with only 1 study distinguishing type of HF into HF with reduced ejection fraction versus HF with preserved ejection fraction. 17 The degree of covariate adjustment varied across studies, with 8 studies accounting for intermediate states such as coronary heart disease (CHD) either through adjustment 14,18,21,24 or restriction of analyses to those with nonischemic HF 16,20,23 or exclusion of those with CHD at baseline (either as part of the original study design or a subgroup analysis).…”

“…26 The combination of the effect estimates from these 2 studies in a random-effects model meta-analysis gave an estimate of 21% (HR, 0.79; 95% CI, 0.75-0.83; P<0.001) lower risk of HF for each 1 U increase in metabolic equivalents of oxygen (Figure 3). …”