Dose-response association between physical activity, BMI and risk of heart failure
Relationship Between Physical Activity, Body Mass Index, and Risk of Heart FailureLiterature - Pandey A, LaMonte M, Klein L, et al. - J Am Coll Cardiol 2017;69:1129–42
Large randomised studies assessing various therapies have failed to improve clinical outcomes among patients with HFpEF, which makes the primary prevention of this condition very important [1,2]. Leisure-time physical inactivity (LTPA) and obesity are important risk factors for the development of HF [3,4]. However, the contribution of different doses of LTPA and levels of BMI to different HF subtypes is unclear, and the optimal goals for HFpEF prevention are not known.
In this study, the dose–response relationship between LTPA levels, BMI, and risk of HFpEF and HFrEF was assessed, by using individual-level pooled data from 3 prospective cohort studies (WHI [Women’s Health Initiative], MESA [Multi-Ethnic Study of Atherosclerosis], and CHS [Cardiovascular Health Study]), including 51 451 participants.
- After 645 515 person-years of follow-up, 3 180 incident HF events were observed, of which 39.4% were HFpEF, 28.7% were HFrEF, and 31.9% were unclassified HF.
- A consistent, dose dependent, inverse association was observed between higher LTPA levels and risk of overall HF. The association was stronger at higher levels of LTPA, with 11% lower HF risk at guideline-recommended levels (500 to 1,000 MET-min/week) and 22% lower at greater than guideline-recommended activity (>1,000 MET-min/week).
- LTPA at levels >1 000 MET-min/week was associated with a 19% lower risk of HFpEF in the most adjusted model.
- A dose-dependent inverse association was observed between LTPA levels and HFpEF risk (adj HR: 0.91; 95% CI: 0.85-0.97).
- The association between LTPA and HFrEF risk was not significant (adj HR: 0.95; 95% CI: 0.89 - 1.02).
- The cumulative incidence of HFpEF was significantly higher across higher BMI categories above the normal range (p log-rank < 0.0001), while the cumulative incidence of HFrEF across higher BMI categories was not significantly different (Plog-rank = 0.154).
- There was a significant, dose-dependent association between BMI and HFpEF risk. Compared with normal weight participants, overweight and obese class I participants had statistically significant 38% and 56% higher risks of HFpEF, respectively.
- Extremely obese participants with a BMI ≥ 35 kg/m2 had the highest risk for both HFpEF and HFrEF.
- A significant association between the waist– hip circumference ratio and risk of overall HF, HFpEF, and HFrEF was observed, independently of other risk factors.
In a pooled analysis from 3 prospective cohort studies, a dose–response association between LTPA, BMI, and risk of HF was observed, particularly in HFpEF patients. These findings suggest that adequate LTPA and appropriate BMI control are important for the prevention of HFpEF.
In his editorial article , Shah summarises the strengths and limitations of the study by Pandey at all. The strengths include the large sample size and number of events, the used meta-analysis methodology and physical activity categories, and the exclusion of patients who developed HF within two years of study start-up. The limitations include the lack of a causal explanation for the findings, the fact that physical activity intensity was self-reported and missing confounders. The author ends: ‘In conclusion, Pandey et al. have provided strong evidence that lack of physical activity is associated with incident HFpEF. Given the critical need to focus on primary prevention to control HFpEF at the population level, the mounting evidence of the harms of a sedentary lifestyle on the heart and extracardiac organs involved in HFpEF, and the fact that physical inactivity is a modifiable risk factor with a low-cost treatment, the time is ripe for considering patient centered HFpEF prevention programs (“huff-puff health clubs”) as a strategy to curb the HFpEF epidemic.’