Lifetime risk of HF
In this cohort of apparently healthy male physicians, we observed that the remaining lifetime risk of HF was about 1 in 7 at age 40, 50, 60, and 70 years. Despite the homogeneity in educational attainment and socioeconomic status, we noted that adherence to healthy lifestyle factors was associated with the remaining lifetime risk of HF in this cohort. As expected, the lifetime risk of HF was higher in hypertensive than normotensive men. We observed a similar relation between HF with antecedent myocardial infarction, type 2 diabetes, or hypertension.
Few studies have examined the remaining lifetime risk of this condition. In the Framingham Heart Study, Lloyd-Jones and colleagues20
found that the lifetime risk of HF in 3757 men age 40 was 21.0%. In the Rotterdam Study,41
the lifetime risk of HF was found to be 33.0%. Contrary to the Framingham Heart Study, where the lifetime risk remained constant from age 40 through age 80, there was a decrease in lifetime risk with advancing age in the Rotterdam Study from 33% at age 55 to 23% at age 85. In the PHS I, we observed a constant lifetime risk of HF from age 40 through age 70 and a drop was only observed in people aged 80. Such lower risk in the oldest age group could be attributable to the shorter remaining time at risk as well as the depletion of susceptible individuals and/or decreased disease ascertainment or reporting with very old ages. Although the lifetime risk of HF in our study (about 1 in 7) was high, it was noticeably lower than the 1 in 5 observed in the Framingham heart Study20
or 1 in 3 reported in the Rotterdam study41
in men of similar ages. What factors could possibly account for the discrepancy?
First, we acknowledge the difficulty of direct comparison of lifetime risk across populations in the absence of comparable mortality rates. A high mortality rate from other causes can lead to lower lifetime risks of HF due to a shorter period a risk. In contrast, longevity can lead to a higher lifetime risk than expected, particularly if the disease is prevalent in old ages. At age 40, PHS I participants have a life expectancy of 49.3 additional years42
; 12 years longer than that of 40-year-old men in the general US population.43
It is noticeable that even though our cohort is longer lived (thus had a longer period at risk for HF) than either the Framingham or the Rotterdam studies, we observed substantially lower lifetime risks of HF. This may be due to the healthy lifestyle factors in our population leading to a decreased incidence of HF. Second, the study period may be a possible contributing source for the variability in estimates of lifetime risk of HF across studies. While there was limited overlap between the Framingham study period (1971 to 1996) and the PHS I (1982 to 2008), the Rotterdam study period (1989 to 2000) was completely included in the PHS study period. A reduction in annual incidence over time (due to better treatment) would partially explain the lower lifetime risk of HF in the most recent study. However, published data on secular trends in HF incidence suggest no substantial change in rate over time.44–47
Third, it is possible that the variability in diagnosis criteria for HF could have led to heterogeneity in cases across studies. Fourth, the PHS I population consisted of adult male physicians recruited for a primary prevention trial. Consequently, it is possible that the fact that physicians may have lower risk of HF given their medical knowledge, their access to state of the art treatment, and early recognition of signs and symptoms leading to the detection of milder cases of HF which may have been missed in the Framingham or the Rotterdam Study. However, early detection of HF in the PHS I would have led to increased rate of HF and not explain the observed lower lifetime risk of HF compared to the Framingham and the Rotterdam studies. Lastly, the healthy volunteer effect could have contributed to the lower lifetime risk of HF in this cohort.
Our finding for HF without antecedent coronary disease was similar to the Framingham data20
in men. As expected, hypertensive men had a higher lifetime risk of HF than normotensive.
Influence of lifestyle factors and lifetime risk of HF
In this cohort, we noted that regular exercise, not smoking, maintaining a normal weight, consumption of fruit and vegetables, breakfast cereal, and moderate alcohol consumption were individually and jointly associated with a lower lifetime risk of HF. The lowest risk was observed in people with 4 or more healthy lifestyle factors. Our data were robust in that restriction to 3 common lifestyle factors (exercise, smoking, and adiposity) yielded similar results and accounting for change in lifestyle factor overtime further strengthened the results.
To the best of our knowledge, this is the first study to examine the influence of modifiable lifestyle factors on the remaining lifetime risk of HF in a large cohort. Of note is that the lifetime risk was 22% in people without any of the desirable healthy lifestyle factors considered. This is about the same risk observed among men in the Framingham Heart Study who were the same age (40 y) and suggests that education alone without adherence to healthy lifestyle factors may not be adequate to lower the lifetime risk of HF. To the contrary, our data suggest that maintenance of healthy habits known to lower the risk of cardiovascular disease remains critical to lowering the risk of HF.
Study strengths and limitations
The large number of participants, 22+ years of follow up, and the standardized methods of endpoints ascertainment are major strengths of this study. On the other hand, the fact that all participants were male physicians, most of whom were Caucasians limits the generalizabilty of the current findings. In addition, we were unable to examine the lifetime risk of systolic versus diastolic HF and we did not have data on the etiology of HF. Although the ascertainment of HF in this study was self-reported, the high confirmation rates of HF diagnosis using Framingham criteria and review of medical records on 2 subsamples is reassuring that we had a reasonable case ascertainment in this study. Nevertheless, we can not exclude misclassification of some cases of HF in this study. It is possible that change in lifestyle factors before incident HF may have led to an underestimation of the effect measure. However, findings accounting for change in lifestyle factors over time yielded similar conclusions, suggesting that such bias may not completely explain our findings. Furthermore, we had reasonable Pearson’s correlation coefficients or levels of agreement across repeated measures as noted above. We were unable to account for early lifestyle factors for men who entered the study at an older age (i.e. 75+ y) despite the 22 years of follow up. Lastly, in the absence of randomization of studied lifestyle factors, we can not exclude unmeasured or residual confounding as partial or complete explanation of these findings.
Public health and clinical implications
Our data provide further evidence supporting a high burden of HF, even among those with a higher educational attainment. Our estimate of lifetime risk of HF could help public health official allocate resources for the prevention and management of this condition. Our findings of a low lifetime risk in people who adhere to modifiable lifestyle factors emphasize the need for incorporation of these behaviors in prevention strategies against HF both at individual and population level.