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Published on: March 6, 2018
Heart rate and prostate cancer mortality: results of a prospective analysis
P H Gann1, M L Daviglus, A R Dyer
1Department of Preventive Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Insights
Higher resting heart rate is linked to increased prostate cancer mortality risk. This finding suggests a potential role for sympathetic nervous activity in prostate cancer progression.
Area of Science:
- Urology
- Cardiology
- Epidemiology
Background:
- Sympathetic nervous system activity may influence prostate tissue growth.
- Resting heart rate (HR), a marker of sympathetic activity, correlates with cancer mortality.
- The specific link between HR and prostate cancer death is not well-established.
Purpose of the Study:
- To investigate the association between resting heart rate and prostate cancer mortality.
- To determine if higher heart rate predicts an increased risk of death from prostate cancer.
Main Methods:
- Analysis of 22,380 men from the Chicago Heart Association cohort (1967-1973).
- Heart rate measured via electrocardiogram, with a mean follow-up of 19.2 years for mortality.
- Proportional hazards models used to calculate relative risks (RRs) adjusted for confounders.
Main Results:
- A 10 beat/min increase in HR was associated with a 1.26 relative risk of prostate cancer death (95% CI = 1.04-1.51).
- Age-adjusted RRs increased progressively across higher quintiles of HR, with a significant trend (P=0.006).
- Elevated risk was observed throughout the follow-up period.
Conclusions:
- Elevated resting heart rate is a significant predictor of prostate cancer mortality.
- Findings support the hypothesis that sympathetic activity influences prostate cancer progression.
- Further research is needed to elucidate the etiological factors involved.
Abstract:
Recent studies suggest that local levels of sympathetic nervous activity influence the growth of prostatic tissue. In several epidemiological studies, resting heart rate, an indicator of overall sympathetic activity, was positively associated with all noncardiovascular and cancer death among men. However, no previous analyses have focused on the specific relationship of heart rate to prostate cancer mortality. We studied 22,380 men enrolled in the Chicago Heart Association cohort from 1967-1973, who had heart rate (HR) determined by electrocardiogram. Mean length of follow-up (for mortality) was 19.2 years. We computed age-adjusted rates for prostate cancer death by variable of interest and fitted proportional hazards models to estimate relative risks (RRs) adjusted for potential confounders. In a model controlling for age, body mass index, blood pressure, serum cholesterol, smoking, postload plasma glucose, and years of education, the RR for a 10 beat/min higher HR was 1.26 (95% confidence interval = 1.04-1.51). Age-adjusted RRs across higher quintiles for HR were 1.00, 1.55, 1.85, 2.18, and 2.69 (P trend = 0.006). Survival curves indicated that the elevated risk was not confined to the early years of follow-up. Because little is known about factors that determine risk of prostate cancer death, these results could prove important even if due to an unmeasured etiological factor other than heart rate itself. The results are consistent with the hypothesis that local neurotrophic factors associated with sympathetic activity influence the progression of prostate cancer
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