PURPOSE: Recent studies have reported conflicting results on a possible rel
ationship between hypertension, heart rate, and prostate cancer. A model ha
s been developed suggesting that high blood pressure and high heart rate ma
y both be markers for increased central sympathetic nervous activity, which
may result in androgen-mediated stimulation of prostate cancer growth.
METHODS: In this study we examined the associations between hypertension, h
eart rate, use of antihypertensive medications, and incident prostate cance
r in a cohort of 2442 men. Data from the Cardiovascular Health Study (CHS),
an NHLBI-sponsored observational study of adults age 65 or older in four U
.S. communities, were analyzed using Cox proportional hazards regression. S
eated systolic and diastolic blood pressures were measured using a standard
ized protocol at the initial clinical examination and annually at follow-up
visits. Medications data were transcribed by trained interviewers from pre
scription medication containers brought into the clinic by participants.
RESULTS: A total of 209 cases of incident prostate cancer were identified f
rom either an ICD-9 code of 185 in hospital medical records (n = 130) or by
self-report from annual surveillance interviews (n = 79). An average of 5.
6 years of follow-up was available for analyses. No associations between bl
ood pressure measures at entry into the study and prostate cancer were foun
d, although these results may have been affected by subsequent treatment of
hypertension. An association between resting heart rate (HR) equal to or g
reater than 80 beats per minute and incident prostate cancer was found comp
ared to men with a rate of less than 60 beats per minute (HR: 1.6, 95% conf
idence interval [Cl]: 1.03-2.5). An inverse association was found between r
isk of incident prostate cancer and use of any antihypertensive medication
(HR: 0.7, 95% Cl: 0.5-0.9). A test of heterogeneity found no difference bet
ween use of the specific classes of antihypertensive medication and the ass
ociation with prostate cancer risk.
CONCLUSIONS: These data tend to support the hypothesized causal pathway bet
ween vascular disease markers and prostate cancer. (C) 2001 Elsevier Scienc
e Inc. All rights reserved.