Although it has been hypothesized that hypertension is in part an inflammatory
disorder, clinical data linking inflammation with incident hypertension are
To examine whether C-reactive protein levels, a marker of systemic inflammation,
are associated with incident hypertension.
Design, Setting, and Participants
A prospective cohort study that began in 1992 of 20 525 female
US health professionals aged 45 years or older who provided baseline blood
samples with initially normal levels of blood pressure (BP) (systolic BP <140
mm Hg and diastolic BP <90 mm Hg, and no history of hypertension or antihypertensive
medications) and then followed up for a median of 7.8 years for the development
of incident hypertension. Plasma C-reactive protein levels were measured and
baseline coronary risk factors were collected.
Main Outcome Measure
Incident hypertension, defined as either a new physician diagnosis,
the initiation of antihypertensive treatment, or self-reported systolic BP
of at least 140 mm Hg or a diastolic BP of at least 90 mm Hg.
During follow-up, 5365 women developed incident hypertension. In crude
models, the relative risks (RRs) and 95% confidence intervals (CIs) of developing
hypertension from the lowest (referent) to the highest levels of baseline
C-reactive protein were 1.00, 1.25 (95% CI, 1.14-1.40), 1.51 (95% CI, 1.35-1.68),
1.90 (95% CI, 1.72-2.11), and 2.50 (95% CI, 2.27-2.75) (linear trend P<.001). In fully adjusted models for coronary risk
factors, the RRs and 95% CIs were 1.00, 1.07 (95% CI, 0.95-1.20), 1.17 (95%
CI, 1.04-1.31), 1.30 (95% CI, 1.17-1.45), and 1.52 (95% CI, 1.36-1.69) (linear
trend P<.001). C-reactive protein was significantly
associated with an increased risk of developing hypertension in all prespecified
subgroups evaluated, including those with very low levels of baseline BP,
as well as those with no traditional coronary risk factors. Similar results
were found when treating C-reactive protein as a continuous variable and controlling
for baseline BP.
C-reactive protein levels are associated with future development of
hypertension, which suggests that hypertension is in part an inflammatory