Hematocrit Predicts Long-Term Mortality in a Nonlinear and Sex-Specific Manner in Hypertensive Adults
Hematocrit has been inconsistently reported to be a risk marker of cardiovascular morbidity and mortality. The Glasgow Blood Pressure Clinic Study cohort included 10951 hypertensive patients, who had hematocrit measured at their initial clinic visit and followed for ≤35 years. Cox proportional hazards models were used to estimate hazard ratios for all-cause, cardiovascular, ischemic heart disease, stroke, and noncardiovascular mortality. There were 3484 deaths over a follow-up period of 173245 person-years. Hematocrit was higher in men (median, 0.44; interquartile range, 0.42–0.47) than in women (median, 0.41; interquartile range, 0.38–0.43). The lowest risk for all-cause mortality was seen in quartile 2 for men (range, 0.421–0.440) and women (range, 0.381–0.400). Compared with quartile 2, the adjusted hazard ratios for quartiles 1, 3, and 4 were, respectively, 1.11 (range, 0.97–1.28), 1.19 (range, 1.04–1.37), and 1.22 (range, 1.06–1.39) in men and 1.17 (range, 1.01–1.36), 0.97 (range, 0.83–1.13), and 1.19 (range, 1.04–1.37) in women. Men showed a J-shaped pattern for cardiovascular mortality and a linear pattern for noncardiovascular mortality in cause-specific analysis, whereas in women a U-shaped pattern was observed for noncardiovascular mortality only. Higher baseline hematocrit was associated with higher on-treatment blood pressure during follow-up. Baseline hematocrit did not affect the time to reach target blood pressure. The increased risk of death attributed to higher hematocrit was seen in men and women irrespective of their achievement of target blood pressure, indicating that the risk is independent of the effect of hematocrit on blood pressure. Hypertensive patients with hematocrit levels outside of the sex-specific reference ranges identified in this study should be targeted for more aggressive blood pressure and cardiovascular risk reduction treatment.
- Received January 17, 2012.
- Revision received February 6, 2012.
- Accepted June 16, 2012.
- © 2012 American Heart Association, Inc.