BALTIMORE, March 24 -- Men whose parents have hypertension are at an increased risk for developing high blood pressure themselves, a longitudinal cohort study showed.
If both of their parents had high blood pressure, participants were 2.4-fold more likely to become hypertensive than men whose parents had normal blood pressure (adjusted HR 2.4, 95% CI 1.8 to 3.2), Nae-Yuh Wang, Ph.D., of Johns Hopkins, and colleagues reported in the March 24 issue of Archives of Internal Medicine.
Action Points
- Explain to interested patients that this study found that a parental history of hypertension is a risk factor for high blood pressure.
- Note that these results are only generalizable to white men with high socioeconomic status.
- Point out that this study cannot determine causality and also cannot rule out possible environmental confounding factors.
When broken down further, if only a man's mother had hypertension, the hazard ratio of developing it himself was 1.5 (95% CI 1.2 to 2.0). If only the father had hypertension, the HR was 1.8 (95% CI 1.4 to 2.4).
If both parents developed hypertension at age 55 or younger, men were 6.2-fold more likely to become hypertensive (adjusted HR 6.2, 95% CI 3.6 to 10.7) at some point in their lives and 20-fold more likely to have developed the condition by age 35 (adjusted HR 20.0, 95% CI 8.4 to 47.9).
"Our findings emphasize the importance of asking patients about parental hypertension to identify those who are at high risk of developing hypertension, especially at a young age, for both population-based and individual-level interventions," the researchers said.
"The [findings] also underscore the importance of primary prevention and [blood pressure] monitoring early in life in men with parental hypertension, especially those who have a parent with early-onset hypertension," they said.
Hypertension is known to run in families, noted the researchers, with genetics and environmental factors sharing the blame.
But the effect of paternal versus maternal hypertension and the long-term association of parental hypertension with lifetime risk in their offspring have not been well studied, they said.
So they turned to the Johns Hopkins Precursors Study, a long-term, longitudinal cohort study whose participants are former medical students from the university's classes of 1948 through 1964.
Only data from 1,160 white male participants were used in this study because of the low numbers in other demographic groups.
At time of enrollment, all participants completed questionnaires about medical history and parental hypertension and underwent physical exams.
Follow-up is ongoing, but for this study the cutoff for data was Dec. 31, 2001; median follow-up was 37 years from graduation.
Participants who reported having at least one parent with hypertension had significantly higher mean systolic (P=0.01) and diastolic (P<0.001) blood pressure levels at baseline than those without a parental history, and the relationship persisted throughout follow-up.
At age 35, mean systolic blood pressure was 1.9 mm Hg higher for men who had only a mother who was hypertensive (95% CI 0.8 to 2.9) compared with participants who had no parental history of high blood pressure. Corresponding numbers were 1.6 mm Hg higher (95% CI 0.4 to 2.8) and 3.2 mm Hg higher (95% CI 1.8 to 4.5) for men with only a hypertensive father, and hypertension in both parents, respectively.
Mean diastolic blood pressure was 0.9 mm Hg higher (95% CI 0.8 to 2.9), 0.6 mm Hg higher (95% CI -0.2 to 1.4), and 2.4 mm Hg higher (95% CI 1.5 to 3.2), respectively.
By the end of follow-up, 448 men had developed hypertension at a median age of 57.
The cumulative incidence of hypertension by age 40 was four times greater in men whose parents had hypertension than in those whose parents did not.
As strengths of the study, the authors listed the repeated assessments of incident parental hypertension, the high response rates at baseline and during follow-up, the repeated measures of blood pressure and possible confounders, and the fact that the participants are physicians and their self-reports have been validated.
Possible limitations included the homogeneity of the cohort, the lack of information on dietary factors that may influence hypertension, and potential residual confounding.
| The study was supported in part by NIH grants. The authors did not report any financial disclosures. |
Primary Source
Archives of Internal Medicine
Wang N-Y, et al Arch Intern Med 2008; 168: 643-648.