Analysis of Recent Papers in Hypertension
Jan Basile, MD, Senior Editor


  • Michael J. Bloch MD,

    1. From the Division of General Internal Medicine/Division of Cardiology, University of Nevada School of Medicine, Reno, NV;1the Risk Reduction Center, Saint Mary's Regional Medical Center, Reno, NV;2the Primary Care Service Line, Ralph H. Johnson VA Medical Center, Charleston, SC;3 and the Division of General Internal Medicine/Geriatrics, Medical University of South Carolina, Charleston, SC4
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  • and 1,2 Jan N. Basile MD 3,4

    1. From the Division of General Internal Medicine/Division of Cardiology, University of Nevada School of Medicine, Reno, NV;1the Risk Reduction Center, Saint Mary's Regional Medical Center, Reno, NV;2the Primary Care Service Line, Ralph H. Johnson VA Medical Center, Charleston, SC;3 and the Division of General Internal Medicine/Geriatrics, Medical University of South Carolina, Charleston, SC4
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Michael J. Bloch, MD, Risk Reduction Center, Saint Mary's Regional Medical Center, 645 North Arlington Street, Suite 460, Reno, NV 89503


Hypertension affects 65 million persons in the United States, or about 1 in every 4 adults. Over our lifetime, about 90% of Americans will develop hypertension. Because the risk of cardiovascular (CV) disease increases in a graded fashion beginning at a blood pressure (BP) of 115/75 mm Hg, well within what is considered the “normal” range, a new category of BP was defined in the most recent guidelines from the Seventh Report of the Joint National Committee for the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). Prehypertension is defined as a systolic BP of 120 to 139 mm Hg or a diastolic BP between 80 and 89 mm Hg. In addition to its being associated with an increased risk of CV events, prehypertension is associated with an increased risk of developing new-onset hypertension. Treating all individuals with prehypertension to prevent the development of hypertension (primordial prevention) would consume substantial medical and economic resources. The goal of the present retrospective observational analysis of the Framingham Offspring Study was to develop a simple risk score to predict the development of new-onset (incident) hypertension in the near term (4 years or fewer) in individuals without hypertension at baseline.

The Framingham Heart Study is a community-based, prospective, CV cohort study that began in 1948; it observed mainly white men and women every 2 years for risk factors that contributed to the development of CV disease. In 1971, researchers began enrolling 5124 children of the original cohort and their spouses into what is known as the Framingham Offspring Study. The records of this cohort were eligible for the present analysis if the participants attended at least 2 consecutive examinations between 1979 and 2001 and if both of their parents were in the original Framingham group. BP was measured at each examination. Participants had to be between the ages of 20 and 69 years and not have diabetes, known hypertension, or moderate to severe renal dysfunction (serum creatinine level >2.0 mg/dL).

After applying the inclusion and exclusion criteria, 1717 offspring participants remained eligible for the analysis. Incident hypertension was defined as systolic BP of at least 140 mm Hg, diastolic BP of at least 90 mm Hg, or use of antihypertensive medications. Independent predictors of incident hypertension were identified by entering available candidate risk factors (age, sex, body weight, body mass index [BMI], physical activity index, diabetes mellitus, systolic BP, diastolic BP, alcohol intake, smoking, and parental hypertension) into a stepwise regression model. A risk prediction index for incident hypertension was then determined using a statistical method called the Weibel regression model. Models for 1-, 2-, and 4-year rates of incident hypertension were calculated; however, the investigators focused on the 4-year rates as they believed they were most clinically relevant. Multiple statistical methods were employed to test the performance of the prediction model.

At baseline, the mean age of this cohort was 42.2 years; 54% were women, 35% were current smokers, and 94% had a history of hypertension in one or more parents. Mean baseline BP was 116/75 mm Hg, and mean baseline BMI was 25.1 kg/m2. Between 2 follow-up visits (at a median of 3.8 years), 796 patients (46.3%) developed incident hypertension. After multivariable analysis, age, sex, systolic and diastolic BP, BMI, parental hypertension, and cigarette smoking were significant predictors of hypertension. Based on these results, a risk prediction model was developed in which each level of these variables was assigned a point value in a manner similar to the well-known Framingham Risk Score for coronary heart disease risk. Using these factors, the researchers developed a risk calculator for new-onset hypertension (available at Based on the factors identified, an individual's 1-, 2-, and 4-year incident hypertension risk can be calculated. For example, as the authors point out, the 4-year risk of incident hypertension for a woman with a baseline BP value of 120/80 mm Hg and no other risk factors is 9%, compared with a 64% risk in a woman with a baseline BP value of 135/85 mm Hg who smokes, has a BMI >30 kg/m2, and a parental history of hypertension. Overall, according to the 4-year risk score, 34% of the cohort was at low risk (<5%), 19% were at moderate risk (5%–10%), and 47% were at higher risk (>10%) for incident hypertension. Finally, the investigators determined that the model had favorable discrimination and was well calibrated.

Using data from the Framingham Offspring cohort, the present simple, office-based hypertension risk prediction tool can be used to estimate an individual's 4-year risk of developing hypertension. It is hoped that this prediction tool will allow clinicians to more appropriately focus interventions, including intensified lifestyle modification and pharmacologic therapy, on individuals at higher risk for incident hypertension.—Parikh NI, Pencina MJ, Wang TJ. A risk score for predicting near-term incidence of hypertension: the Framingham Heart Study. Ann Intern Med. 2008;148(2):102–110.


The Framingham Heart Study has established that the risk of having a CV event increases continuously with increases in BP. With no absolute threshold for defining risk, the current definition of hypertension >140/90 mm Hg is considered to be somewhat arbitrary. By defining a new category of BP, prehypertension, the JNC 7 has focused our attention on the prevention of hypertension, often referred to as primordial prevention. For the approximately 70 million persons in the United States who have prehypertension, the JNC 7 recommends treatment with lifestyle modification alone. At least in the short term, lifestyle interventions, including the Dietary Approach to Stop Hypertension (DASH) eating plan, weight loss, sodium restriction, moderation of alcohol, and physical activity have all been shown to decrease BP or the development of hypertension in these individuals. Since the publication of the JNC 7, one study of pharmacologic treatment of prehypertension has also demonstrated a decrease in the incidence of new-onset hypertension. In the Trial of Preventing Hypertension (TROPHY), patients with baseline systolic BP levels of 130 to 139 mm Hg or diastolic BP levels of 85 to 89 mm Hg were randomized to treatment with the angiotensin receptor blocker candesartan or placebo. After completion of active study medication at 2 years, randomization to candesartan was associated with a 27% absolute risk reduction in incident hypertension. Of interest, the reduction in incident hypertension persisted long after the discontinuation of study medication; there was still a 10% risk reduction that persisted during the final 2 years of the study while all participants continued to receive placebo. Some questions remain about the definition of hypertension in this study. While delaying the onset of incident hypertension in those with prehypertension (primordial prevention) would appear to be beneficial, as there is a direct log-linear relationship between BP and the risk of subsequent CV events, no clinical trial has yet demonstrated that intervening with either life-style modification or antihypertensive medication in people with prehypertension reduces rates of CV events. Given the low short-term CV risk of many individuals with prehypertension, it has been suggested that a strategy of watchful waiting would still allow ample time to offer treatment of BP before any excess CV morbidity and mortality develops.

There remain 2 primary concerns for prehypertensive individuals: the risk of future CV events and the risk of developing incident hypertension. We now have 2 risk calculators from the Framingham investigators, both of which are simple, easy to use, and clinically relevant to estimate the near-term risk of both of these end points. Physicians should familiarize themselves with this new, simple-to-use office-based tool that may better identify individuals with prehypertension who are more likely to develop hypertension in the next 4 years. That said, it is imperative that this tool is validated in an independent cohort, outside of the mostly white 20- to 69-year-old population which was studied.

One other question remains: Do we really need a “risk calculator” or is clinical judgment adequate? Shouldn't it be obvious that an obese, smoker, an older person, or a person with a strong family history of hypertension is more likely to develop hypertension than a person without these characteristics?