There is sufficient evidence to demonstrate that lowering BP to less than 140/90 mm Hg offers cardiovascular and renal protection.

In addition, clinical trials have demonstrated that a BP goal of less than 130/80 is preferable in individuals with diabetes mellitus or CKD. While these goal BP levels offer a general threshold to direct antihypertensive therapy, whether more intense BP lowering offers additional benefit remains undecided. To date, most clinical trials in hypertension have not been designed to evaluate the effect of intensive BP lowering.

A 2003 meta-analysis provides the best evidence thus far for a threshold BP above which the risk of cardiovascular mortality increases (Lancet. 2002;360:1903–1913). This meta-analysis included 61 prospective observational studies of BP and mortality and involved 1 million adults without documented vascular disease at baseline. Results indicated that increased risk for cardiovascular mortality begins at BP above 115/75.

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Based on these data, the authors of The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) created a new category called “prehypertension,” which included individuals with BP levels in the range of 120-139/80-89.

Researchers debate whether raw BP readings alone should be used to classify patients into various stages of hypertension or if such classification should involve a more comprehensive evaluation that includes risk factors as well as baseline BP assessment.

The latter approach is evidence-based and readily acceptable for individuals with comorbid cardiovascular and renal disease, in whom intense BP control has been shown to be beneficial. The value of applying a similar approach to healthy individuals who present with BP in the prehypertension range, however, is less clear and subject to debate.

Current European guidelines on hypertension attempt to address this undecided clinical question by stratifying individuals based on both known risk factors and early markers of subclinical target-organ damage. The data are limited, and no large outcome studies have investigated the presence of these markers and an increase in cardiovascular or renal events in healthy individuals. Modifying these early risk factors may improve cardiovascular and renal outcomes, but there is no evidence to verify this.

The concept of prehypertension was based on the lifetime risk of hypertension and an increased risk for cardiovascular complications associated with BP levels previously considered to be normal. The data were derived from the general population, which included individuals who were at higher risk due to comorbid conditions. The time has come to clearly define the role of BP elevation in the prehypertension range as it affects healthy individuals.

In a study presented at the American Heart Association 2008 Scientific Sessions, we evaluated a relatively healthy group of individuals with BP less than 140/90. In this study, we evaluated cardiovascular and renal risk parameters after stratifying patients into two groups based on a systolic BP (SBP) of 115 mm Hg.

Although all parameters were within normal range for both groups, the group with SBP greater than 115 had significantly higher BMI, worse lipid panel parameters, higher C-reactive protein levels, elevated renal hemodynamic parameters, and higher blood glucose levels both in a fasting state and at all stages of the oral glucose tolerance test.

These results demonstrate that cardiovascular and metabolic disarray begins much earlier in healthy individuals than previously thought and that SBP may be a useful surrogate marker. Conclusions drawn from these data may help guide management of healthy individuals with BP in the prehypertension range.

The prehypertension state probably begins at an SBP of 115 instead of the currently recognized threshold of 120. Nonpharmacologic, multipronged interventions based on healthy diet and exercise may be more effective in prevention of this subclinical metabolic disarray and progressive target-organ damage than treatment of elevated BP with antihypertensive therapy alone. Large, prospective clinical trials are needed.