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Malaysian Family Physician, a peer-reviewed open-access journal of family practice
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REVIEW ARTICLE
PREHYPERTENSION: WHAT IS THE CURRENT STATUS?
EXCESS CVD RISK ASSOCIATED WITH PREHYPERTENSION
It is well known that the risk of CVD events rises with rises in BP and this risk is a continuum.14 Consequently, those with prehypertension has twice the risk of someone with a SBP of 115 mmHg of getting coronary heart disease or stroke.15 In fact there is a 27% increase in all cause mortality and a 66% increase in CVD mortality in prehypertensives compared to normotensive individuals. Thirty-two percent of BP related deaths occur in those with SBP of 110-139 mmHg.10
Although the absolute CVD events associated with prehypertension is relatively low, the morbidity, mortality and health care costs attributable to prehypertension is substantial because of the large number of prehypertensives involved. In a simulation of the NHANES I cohort with a follow-up of >20 years, it was estimated that 3.4% of hospitalizations, 6.5% of nursing home stays and 9.1% of deaths could be attributed to prehypertension.16
This excess CVD risk in prehypertension is due to subclinical atherosclerosis. Prehypertensives have
- increased coronary atherosclerosis17
- increased carotid and brachial intima-media thickness, a surrogate for atherosclerosis18
- elevated C-reactive proteins (CRP)19,20
- elevated tumour necrosis factor-α (TNF-α)20
- elevated serum homocysteine levels20
- elevated oxidized LDLcholesterol18
- microalbuminuria which is more common in prehypertension than normotension21
- presence of other inflammatory markers like interleukin6,19,20
Management of prehypertension
Obviously because of all the reasons above, the aim of management of prehypertension would be to
- lower BP to within normal range
- prevent a rise in BP with age
- prevent BP related CVD events
Unfortunately to date, the impact of treatment of prehypertension on outcome is still unknown. However what is known is that in the treatment of hypertension, reduction of BP is associated with reductions in CVD events. There is abundant evidence that life-style changes22 like dietary modification,23 weight loss,24-28 reduction in sodium intake,24,27-29 regular physical activity30-33 and limiting alcohol intake34,35 can reduce BP (Table 2). While the BP lowering effect of each individual life-style change is modest, when taken together the benefit can be substantial. Furthermore it is also relatively free of much added costs and adverse events. Life-style changes not only benefit those with prehypertension but it will also benefit those with diabetes mellitus, dyslipidemia, the metabolic syndrome, overweight/obesity and other cardiovascular disease or risk.
Table 2. Lifestyle modifications to prevent and manage hypertension1| Modification | Recommendation | ~ SBP reduction |
| Weight reduction | Aim for BMI 18.5-25 kg/m2 | 5-20 mmHg/10 kg wt loss |
| Sodium intake | < 100 mmol Na/ 6 g NaCl (1 ¼ tsp salt) | 2-8 mmHg |
| Physical exercise | Aerobic activity e.g. brisk walking 30-60 mins, minimum 3x/ wk | 4-9 mmHg |
| DASH Diet | Rich in fruit, vegetable and low-fat diary products | 8-14 mmHg |
| Alcohol | 2 units/day in men, 1 unit/day in women | 2-4 mmHg |
DASH, Dietary Approaches to Stop Hypertension; SBP, systolic blood pressure
Note: For overall cardiovascular risk reduction, stop smoking. The effects of implementing these lifestyle modifications are dose- and time-dependent, and could be greater for some individuals
IS THERE A ROLE FOR PHARMACOLOGICAL TREATMENT OF PREHYPERTENSION?
There is again abundant evidence for the use of pharmacological agents in those with diabetes mellitus and chronic kidney disease and prehypertensive range of BP especially if it is ≥130/80 mm Hg.1,36,37 For those with other established CVD like stroke,38 coronary heart disease (CHD), there is also evidence that pharmacological treatment is beneficial.39
Whether treating prehypertension with pharmacological agents can prevent hypertension has been looked at in one study.12 The use of an angiotensin receptor blocker, candesartan did reduce the risk of developing hypertension compared to placebo but this reduction was very minimal once the drug was withdrawn.12 One can surmise that pharmacological agents can delay the progression of prehypertension to hypertension but it did not alter or prevent the progression into hypertension.
The greater difficulty is whether prehypertension should be treated as primary prevention of CVD events in circumstances other than those above. Because there are no outcome studies of pharmacological treatment of prehypertension, one approach would be to do a global cardiovascular risk assessment using for example the Framingham Heart Study multivariate risk algorithm. If the risk is medium (10-20% 10-year risk) or high (> 20% 10-year risk) then pharmacological treatment in addition to life-style changes should be considered.4,5
