GOALS OF ANTIHYPERTENSIVE THERAPY

Antihypertensive therapy has been used for almost 40 years to reduce b lood pressure and to prevent morbidity and mortality related to the hy pertensive state. Cardiovascular events are related to the initial ele vation of blood pressure; the benefits of treating malignant, severe o r moderate hypertension are well established. Although large scale cli nical trials have demonstrated a decrease in morbid events when mildly elevated blood pressures is treated, the benefits are neither univers al or dramatic and treatment is certainly less cost effective than no treatment. Recently it has been emphasised that the absolute risk of c ardiovascular events is determined only in part by blood pressure, and that it is also influenced by age, gender, race and the presence of o ther cardiovascular risk factors. For example, in older individuals wh ere the absolute risk of vascular complications is greater than in you nger individuals for any given level of blood pressure, the benefits o f therapy will be greater. It has been suggested that in younger indiv iduals with mild hypertension and a low absolute risk of developing ca rdiovascular morbid events it may be more appropriate to monitor the e ffects of drug therapy on measures of cardiac and vascular damage that are associated with the hypertensive state. Drug therapy has been sho wn to be extremely effective in reducing the incidence of stroke, cong estive cardiac failure and renal failure associated with elevated bloo d pressure. Meta-analysis of randomised large scale clinical trials in dicates that drug therapy may not reduce coronary events to the extent expected in patients with hypertension. One plausible explanation is that the trials have been of insufficient duration to detect the benef it of blood pressure lowering on coronary heart disease. It has also b een suggested that certain adverse metabolic effects associated with t he use of thiazide diuretics and beta-blockers employed in these trial s may have partially offset the benefits of blood pressure reduction. However, the clinical significance of these drug-induced metabolic dis turbances remains unclear. Experimental data suggesting differences in the ability of antihypertensive drugs to inhibit atherosclerosis in a nimal models are also of interest, but again the relation of the findi ngs to the clinical situation is unknown. Thiazide diuretics, beta-blo ckers, calcium antagonists, angiotensin-converting enzyme (ACE) inhibi tors and alpha-blockers can produce regression of left ventricular hyp ertrophy (LVH). While LVH is clearly a strong and independent predicto r for coronary disease, it remains to be shown that a lower risk for c oronary morbid events exists in patients whose LVH has undergone regre ssion over and above that attributable to blood pressure reduction. Th us, although ACE inhibitors, calcium antagonists and alpha-blockers ma y have some advantages for the prevention of cardiovascular disease pr ogression, until randomised trials show that they are more effective t han diuretics or beta-blockers in terms of preventing cardiovascular e vents, they should probably be considered as second-line treatment for patients with mild hypertension.