Antihypertensive Drugs and Lipid Profiles

The large clinical trials of the treatment of hypertension, in which diuretics were used as initial drug therapy, have demonstrated a major reduction in stroke hut little benefit in the incidence of coronary heart disease. The limited effect of treatment on coronary disease is surprising given the strong risk factor relationship to pre-existing hypertension. This may mean that the risk factor relationship is not a causal one. Alternatively, the drug therapy may have subtle toxicity that in the long term offsets the benefit of lowering blood pressure. This review explores the latter possibility by reviewing the evidence that the antihypertensive drugs used preferentially heretofore have adverse effects on the lipid profile. Diuretics increase triglycerides (average of 30%), total cholesterol (average of 6-8%), and LDL or VLDL cholesterol β-1 selective and nonselective β-blockers increase triglycerides (average of 30%) and lower HDL cholesterol (average of 5-15%). Whereas the adverse modifications of the lipid profile appear small and inconsequential, the increase in total cholesterol during diuretic therapy is of the same magnitude as observed in the Lipid Research Clinic trial (although opposite in direction) that significantly affected coronary events. The persistence of the lipid changes during long-term treatment is unresolved due to fragmentary and poorly controlled observations. Nevertheless, considerable data suggest that it continues during extended therapy. Selective α-1 adrenoceptor blocking drugs and perhaps calcium antagonists and β-blockers with intrinsic sympathomimetic activity have a favorable influence on the lipid profile. Drugs with a favorable effect on both blood pressure and lipids hold promise of much greater gains against coronary disease. However, it remains unproved whether the newer agents provide the same large protection against stroke as diuretic-based regimens. Hence, additional large trials will be needed to prove whether the newer agents fulfill their promise against coronary disease and at the same time hold the line against stroke and congestive heart failure. Am J Hypertens 1988;1:421-427