University of California, Davis, conference: Mild hypertension

Prevalence of "higher than normal" blood pressures in a community is inversely related to the magnitude of the elevation; the milder grades of elevation are far more prevalent. A multifactorially inherited tendency to develop hypertension is modulated by multiple environmental influences. Autonomic nervous and behavioral factors plausibly appear to contribute to the initiating mechanisms of hypertension; the associated hemodynamic changes and the resulting cardiovascular structural changes interact to perpetuate the process. The complex interaction of hypertension and atherosclerosis is further complicated by direct as well as secondary effects of antihypertensive drugs on atherogenesis. Attributable cardiovascular risk is generally proportional to the degree of hypertension across the entire range of elevated blood pressure; this kind of relationship holds also for normal versus subnormal blood pressure values. Pharmacologic lowering of blood pressure, however, does not confer proportional benefit. Thus, such lowering of blood pressure to normotensive levels does not reduce the risk level to that in the normotensive population. Therapeutic outcome is influenced by the interaction of blood pressure lowering, type of antihypertensive agents used, existing risk factors, and target organ damage. Benefits of lowering blood pressure in established mild hypertension (diastolic blood pressure greater than 95 mm Hg) are confirmed. Drug treatment of patients with lower diastolic blood pressure or with isolated elevations of systolic blood pressures continues to be controversial as does the choice of initial therapeutic agent(s). The large-scale experience of clinical trials encompassing the long-term risks and benefits of the drug treatment of mild hypertension is limited to the use of diuretics and adrenergic beta blockers. A variety of new and promising therapeutic agents for use as alternate choices for initial therapy needs to undergo comparative evaluation.