Obvious, but often forgotten, is the premise that blood pressure reduction in the patient with hypertension is a surrogate for our real goal, which is reduction in the risks consequent to hypertension. This surrogate, a convenience for regulatory agencies, has therapeutic implications. As the array of antihypertensive agents available has grown, along with information from clinical trials and insights into underlying mechanisms, it has become reasonable to examine that premise. The overall success of antihypertensive therapy has been undeniable, but has not influenced the advance of atherosclerosis, primarily coronary events. Multiple observations suggest that metabolic disarray consequent to the use of antihypertensive agents, especially thiazides and β-blockers, may have contributed to this scenario. Electrolyte abnormalities predispose to malignant arrhythmias and sudden death during myocardial infarction. Left ventricular hypertrophy, a major risk factor for coronary events, arrhythmias, and heart failure, responds selectively to antihypertensive agents. Similarly, the progression of renal injury in the hypertensive patient may be sensitive to the agents employed. Obesity and hypertension coexist frequently. moreover, evidence is growing that atherogenic abnormalities common in the obese patient, such as insulin resistance, not only occur frequently in the nonobese patient. but are also sensitive to the antihypertensive agent selected. Although predictions are risky, it seems safe to predict that the next chapter in antihypertensive therapy will examine whether we need to go beyond blood pressure reduction in selecting such therapy.
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