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Metabolic effects of antihypertensive treatment: long live the debate.

Thiazide diuretics and -adrenergic blockers, alone or in combination, have long been suspected of having an unfavourable metabolic impact: deterioration of glucose tolerance and insulin sensitivity, worsening of the serum lipid profile and potassium depletion are the chief imputations [1]. By contrast, in many clinical trials [2–6], these drugs improved the cardiovascular outcome of hypertensive patients, although it has been noted that the cardiac protection they offered was less than what could be expected on the basis of the known epidemiology [7]. Both thiazide diuretics and -adrenergic blockers are efficacious, safe and cheap. More recently developed antihypertensive agents, such as calcium-channel blockers, angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin II receptor blockers (ARB), generally have a better metabolic profile than thiazide diuretics or -adrenergic blockers: essentially neutral or even beneficial depending on the evidence one favours [8–15]. These newer drugs, which are proving their non-inferiority to the older ones in outcomes trials [2–6,13], are efficacious and safe, but expensive. The question then arises: should the new kids on the block replace the old cronies as first choice in the pharmacological treatment of hypertension? A clear-cut answer, free of the opposing pressures of budget and marketing, depends on several subordinate questions: (i) Is the untoward metabolic profile of thiazide diuretics and -adrenergic blockers conclusively proven? (ii) What is the size of these undesirable effects? (iii) What is their clinical relevance in which category of patients? (iv) How compelling are the cost considerations? (v) Can a general recommendation be made?