Echocardiography in clinical pharmacology: developing new concepts on the pathophysiology of left ventricular hypertrophy in arterial hypertension.

By using echocardiography it is possible to quantify accurately and repeatedly the degree of left ventricular hypertrophy (LVH) in patients with arterial hypertension. It therefore appears to be a valuable tool for investigating the mechanisms that may be involved in the pathogenesis of this condition in hypertensive patients. The role of increased afterload in LVH induction is well established, and results of several independent laboratories concord in indicating blood pressure as a major independent factor in the pathogenesis of LVH in hypertensive patients. The role of factors other than blood pressure has not yet been fully established, however, in this setting. Animal and human studies from different laboratories are providing conflicting results on the possible role of factors such as the catecholamines or the renin-angiotensin system as additional stimuli facilitating LVH development. Clinical pharmacology could be a useful tool in seeking to clarify this important question. Drugs that lower blood pressure without consistently affecting the humoral factors possibly responsible for LVH might be expected to induce a lesser degree of LVH reversal than drugs that lower blood pressure while at the same time reducing or inhibiting the factors responsible for LVH. This experimental approach raises several methodological and technical points which are crucial in the trial planning stages. The question whether borderline hypertensive patients should be considered separately from stable hypertensive patients in the search for relationships between LVH and possible pathogenic factors is also discussed.