Relevance of 24 H blood pressure profile and sympathetic activity for outcome on short- versus long-acting 1,4-dihydropyridines.

Short-acting formulations of nifedipine-like 1,4-dihydropyridines cause clearly less regression of left ventricular hypertrophy (LVH) than anticipated from their antihypertensive effect. Moreover, these compounds increase the risk of cardiac death and myocardial reinfarction in patients with coronary artery disease (CAD) not on concomitant beta-blocker therapy. Increased sympathetic activity is one of the non-pressure-related risk factors for LVH and atherosclerosis in hypertensives. In addition, increased sympathetic tone may precipitate clinical events in subclinical or stable CAD. Intermittent increases in sympathetic activity persist during chronic treatment with those 1,4-dihydropyridines that have a poor peak/trough ratio with a rapid fall of BP and deactivation of the arterial baroreflex. On the other hand, these intermittent increases in sympathetic activity do not occur for formulations and compounds with a gradual and sustained antihypertensive effect over the dosing interval. Such long-acting 1,4-dihydropyridines cause regression of LVH as anticipated from their antihypertensive effect, and are similar to angiotensin converting enzyme inhibitors. In contrast to short-acting 1,4-dihydropyridines, long-acting 1,4-dihydropyridines appear not to be detrimental for patients with stable CAD. However, the evidence is still missing for patients with unstable CAD. Neither is there evidence that they will reduce cardiovascular morbidity and mortality in patients with CAD when used for the chronic treatment of hypertension.