Messerli F H
Clinical Hypertension Laboratory, Ochsner Clinic, New Orleans, Louisiana 70121.
Am J Med. 1991 May 17;90(5A):27S-31S. doi: 10.1016/0002-9343(91)90482-d.
Left ventricular hypertrophy (LVH) of the concentric type is the classic cardiac adaptation to sustained arterial hypertension. Data from the Framingham cohort have shown that patients with LVH have a severalfold higher risk of sudden death, acute myocardial infarction, and other cardiovascular morbidity than those with normal hearts. Common sequelae of LVH are ventricular ectopy, impaired ventricular contractility, myocardial ischemia, and decreased left ventricular filling. The benefits of antihypertensive therapy should not be limited to lowering arterial pressure, but should extend to preventing or reducing target organ damage. A variety of antihypertensive agents, such as calcium channel blockers, angiotensin-converting enzyme inhibitors, antiadrenergic drugs, and, to a lesser extent, beta blockers, have been shown to reduce LVH and to improve left ventricular filling. We have shown that calcium channel blockers diminish ventricular ectopy in parallel with the reduction of LVH, whereas antihypertensive therapy with diuretics neither reduced LVH nor suppressed ventricular ectopy, although it lowered arterial pressure to a similar extent. Whether or not these cardiac changes with antihypertensive therapies will improve cardiovascular morbidity and mortality in patients with LVH remains to be documented.
