Exacerbation of atherosclerosis by hypertension. Potential mechanisms and clinical implications.

Recent experimental data suggest marked similarities between the effects of hypertension and hypercholesterolemia on the arterial intima. Both conditions also seem to exert proinflammatory effects on the artery, resulting in the recruitment of monocytes into the intima. These effects may be due to production of oxygen-free radicals, which in turn may stimulate genes involved in the recruitment of inflammatory cells into the arterial wall. Plaque rupture and acute myocardial infarction are related to local accumulation of inflammatory cells in vulnerable areas of the plaque. Recent clinical trials using cholesterol-lowering or antihypertensive therapies have shown a decrease in cardiovascular events that may have resulted from withdrawal of inflammatory effects on the arterial wall. Angiotensin-converting enzyme inhibitors decrease the rate of myocardial infarction in patients with overt congestive heart failure or left ventricular dysfunction. These drugs probably affect several mechanisms related to the inhibition of angiotensin production and the potentiation of bradykinin and resultant enhancement of nitric oxide and prostacyclin. The mechanisms could include reversing the proinflammatory effects of angiotensin and hypercholesterolemia on the arterial wall. Future therapeutic strategies of vascular protection in hypertension may include direct attacks on proinflammatory or pro-oxidant vascular mechanisms.