Rigidity of large arteries and cardiovascular risk. Epidemiological considerations and genetic determinants.

Most of the morbid events due to hypertension and other risk factors an rel ated to alterations of the large arteries of the brain, the heart or the ki dney. Historically large arteries have been considered as passive conduits of blood, and physicians, surgeons and pathologists were mainly interested on their anatomical lesions such as rupture, stenosis, aneurysm, or thrombo sis. However we know that large arteries are not passive conduit tubes but are characterized by elastic properties and are able to synthesize many vas oactive substances. These properties make the arterial wall a major modulat or of the blood pressure and more generally of the cardiovascular regulatio n. Aging, environmental and genetic factors are responsible for structural and functional changes of the arterial wall media (hypertrophy, extracellul ar matrix accumulation, calcium deposits) and of the vascular endothelium ( decrease in the release of vasodilators and increased synthesis of vasocons trictors), all that leading to a diminution of elasticity and increased sti ffness. The alteration of large arteries elasticity has deleterious effects on the heart upstream being responsible for an inadequate increase in syst olic pressure and a relative decrease in aortic diastolic pressure at any g iven value of mean arterial pressure. The elevation in systolic pressure ca uses a disproportonate increase in end-systolic stress, which is the princi pal hemodynamic factor which promotes the development of cardiac hypertroph y, increased ventricular oxygen consumption, and left ventricular hypertrop hy and can compromise capacity for coronary perfusion. Clinical and epidemi ological studies have raised the possibility that subjects with stiffer art eries have wide pulse pressure, and that stiffening of large arteries is as sociated with excess morbidity and mortality independently of mean blood pr essure. In addition to its etiologic role in cardiovascular disease, increa sed arterial stiffness may serve as an early marker for the diagnosis of as ymptomatic atherosclerotic lesions, or for the evaluation of the severity o f these lesions. In this review we report data from clinical, epidemiologic al and genetic studies, suggesting that arterial stiffness may be considere d as a significant marker and/or an independent cardiovascular risk factor. This new concept should lead physicians to evaluate arterial stiffness for the prognosis and treatment of cardiovascular patients.