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Over the past decade, increased aortic stiffness has emerged as an important risk factor for target organ damage and cardiovascular disease events. Aortic stiffness can be assessed as pulse wave velocity (PWV), which is a measure of aortic wall stiffness, and pulse pressure (PP), which is affected by wall stiffness and the interaction between flow and diameter. Because these stiffness measures have different sensitivities to geometry and other factors, they are only moderately correlated and play a complementary role in risk prediction. Arterial stiffness has long been viewed as a complication of hypertension that integrates long-term adverse effects of elevated blood pressure and other risk factors. However, PWV is only modestly correlated with risk factors other than age and blood pressure, which likely explains the ability of PWV to add to standard risk prediction models and reclassify risk in a clinically relevant manner. Recent studies have demonstrated that stiffness can antedate and contribute to the pathogenesis of hypertension, raising the possibility that early assessment of arterial stiffness may provide insight into complications including hypertension that develop years later. The role that stiffness plays in the pathogenesis of hypertension and cardiovascular disease has sparked considerable interest in defining basic mechanisms that stiffen the aortic wall, increase PP and contribute to target organ damage with a hope that elucidation of these mechanisms will allow for development of more effective treatments.
Gary F. Mitchell (Tue,) studied this question.
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