Aortic Elasticity Evaluation: Ongoing Assertion of M-Mode Measurements.

Abstract

A therosclerosis, a chronic inflammatory disease, is a leading cause of cardiovascular diseases (CVDs) and requires early detection for effective prevention. 1 Arterial stiffness, characterized by the imbalance of elastin and collagen content in the vessel wall, is an early indicator of atherosclerosis. 2 While arterial stiffness is a useful measure for the prediction of stiffness level of all arteries, the concept of aortic stiffness is frequently used in the clinical assessment of it. In clinical practice, it is an important issue to understand the relationship between aortic stiffness and cardiovascular risk factors. Possible mechanisms linking aortic stiffness and atherosclerosis include common risk factors, mechanical stress on arterial walls, altestress, modynamics, vascular remodeling, and impaired endothelial repair mechanisms. 2 Hypertension, diabetes, dyslipidemia and smoking, which are risk factors for aortic stiffness and atherosclerosis, induce both conditions and lead to endothelial dysfunction, oxidative stress and chronic inflammation. As aortic stiffness increases, it exerts mechanical pressure on the endothelium, impairs its function, increases inflammation and causes plaque formation. 3 Altered hemodynamics due to aortic stiffness raises blood pressure and pulse wave velocity, thereby accelerating atherosclerotic processes in smaller vessels. 4 Arterial stiffness also induces vascular remodeling, stimulating smooth muscle cell proliferation, collagen deposition, and structural changes that promotes plaque formation and aortic stiffness. 2,5 Moreover, aortic stiffness affects endothelial progenitor cells by reducing their mobilization and impairing repair capacity. 6 Knowing these mechanisms focus on the importance of considering aortic stiffness as a modifiable