Arteriosclerosis/Large Artery Disease

Abstract

“Arteriosclerosis” is an entirely different condition to atherosclerosis, as emphasised by William Osler in his “Principles and Practice of Medicine” over 100 years ago. At that time, atherosclerosis was called nodular arteriosclerosis, and arteriosclerosis, as we now know it, was called senile arteriosclerosis. Arteriosclerosis is caused by fatigue and fracture of elastin laminae in the proximal aorta. The proximal thoracic aorta is principally involved because it expands more with each beat of the heart than any other systemic artery. Fracture of elastin lamellae is associated with stretching of the wall and dilation of the aorta. Stiffening is due to transfer of stresses to collagenous elements in the aortic wall. While physical damage to elastin lamellae is the primary cause of damage, secondary inflammatory and chemical changes occur in the aorta, associated with an attempt at repair. Ill-effects on the heart are attributable to increased load and compromised coronary flow as a consequence of increased characteristic impedance (Zc) with rise in systolic pressure and early wave reflection caused by concomitant increase in aortic pulse wave velocity (PWV). Numerically, PWV in cm/s and Zc are virtually identical, differing only with blood density which is almost unity (1.05). Arteriosclerosis leads indirectly to cerebral and renal microvascular damage with dementia and renal failure. Conventional blood pressure recordings underestimate the ill-effects of arteriosclerosis. With modern techniques, intelligently used, arteriosclerosis can be viewed as quantitatively the most extreme effect of the aging process as seen anywhere in the body. Prevention and future treatment will entail reduction of wave reflection from the body’s periphery with drugs together with surgical and other techniques for decreasing aortic stiffness.