Arterial Stiffness, Vascular Aging, and Intracranial Large Artery Disease

Vascular aging is described as a gradual process involving biochemical, enzymatic, and cellular changes of the vasculature and modification of the signals that modulate them.1,2 In susceptible individuals this process appears to be accelerated, leading ultimately to several features that collectively comprise a condition characterized as early vascular aging. Increased arterial stiffness, increased intima-media thickness, dilation of central elastic arteries, and impaired endothelial function are dominant aspects of this premature process. Aging represents a major determinant of arterial stiffness. Histological studies have shown extensive impairment to the medial elastin fiber network on central elastic arteries, such as the proximal aorta and the carotid artery, while subtle aging alterations have been found in distal muscular arteries because of impaired distensibility.3 Several years ago, we found that the intima-media thickness of carotid arteries was significantly correlated with coronary artery lesions.4 Atherosclerosis is considered to be a generalized disease of the vascular system; if it is detected in any one artery, it is possibly present in one or more other sites of the arterial tree. There is a linear relationship between coronary artery disease and diseases of peripheral, carotid, and intracranial arteries. From the results of the study to which our response refers, Zhang et al.5 reported that intracranial large artery disease was positively associated with arterial stiffness in patients with hypertension, thereby suggesting an association between atherosclerosis (stenosis, calcification) of brain arteries and arteriosclerosis of large arteries. In their study, the patients with intracranial artery disease were also significantly older, with isolated instances of office-recorded and ambulatory systolic hypertension and consequent increase in pulse pressure (PP). As elastic arteries become stiffer, they lose their ability to absorb the energy released by ventricular ejection, resulting in a recoil effect. Systolic blood pressure increases as the waves reflected by the recoil in the peripheral arteries arrive at the central arteries earlier than normal, whereas diastolic blood pressure falls, resulting in increased central PP. As a consequence, left ventricular afterload increases, forcing the heart to generate higher end-systolic pressures to sustain the constancy of blood flow in the stiffened arteries. The rise in central PP may be the cause for the modification of the arterial wall, including elastin degeneration and collagen deposition that occurs order to reduce increased cyclical vascular shear stress. The brain may be more susceptible to variations in pressure transmitted by larger arteries, resulting in earlier vascular remodeling and predisposition to cognitive decline and stroke. Nevertheless, it is important to evaluate the predictive significance of arterial stiffness for future cardiovascular events, and a prospective study could provide such pointers that could signal the likelihood of future events in a patient, such as stroke or other brain vascular events such as those associated with dementia. It has been demonstrated that aortic stiffness and central aortic pulse pressure are important independent predictors of cardiovascular events. Indeed, given the correlation between the identified cardiovascular risk factors and vascular aging, aortic stiffness may represent the true burden on the arterial wall, whereas the levels of blood pressure, glucose, and lipids may not, because they vary from period to period. Therefore the measurement of arterial stiffness can quantify the arterial impairment and identify patients who are at a higher level of cardiovascular risk. The authors declared no conflict of interest.