Age-Related Changes Affecting Atherosclerotic Risk

Abstract

The incidence of cardiovascular diseases that are related to the atherosclerotic process increases exponentially with age. Organ lesions, the clinical manifestation of atherosclerotic disease, are late events due to complications in the plaque (ulceration, thrombosis, calcification) which are the result of an increased vulnerability to disruption of a previously stable plaque. The higher incidence of age-related clinical events could be explained by a rising sensitivity of plaques to destabilising factors, both parietal and humoral. The increased probability that a plaque in an elderly patient will became vulnerable could be related to those destabilising factors that significantly increase with aging, such as advanced glycation end-products. For these reasons, it seems most important that the analysis of these age-related destabilising factors, rather than those factors that promote the development of early atherosclerotic plaques, should be undertaken. Taking the point of view of a pharmacological intervention, this should eventually lead to a more complete understanding of this process.

Carotid Intima Media Thickness Is Independently Associated with Male Gender, Middle Age, and IGF-1 in Metabolically Healthy Obese Individuals

“…Aging induces intrinsic changes in the arterial wall including progressive increase in intimal thickness [32], and this constant increase in IMT over age is an effect present in both male and female [33]. …”

Molecular Pathways Regulating Macrovascular Pathology and Vascular Smooth Muscle Cells Phenotype in Type 2 Diabetes

“…Diabetes-induced vascular alterations share same aspects with age-related macroangiopathy, and both represent a risk factor for atherosclerosis [ 49 , 51 ]. Aging potentiates other atherogenic risk factors, including diabetes [ 52 ] and VSMCs, also drive the age-related vascular changes [ 53 ]. The age-related diffuse intimal thickening in great vessels the principal site for the progression of atherosclerotic lesions [ 49 , 51 ].…”

Serum Pentosidine Level in Healthy Ageing and Its Association with Age-Related Disease

“…The injuries between the extracellular matrix (ECM) and cells are stimulated by AGEs in three interesting ways. (1) Accretion of AGEs creates a cross-linking between extracellular matrix and AGEs, and this causes a decrease in elasticity of connective tissue and affects vascular function [9]. (2) There are no enzymes to get rid of the glycated product as of the human body; glycated proteins are generally removed via ubiquitin-dependent 20S proteasome-mediated proteolysis [10].…”