Atherosclerosis Pathophysiology and the Role of Novel Risk Factors: A Clinicobiochemical Perspective

Abstract

Atherosclerosis is the root cause of the biggest killer of the 21st century. Mechanisms contributing to atherogenesis are multiple and complex. A number of theories-including the role of dyslipidemia, hypercoagulability, oxidative stress, endothelial dysfunction, and inflammation and infection by certain pathogens-have been propounded from time to time explain this complex phenomenon. Recently it has been suggested that atherosclerosis is a multifactorial, multistep disease that involves chronic inflammation at every step, from initiation to progression, and that all the risk factors contribute to pathogenesis by aggravating the underlying inflammatory process. A better understanding of the pathogenesis of atherosclerosis will aid in devising pharmaceutical and lifestyle modifications for reducing mortality resulting from coronary artery disease (CAD).A comprehensive literature search was conducted using the Web sites of the National Library of Medicine (http:// www.ncbl.nlm.nih.gov/) and PubMed Central, the US National Library of Medicine's digital archive of life sciences literature (http:// www.pubmedcentral.nih.gov/). The data were accessed from books and journals in which relevant articles in this field were published. The whole spectrum of coronary artery disease evolves through various events that lead to the formation and progression of atherosclerotic plaque and finally its complications. Atherosclerosis is the culprit behind coronary artery disease, cerebral vascular disease, and peripheral vascular disease. The pathogenic mechanisms are varied and complex. Of late, the role of lipoprotein (a), homocysteine, and inflammation and infection as prime culprits in pathogenesis of CAD is the subject of intense research and debate. The appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework to understand the clinical benefits of newer therapeutic strategies, and a better understanding of pathogenesis aids in formulating preventive and therapeutic strategies in reducing mortality resulting from CAD.An in-depth knowledge of the various pathogenic mechanisms involved in atherosclerosis can help in substantiating the current existing knowledge about the CAD epidemic. This knowledge will help clinicians to better manage the disease, which affects Indians in its most severe form.

White blood cell subsets are associated with carotid intima-media thickness and pulse wave velocity in an older Chinese population: the Guangzhou Biobank Cohort Study

“…1 Given this association, research has concentrated on risk factors for or markers of the risk of atherosclerosis itself. For example, metabolic syndrome, a constellation of biological and anthropometric indicators, including high blood pressure, glucose, triglycerides, abdominal obesity and low highdensity lipoprotein cholesterol, is strongly predictive of atherosclerosis risk.…”

An alternative marker of low-density lipoprotein cholesterol in coronaryartery disease: non-high-density lipoprotein cholesterol

“…Atherosclerotic coronary artery disease is one of the most common causes of morbidity and mortality in developed countries (1). Age, sex, family history, diabetes, hypertension, dyslipidemia, smoking, obesity, sedentary lifestyle, and psychosocial factors can be considered as the main risk factors for atherosclerotic heart disease (2).…”

“…The main source of cholesterol in the atherosclerotic plaque is the esterified cholesterol in low-density lipoprotein cholesterol (LDL-C). The main factors that determine the migration of lipoproteins into subintimal spaces are the molecular size of lipids and gradient degree (1). Although LDL-C is known as the major factor in the process of atherogenesis, the higher levels and the migration of triglyceride-enriched lipoproteins [very-low-density lipoprotein cholesterol (VLDL-C)], intermediate-density lipoprotein cholesterol (IDL-C), chylomicron remnant, and lipoprotein a into the subendothelial space through damaged vascular endothelium can also have an important role in the formation of atheromatous plaque (2).…”

Ateroskleroz ile il-1α (interleukin-1α -889 c/t) gen polimorfizmi arasındaki ilişkinin araştırılması

“…Günümüzde ateroskleroz; multifaktöriyel, başlangıçtan progresyona kadar her basamağında kronik inflamasyonun rol oynadığı ve her risk faktörünün altta yatan inflamatuvar süreci hızlandırarak patogeneze katkıda bulunduğu bir hastalık olarak tanımlanmaktadır [2]. İnflamatuvar süreçte rol alan genlerin, ateroskleroz gelişimine direkt ve dolaylı olarak katkıda bulunabileceği gösterilmiştir [4].…”