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Coronary Artery Calcium and Carotid Artery Intima Media Thickness and Plaque: Clinical Use in Need of Clarification

View Article: PubMed Central - PubMed

ABSTRACT

Atherosclerosis begins in early life and has a long latent period prior to onset of clinical disease. Measures of subclinical atherosclerosis, therefore, may have important implications for research and clinical practice of atherosclerotic cardiovascular disease (ASCVD). In this review, we focus on coronary artery calcium (CAC) and carotid artery intima-media thickness (cIMT) and plaque as many population-based studies have investigated these measures due to their non-invasive features and ease of administration. To date, a vast majority of studies have been conducted in the US and European countries, in which both CAC and cIMT/plaque have been shown to be associated with future risk of ASCVD, independent of conventional risk factors. Furthermore, these measures improve risk prediction when added to a global risk prediction model, such as the Framingham risk score. However, no clinical trial has assessed whether screening with CAC or cIMT/plaque will lead to improved clinical outcomes and healthcare costs. Interestingly, similar levels of CAC or cIMT/plaque among various regions and ethnic groups may in fact be associated with significantly different levels of absolute risk of ASCVD. Therefore, it remains to be determined whether measures of subclinical atherosclerosis improve risk prediction in non-US/European populations. Although CAC and cIMT/plaque are promising surrogates of ASCVD in research, we conclude that their use in clinical practice, especially as screening tools for primary prevention in asymptomatic adults, is premature due to many vagaries that remain to be clarified.

No MeSH data available.


Related in: MedlinePlus

A schematic of the theoretical LDL-initiated formation of atherosclerotic plaques in the arterial wallA high concentration of circulating LDL causes damage to the arterial wall and allows for entry and oxidization of LDL in the intimal layer. This leads to the secretion of chemokines and expression of leukocyte adhesion markers by endothelial cells. Monocytes are recruited to the site of injury. Once inside the intima, monocytes differentiate into macrophages and engulf the oxidized LDL. Continual uptake of oxidized LDL (due to prolonged high levels of circulating LDL) causes macrophages to become lipid-laden foam cells. Foam cells remain in the intima, secrete proinflammatory cytokines and chemokines, thus recruiting more monocytes. Dying foam cells lead to the formation of the necrotic core, which may become calcified. Smooth muscle cells migrate to the lipid pool of foam cells in an attempt to stabilize the plaque, however, local macrophages secrete enzymes that degrade the fibrous cap, causing the plaque to be vulnerable to rupture. Once ruptured, thrombosis ensues and may lead to myocardial infarction or stroke.
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Figure 1: A schematic of the theoretical LDL-initiated formation of atherosclerotic plaques in the arterial wallA high concentration of circulating LDL causes damage to the arterial wall and allows for entry and oxidization of LDL in the intimal layer. This leads to the secretion of chemokines and expression of leukocyte adhesion markers by endothelial cells. Monocytes are recruited to the site of injury. Once inside the intima, monocytes differentiate into macrophages and engulf the oxidized LDL. Continual uptake of oxidized LDL (due to prolonged high levels of circulating LDL) causes macrophages to become lipid-laden foam cells. Foam cells remain in the intima, secrete proinflammatory cytokines and chemokines, thus recruiting more monocytes. Dying foam cells lead to the formation of the necrotic core, which may become calcified. Smooth muscle cells migrate to the lipid pool of foam cells in an attempt to stabilize the plaque, however, local macrophages secrete enzymes that degrade the fibrous cap, causing the plaque to be vulnerable to rupture. Once ruptured, thrombosis ensues and may lead to myocardial infarction or stroke.

Mentions: Atherosclerosis, a chronic condition of the arterial wall, is a leading cause of death worldwide1) and is characterized by the accumulation of lipids in arteries, leading to plaque formation and eventually to coronary heart disease (CHD) or stroke2). Various lifestyle-related factors that contribute to the development of atherosclerosis have been identified (called “risk factors”). These include elevated plasma concentrations of low-density lipoprotein (LDL) cholesterol, increased local shear forces from elevated blood pressure, chemical toxins from cigarette smoke, insulin resistance, and glycosylated end-product formation in diabetes mellitus3). One of the widely-accepted models of plaque formation, LDL-initiated atherogenesis, is depicted in Fig. 1.


Coronary Artery Calcium and Carotid Artery Intima Media Thickness and Plaque: Clinical Use in Need of Clarification
A schematic of the theoretical LDL-initiated formation of atherosclerotic plaques in the arterial wallA high concentration of circulating LDL causes damage to the arterial wall and allows for entry and oxidization of LDL in the intimal layer. This leads to the secretion of chemokines and expression of leukocyte adhesion markers by endothelial cells. Monocytes are recruited to the site of injury. Once inside the intima, monocytes differentiate into macrophages and engulf the oxidized LDL. Continual uptake of oxidized LDL (due to prolonged high levels of circulating LDL) causes macrophages to become lipid-laden foam cells. Foam cells remain in the intima, secrete proinflammatory cytokines and chemokines, thus recruiting more monocytes. Dying foam cells lead to the formation of the necrotic core, which may become calcified. Smooth muscle cells migrate to the lipid pool of foam cells in an attempt to stabilize the plaque, however, local macrophages secrete enzymes that degrade the fibrous cap, causing the plaque to be vulnerable to rupture. Once ruptured, thrombosis ensues and may lead to myocardial infarction or stroke.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5383538&req=5

Figure 1: A schematic of the theoretical LDL-initiated formation of atherosclerotic plaques in the arterial wallA high concentration of circulating LDL causes damage to the arterial wall and allows for entry and oxidization of LDL in the intimal layer. This leads to the secretion of chemokines and expression of leukocyte adhesion markers by endothelial cells. Monocytes are recruited to the site of injury. Once inside the intima, monocytes differentiate into macrophages and engulf the oxidized LDL. Continual uptake of oxidized LDL (due to prolonged high levels of circulating LDL) causes macrophages to become lipid-laden foam cells. Foam cells remain in the intima, secrete proinflammatory cytokines and chemokines, thus recruiting more monocytes. Dying foam cells lead to the formation of the necrotic core, which may become calcified. Smooth muscle cells migrate to the lipid pool of foam cells in an attempt to stabilize the plaque, however, local macrophages secrete enzymes that degrade the fibrous cap, causing the plaque to be vulnerable to rupture. Once ruptured, thrombosis ensues and may lead to myocardial infarction or stroke.
Mentions: Atherosclerosis, a chronic condition of the arterial wall, is a leading cause of death worldwide1) and is characterized by the accumulation of lipids in arteries, leading to plaque formation and eventually to coronary heart disease (CHD) or stroke2). Various lifestyle-related factors that contribute to the development of atherosclerosis have been identified (called “risk factors”). These include elevated plasma concentrations of low-density lipoprotein (LDL) cholesterol, increased local shear forces from elevated blood pressure, chemical toxins from cigarette smoke, insulin resistance, and glycosylated end-product formation in diabetes mellitus3). One of the widely-accepted models of plaque formation, LDL-initiated atherogenesis, is depicted in Fig. 1.

View Article: PubMed Central - PubMed

ABSTRACT

Atherosclerosis begins in early life and has a long latent period prior to onset of clinical disease. Measures of subclinical atherosclerosis, therefore, may have important implications for research and clinical practice of atherosclerotic cardiovascular disease (ASCVD). In this review, we focus on coronary artery calcium (CAC) and carotid artery intima-media thickness (cIMT) and plaque as many population-based studies have investigated these measures due to their non-invasive features and ease of administration. To date, a vast majority of studies have been conducted in the US and European countries, in which both CAC and cIMT/plaque have been shown to be associated with future risk of ASCVD, independent of conventional risk factors. Furthermore, these measures improve risk prediction when added to a global risk prediction model, such as the Framingham risk score. However, no clinical trial has assessed whether screening with CAC or cIMT/plaque will lead to improved clinical outcomes and healthcare costs. Interestingly, similar levels of CAC or cIMT/plaque among various regions and ethnic groups may in fact be associated with significantly different levels of absolute risk of ASCVD. Therefore, it remains to be determined whether measures of subclinical atherosclerosis improve risk prediction in non-US/European populations. Although CAC and cIMT/plaque are promising surrogates of ASCVD in research, we conclude that their use in clinical practice, especially as screening tools for primary prevention in asymptomatic adults, is premature due to many vagaries that remain to be clarified.

No MeSH data available.


Related in: MedlinePlus