{"id":9642,"date":"2021-12-28T17:54:54","date_gmt":"2021-12-28T15:54:54","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/cardiology\/atherosclerosis-risk-factors-pathomechanism-organ-complications-prevention-and-treatment\/"},"modified":"2022-01-03T11:59:39","modified_gmt":"2022-01-03T09:59:39","slug":"atherosclerosis-risk-factors-pathomechanism-organ-complications-prevention-and-treatment","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/cardiology\/atherosclerosis-risk-factors-pathomechanism-organ-complications-prevention-and-treatment\/","title":{"rendered":"Atherosclerosis (risk factors, pathomechanism, organ complications, prevention and treatment)"},"content":{"rendered":"<span class=\"block-heading\" id=\"header_1\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Definition<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">Hardening of arteries brought by lesions known as atherosclerotic plaques,&nbsp;or&nbsp;<strong>atheromas<\/strong>.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Generally, atheromas are nodules containing&nbsp;gruel, fatty, wax-like substance<ul><li>Composed of a soft, necrotic, lipid core (mainly cholesterol and cholesterol esters)<\/li><li>Covered by a fibrous cap<\/li><\/ul><\/li><li>As the plaques enlarge, they obstruct the vessel (stenosis) and change the flow hemodynamics<\/li><li>The change in flow increases the shear stress, which often causes the rupture of the plaque<ul><li>Plaque fate is discussed in detail below<\/li><\/ul><\/li><li>Atherosclerosis common occurs in the coronary arteries and is responsible for the majority of myocardial infarctions<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Risk factors<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<p class=\"wp-block-paragraph\">Atherosclerosis is a complex, multifactorial chronic condition with many known risk&nbsp;factors. We can classify them into modifiable (factors under our influence) and non-modifiable factors:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Modifiable<\/strong><ul><li><strong>Hyperlipidemia and hypercholesterolemia<\/strong><ul><li>Increased levels of LDL and decreased levels of HDL<ul><li>LDL mobilizes lipids from the liver to the periphery (&#8220;bad cholesterol&#8221;)<\/li><li>HDL mobilizes lipids from the periphery to the liver (&#8220;good cholesterol&#8221;)<\/li><\/ul><\/li><\/ul><\/li><li><strong>Hypertension<\/strong><\/li><li><strong>Cigarette smoking<\/strong><\/li><li><strong>Diabetes Mellitus<\/strong><ul><li>Associated with hypercholesterolemia<\/li><li>The cytological metabolic changes provide a favorable environment for the formation of atherosclerosis<\/li><\/ul><\/li><li><strong>Metabolic syndrome<\/strong><ul><li>Obesity and obesity-related diseases<\/li><\/ul><\/li><li><strong>Diet<\/strong><ul><li>Although some authors state that a diet high in cholesterol increases the risk for atherosclerosis and cardiovascular-related diseases, the current data suggests no link between the two<sup>1<\/sup><\/li><li>Omega-3 fatty acids generally aid in the prevention of\u00a0atherosclerosis and cardiovascular-related diseases<\/li><li>Trans fats\u00a0adversely affect lipid profiles<\/li><\/ul><\/li><li><strong>Exercise <\/strong>(generally improves lipid profiles)<\/li><\/ul><\/li><li><strong>Somewhat-modifiable<\/strong><ul><li>Hyper-lipoprotein A<\/li><li>Hyperhomocytinemia<\/li><\/ul><\/li><li><strong>Non-modifiable<\/strong><ul><li>Age<ul><li>Generally, the occurrence and severity of atherosclerosis increases as we age<\/li><\/ul><\/li><li>Gender<ul><li>Pre-menopausal women can be compared to men of the same age<\/li><li>Post-menopausal women have an increased risk of developing atherosclerosis-related diseases, however, men are more commonly developing atherosclerosis<\/li><\/ul><\/li><li>Genetics<ul><li>Certain genetic traits have been linked to an increase in developing atherosclerosis<\/li><\/ul><\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Pathomechanism<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<p class=\"wp-block-paragraph\">The precise mechanism is not fully understood yet, but the current model suggests an initial phase that includes the following events that occur simultaneously:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Endothelial injury and dysfunction<ul><li>Due to a variety of both <strong>mechanical<\/strong> (hypertension) and <strong>chemical<\/strong> (toxins, metabolic disruption) causes<\/li><li><strong>Increases the permeability<\/strong> (the endothelium becomes <strong>leaky<\/strong>)<\/li><li>Platelet adhesion, and monocyte adhesion and transmigration into the intimal layer<\/li><\/ul><\/li><li>Accumulation of lipoprotein (LDL) in the vessel wall<ul><li>LDL particles will oxidize and cause further endothelial damage<\/li><\/ul><\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">Once in the intimal layer, monocytes differentiate into macrophages and phagocytose the oxidized LDL particles, forming <strong>foam cells<\/strong>, and releasing pro-inflammatory cytokines, causing:<\/p>\n\n\n\n<ol class=\"wp-block-list\"><li>Smooth muscle cells recruitment<\/li><li>Formation of a necrotic core containing cellular and lipid debris (mainly in the form of cholesterol crystals) &#8212;&nbsp;<strong>fatty streaks<\/strong><ul><li>These fatty streaks can be seen macroscopically as elongated, slightly raised lesions containing foam cells<\/li><li>Fatty streaks are normally present in healthy individuals and even infants;<strong> not all of them progress to atherosclerotic plaques<\/strong><\/li><\/ul><\/li><li>Lymphocyte recruitment<ul><li>Chronic inflammatory process, releasing even more inflammatory cytokines<\/li><\/ul><\/li><li>Smooth muscle proliferation and ECM deposition &#8212;&nbsp;<strong>intimal thickening<\/strong><ul><li>Caused by the inflammatory cytokines (<strong>INF-gamma<\/strong>, amongst others)<sup>3<\/sup><\/li><\/ul><\/li><li>Formation of a fibrous cap overlying the necrotic core &#8212; <strong>atheroma&nbsp;<\/strong>(at this stage we can refer to it as an&nbsp;<strong>atherosclerotic\/atheromatous plaque<\/strong>)<ul><li>At this stage, the plaque will consist of all of the components described above:<ul><li><strong>Cells<\/strong> &#8212; Smooth muscle cells, macrophages, and lymphocytes<\/li><li><strong>ECM<\/strong> &#8212; Collagen, elastic fibers, and proteoglycans<\/li><li><strong>Lipids<\/strong><\/li><\/ul><\/li><\/ul><\/li><\/ol>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">The fate of atherosclerotic plaques<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<p class=\"wp-block-paragraph\">Once large enough, atherosclerotic plaques begin to restrict blood flow.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Depending on the conditions,&nbsp;atherosclerotic plaques can progress even further and undergo organization and remodeling. The chronic inflammation causes together with the associated hemodynamic changes cause:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>The increase of lipid contents (plaque growth), loss of smooth muscle tissue (apoptosis) and its fibrosis form a\u00a0<strong>fibroatheroma\u00a0<\/strong>(an atherosclerotic plaque with fibrosis)<ul><li>Not to be confused with <strong>fibrous plaques\u00a0<\/strong>which are atherosclerotic lesions composed exclusively of smooth muscle and collagen<\/li><\/ul><\/li><li>Progressive loss of smooth muscle tissue, increased degradation and reduced synthesis of\u00a0collagen destabilizes the structural integrity of the plaque and can form a\u00a0<strong>vulnerable plaque<\/strong><ul><li>As their name suggests, these plaques have an increased risk to:<ul><li><strong>Rupture<\/strong>. Bursting of the vessel wall.<\/li><li><strong>Erode<\/strong>. Sloughing off of the plaque, exposure of the subendothelial basement membrane and formation of an embolus<\/li><li><strong>Hemorrhage<\/strong>. Bleeding into the plaque<\/li><li><strong>Thrombosis<\/strong>. Partial fissure exposes a highly thrombogenic surface, thus creating a thrombus<\/li><li><strong>Dilatation<\/strong>. Formation of an aneurysm<\/li><\/ul><\/li><\/ul><\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">Once a plaque has undergone one of the above changes (thrombosis for example), it is considered to be a <strong>complicated plaque<\/strong>.<\/p>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Complications<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<p class=\"wp-block-paragraph\">Atherosis is typically asymptomatic for decades. Complications begin to appear once the atherosclerotic plaque becomes complicated.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Anyeurysm and aortic dissection<\/li><li>Renovascular disease leading to CKD<\/li><li>Coronary artery disease and agina<\/li><li>Carotid artery disease and stroke<\/li><li>Peripheral artery disease<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<ul class=\"wp-block-list\"><li>Non-invasive techniques<ul><li>Vascular US<\/li><li>CT angiography<\/li><li>MRI angiography<\/li><li>PET<\/li><\/ul><\/li><li>Invasive techniques<ul><li>Intravascular US<\/li><li>Angioscopy<\/li><li>Coronarography<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Prevention and treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<ul class=\"wp-block-list\"><li><strong>Lifestyle modifications<\/strong><ul><li>Diet<\/li><li>Exercise<\/li><li>Smoking cessation<\/li><\/ul><\/li><li><strong>Antihypertensives<\/strong><ul><li>For primary hypertension, use the NICE pathway<\/li><li>For secondary hypertension, treat the cause<\/li><\/ul><\/li><li><strong>Glycemic control in DM<\/strong><\/li><li><strong>Lipid reduction<\/strong><ul><li>Statins (atorvastatin 20mg\/day)<\/li><li>Ezetimibe (10mg\/day)<\/li><li>PCSK9 inhibitors<\/li><li>Bile sequesterants<\/li><li>Fibrates<\/li><\/ul><\/li><li><strong>Antiplatelet drugs<\/strong><ul><li>Aspirin (100mg\/day)<\/li><li>Clopidogrel, prasugrel (75mg\/day)<\/li><\/ul><\/li><\/ul>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Definition<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Risk factors<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Pathomechanism<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">The fate of atherosclerotic plaques<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Complications<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Prevention and treatment<\/h4><\/div>","protected":false},"excerpt":{"rendered":"<p>Definition Hardening of arteries brought by lesions known as atherosclerotic plaques,&nbsp;or&nbsp;atheromas. Generally, atheromas are nodules containing&nbsp;gruel, fatty, wax-like substance Composed of a soft, necrotic, lipid core (mainly cholesterol and cholesterol esters) Covered by a fibrous cap As the plaques enlarge, they obstruct the vessel (stenosis) and change the flow hemodynamics The change in flow increases [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":410,"menu_order":24,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-9642","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.9 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Atherosclerosis (risk factors, pathomechanism, organ complications, prevention and treatment) &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/cardiology\/atherosclerosis-risk-factors-pathomechanism-organ-complications-prevention-and-treatment\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"4 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/cardiology\\\/atherosclerosis-risk-factors-pathomechanism-organ-complications-prevention-and-treatment\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/cardiology\\\/atherosclerosis-risk-factors-pathomechanism-organ-complications-prevention-and-treatment\\\/\",\"name\":\"Atherosclerosis (risk factors, pathomechanism, organ complications, prevention and treatment) &#8211; 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