C. Tejada-González, A.J. Herruzo-León, F. Luquero-Bachiller, J. Serpa-Morán, A. Leandro-Barros, A. Ruiz-Saavedra, C. Torán-Martínez, A. García-Lledó
{"title":"Ateroesclerosis. Etiopatogenia. Placa estable y placa vulnerable. Rotura de placa. Resumen de las manifestaciones clínicas a nivel sistémico","authors":"C. Tejada-González, A.J. Herruzo-León, F. Luquero-Bachiller, J. Serpa-Morán, A. Leandro-Barros, A. Ruiz-Saavedra, C. Torán-Martínez, A. García-Lledó","doi":"10.1016/j.med.2025.08.009","DOIUrl":null,"url":null,"abstract":"<div><div>Atherosclerosis is a chronic disease characterized by the deposition of lipids in the intima layer of medium- and large-caliber arteries that causes the formation of atheromatous plaques. It is one of the main causes of morbidity and mortality worldwide. Risk factors include hypercholesterolemia, diabetes, hypertension, and unhealthy habits. The development of plaques, which is closely linked to risk factors, begins with endothelial dysfunction and the accumulation of oxidized LDL cholesterol followed by inflammation and cell migration. This generates a vicious cycle that increases the risk of cardiovascular events such as heart attacks and strokes. It is a phenomenon of lipid infiltration, inflammation, and repair whose balance depends on the stability of the plaques, which can be stable or vulnerable. Inflammation plays a central role in disease progression. It is mediated by macrophages and foam cells that secrete proinflammatory cytokines. Other mechanisms, such as hypoxia and reverse cholesterol transport, influence plaque stability. Clinical manifestations include ischemic heart disease, cerebrovascular disease, peripheral arterial disease, and renal and oncologic complications. The therapeutic approach includes primary and secondary prevention by controlling risk factors and specific therapies to stabilize plaques and reduce acute events.</div></div>","PeriodicalId":100912,"journal":{"name":"Medicine - Programa de Formación Médica Continuada Acreditado","volume":"14 39","pages":"Pages 2349-2356"},"PeriodicalIF":0.0000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medicine - Programa de Formación Médica Continuada Acreditado","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304541225002094","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Atherosclerosis is a chronic disease characterized by the deposition of lipids in the intima layer of medium- and large-caliber arteries that causes the formation of atheromatous plaques. It is one of the main causes of morbidity and mortality worldwide. Risk factors include hypercholesterolemia, diabetes, hypertension, and unhealthy habits. The development of plaques, which is closely linked to risk factors, begins with endothelial dysfunction and the accumulation of oxidized LDL cholesterol followed by inflammation and cell migration. This generates a vicious cycle that increases the risk of cardiovascular events such as heart attacks and strokes. It is a phenomenon of lipid infiltration, inflammation, and repair whose balance depends on the stability of the plaques, which can be stable or vulnerable. Inflammation plays a central role in disease progression. It is mediated by macrophages and foam cells that secrete proinflammatory cytokines. Other mechanisms, such as hypoxia and reverse cholesterol transport, influence plaque stability. Clinical manifestations include ischemic heart disease, cerebrovascular disease, peripheral arterial disease, and renal and oncologic complications. The therapeutic approach includes primary and secondary prevention by controlling risk factors and specific therapies to stabilize plaques and reduce acute events.