Post by Nadica (She/Her) on Aug 19, 2024 2:04:15 GMT
COVID-19 in the Initiation and Progression of Atherosclerosis: Pathophysiology During and Beyond the Acute Phase - Published July 17, 2024
Highlights
•SARS-CoV-2 infection can markedly influence the initiation and progression of atherosclerotic lesions.
•Endothelial dysfunction, platelet activation, and persistent inflammation are potential drivers of increased atherosclerosis following COVID-19.
•Understanding the pathogenesis of atherosclerosis in COVID-19 can provide insights into cardiovascular disease mechanisms in other chronic infections.
•Recognizing the cardiovascular implications of long COVID-19 highlights the importance of proactive risk management and advocates for further research into this topic.
Abstract
The incidence of atherosclerotic cardiovascular disease is increasing globally, especially in low- and middle-income countries, despite significant efforts to reduce traditional risk factors. Premature subclinical atherosclerosis has been documented in association with several viral infections. The magnitude of the recent COVID-19 pandemic has highlighted the need to understand the association between SARS-CoV-2 and atherosclerosis. This review examines various pathophysiological mechanisms, including endothelial dysfunction, platelet activation, and inflammatory and immune hyperactivation triggered by SARS-CoV-2 infection, with specific attention on their roles in initiating and promoting the progression of atherosclerotic lesions. Additionally, it addresses the various pathogenic mechanisms by which COVID-19 in the post-acute phase may contribute to the development of vascular disease. Understanding the overlap of these syndromes may enable novel therapeutic strategies. We further explore the need for guidelines for closer follow-up for the often-overlooked evidence of atherosclerotic cardiovascular disease among patients with recent COVID-19, particularly those with cardiometabolic risk factors.
Highlights
•SARS-CoV-2 infection can markedly influence the initiation and progression of atherosclerotic lesions.
•Endothelial dysfunction, platelet activation, and persistent inflammation are potential drivers of increased atherosclerosis following COVID-19.
•Understanding the pathogenesis of atherosclerosis in COVID-19 can provide insights into cardiovascular disease mechanisms in other chronic infections.
•Recognizing the cardiovascular implications of long COVID-19 highlights the importance of proactive risk management and advocates for further research into this topic.
Abstract
The incidence of atherosclerotic cardiovascular disease is increasing globally, especially in low- and middle-income countries, despite significant efforts to reduce traditional risk factors. Premature subclinical atherosclerosis has been documented in association with several viral infections. The magnitude of the recent COVID-19 pandemic has highlighted the need to understand the association between SARS-CoV-2 and atherosclerosis. This review examines various pathophysiological mechanisms, including endothelial dysfunction, platelet activation, and inflammatory and immune hyperactivation triggered by SARS-CoV-2 infection, with specific attention on their roles in initiating and promoting the progression of atherosclerotic lesions. Additionally, it addresses the various pathogenic mechanisms by which COVID-19 in the post-acute phase may contribute to the development of vascular disease. Understanding the overlap of these syndromes may enable novel therapeutic strategies. We further explore the need for guidelines for closer follow-up for the often-overlooked evidence of atherosclerotic cardiovascular disease among patients with recent COVID-19, particularly those with cardiometabolic risk factors.