Key result
Herpesviruses, particularly cytomegalovirus, are implicated in the pathogenesis of coronary atherosclerosis through mechanisms involving inflammatory reactions, endothelial injury, and lipid deposition.
Why the study?
The viral etiology of the development and progression of coronary atherosclerosis remains a subject of ongoing debate.
This review highlights the potential role of latent viral infections, specifically herpesviruses, as an etiopathogenetic factor in the development and progression of coronary atherosclerosis.
No immediate change to clinical practice; leaves open whether targeting latent herpesviruses modifies atherosclerosis risk.
Cardiovascular diseases are still the dominant cause of death worldwide. Coronary artery disease (CAD) is the most common type of heart disease and the leading cause of death for both men and women. Coronary atherosclerosis underlies multiple clinical manifestations ranging from asymptomatic to stable angina, acute coronary syndrome, MI, heart failure, and sudden cardiac death. The prerequisites for a closer study of the pathogenesis of the atherosclerotic process were the development of atherosclerotic vascular lesions at a younger age and the rapid progression of the process. Currently, it is generally accepted that CAD is a multifactorial disease. Attention is drawn to hereditary disorders of the receptor apparatus, endothelial dysfunction, and lipid metabolism disorders. In addition, latent viral infections are one of the etiopathogenetic factors in the development of atherosclerosis. A number of scientific studies have confirmed the relationship between infectious agents and the development of atherosclerotic vascular lesions. The viral etiology of the development and progression of atherosclerosis is the subject of debate among scientists around the world.
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Julia Kotova (2021) conducted a review in Coronary atherosclerosis. Herpesviruses (CMV, EBV, HSV) was evaluated. Herpesviruses, particularly cytomegalovirus, are implicated in the pathogenesis of coronary atherosclerosis through mechanisms involving inflammatory reactions, endothelial injury, and lipid deposition.
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