Abstract
Atherosclerosis is a chronic long-lasting vascular disease leading to myocardial infarction and stroke. Vulnerable atherosclerotic (AS) plaques are responsible for these life-threatening clinical endpoints. To more successfully work against atherosclerosis, improvements in early diagnosis and treatment of AS plaque lesions are required. Vulnerable AS plaques are frequently undetectable by conventional imaging because they are non-stenotic. Although blood biomarkers like lipids, C-reactive protein, interleukin-6, troponins, and natriuretic peptides are in pathological ranges, these markers are insufficient in detecting the critical perpetuation of AS anteceding endpoints. Thus, chances to treat the patient in a preventive way are wasted. It is now time to solve this dilemma because clear results indicate a benefit of anti-inflammatory therapy per se without modification of blood lipids (CANTOS Trial, NCT01327846). This fact identifies modulation of immune-mediated inflammation as a new promising point of action for the eradication of fatal atherosclerotic endpoints.
Highlights
Myocardial infarction and stroke are still the leading causes of death worldwide.Atherosclerosis (AS) a sub-acute immune-mediated inflammation around lipid accumulations of the vascular wall is responsible for this burden
Immune-mediated inflammation is a main driver of AS, and monocytes/macrophages are principal offenders [25,26]
Allahverdian et al suggest that vascular smooth muscle cells (VSMCs) can gain functions of a macrophage, like lipid uptake [30] or phenotypic conversion toward monocyte descent [31,32]
Summary
Myocardial infarction and stroke are still the leading causes of death worldwide. Atherosclerosis (AS) a sub-acute immune-mediated inflammation around lipid accumulations of the vascular wall is responsible for this burden. A main feature of AS is infiltration of the vessel wall by monocytes and T-cells. These cells interact with one another and with the arterial wall cells [1,2,3]. Effective identification methods and techniques to follow the development of AS-plaques before clinical events occur are missing. This is caused by the lacking performance of blood biomarkers and imaging techniques and by the availability of specific molecules for targeted recognition [1,8,9]. In most cases, vulnerable AS lesions become detectable too late by either incidence of myocardial infarction or stroke or the effect of arterial stenosis on organ perfusion. As vulnerable AS plaques are frequently non-stenotic, preclinical identification is not possible [1,9,10]
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