Coronary “Microvascular Dysfunction”: Evolving Understanding of Pathophysiology, Clinical Implications, and Potential Therapeutics
نویسندگان
چکیده
Until recently, it has been generally held that stable angina pectoris (SAP) primarily reflects the presence of epicardial coronary artery stenoses due to atheromatous plaque(s), while acute myocardial infarction (AMI) results from thrombus formation on ruptured plaques. This concept is now challenged, especially by ORBITA and ISCHEMIA trials, which showed angioplasty/stenting does not substantially relieve SAP symptoms or prevent AMI death in such patients. These disappointing outcomes serve redirect attention towards anomalies small physiology. Recent studies suggest microvasculature often both structurally physiologically abnormal irrespective absence large stenoses. Structural remodelling appears be induced inflammation initiated mast cell, platelet, neutrophil activation, leading erosion endothelial glycocalyx. leads disruption laminar flow facilitation platelet interaction. Glycocalyx shedding implicated pathophysiology spasm, cardiovascular ageing, AMI, viral vasculitis. Physiological dysfunction closely linked structural occurs most patients with ischemia, large-vessel Dysfunction includes impairment vascular responsiveness autocidal vasodilators, as nitric oxide, prostacyclin, hydrogen sulphide, predisposes vasoconstriction a propensity for microthrombus formation. findings emphasise need new directions medical therapeutics SAP, well wide range other disorders.
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ژورنال
عنوان ژورنال: International Journal of Molecular Sciences
سال: 2023
ISSN: ['1661-6596', '1422-0067']
DOI: https://doi.org/10.3390/ijms241411287