200 Chapter 10 Part 1. Endotypes of Chronic Coronary Syndrome Each year in the Netherlands, over 20.000 patients visit their general practitioner for newly onset anginal complaints.1 Often, the first diagnostic step is to evaluate if patients suffer from ischemia due to obstructive coronary arteries (CAD) via invasive coronary angiography (CAG) or coronary computed tomography angiography (CCTA). Approximately half of these patients do not have obstructive CAD and are classified as having Angina with Non-Obstructive Coronary Arteries (ANOCA).2, 3 ANOCA is found in approximately 65% of women and 30% of men after evaluation for obstructive CAD. Among these patients, in the ESC-guidelines is recommended to determine whether the patient is symptomatic due to coronary vasomotor dysfunction, such as enhanced vasoconstriction or impaired vasodilation, or if they have non-cardiac chest pain.4 The ANOCA population is very heterogeneous, which makes it difficult to distinguish between the various endotypes. The MICORDIS study showed that 39% of ANOCA patients exhibited microvascular vasospasm, while 25% had CMD, of which 14% met the criteria for both microvascular vasospasm and CMD. This heterogeneity, in combination with lack of evidence-based medical therapies and lacking sufficient pathophysiological knowledge, results in an reduced quality of life for ANOCA patients.5 Invasive CAG alone is insufficient to detect all endotypes of chronic coronary syndrome (CCS), due to several reasons. Invasive CAG has a spatial resolution of 0.3mm, making it impossible to detect microvascular rarefaction and inward remodeling, responsible for structural CMD. Moreover, functional CMD and enhanced vasoconstriction due to endothelial or smooth muscle dysfunction cannot be detected using CAG alone.6 Current guidelines recommend invasive coronary function testing (CFT), allowing diagnosis of the various endotypes of ANOCA.4 However, invasive assessment is accompanied by additional risks, such as bleeding, arterial damage and infection, and often CFT is performed in a step-wise approach after CAG, doubling the risk of complications. The CorMicA trial demonstrated that while ICFT helps to identify distinct ANOCA endotypes, a significant proportion of patients still do not receive a conclusive diagnosis after these tests.7 This highlights the need for a better understanding of the distribution and characteristics of the different CCS endotypes is essential. This will allow for more effective stratification of patients, ensuring that the appropriate invasive assessment is conducted in each patient. Large atherosclerotic plaques are the cause of obstructive CAD. Atherosclerosis is a chronic inflammatory condition of the vasculature, provoked by cardiovascular risk factors such as hypertension, diabetes mellitus, smoking and dyslipidemia. These cardiovascular risk factors damage the endothelial cells, resulting in a loss of anti-inflammatory and antithrombotic properties. This endothelial dysfunction stimulates monocytes to infiltrate the vasculature and differentiate into macrophages and foam cells.8 These foam cells constitute a plaque, which, when larger than >70% stenosis, cause insufficient coronary flow to the myocardium resulting in ischemia. However, women are relatively protected from atherosclerotic vascular disease until menopause, due to the possible protective effect of estrogen on atherosclerosis. Estrogen is known to increase HDL-cholesterol
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