Abstract

Just as in epicardial coronary stenosis, coronary microvascular dysfunction (CMD) also leads to an imbalance of myocardial oxygen supply and demand. The dysfunction is located at the level of the coronary microcirculation with vessel diameters < 500µm and structural as well as functional alterations have been described. The underlying mechanisms are diverse, frequently overlap and are still incompletely understood. Among others, conditions such as chronic inflammation, estrogen deficiency and a genetic familial predisposition have been reported. A common and often underdiagnosed clinical manifestation of CMD is found in patients who have symptoms of angina pectoris but no obstructive epicardial coronary artery disease or myocardial disease. The CMD can be diagnosed using non-invasive procedures, such as the combination of coronary computed tomography (CT) angiography and cardiac stress magnetic resonance imaging (MRI) or coronary CT and positron emission tomography (PET). In addition, invasive coronary vasomotor assessment is also suitable. Very little evidence is available regarding the effectiveness of pharmacological treatment of CMD. The current European Society of Cardiology (ESC) guidelines on the management of stable coronary artery disease from 2013 recommend using acetylsalicylic acid (ASS) and a statin as well as beta blockers and/or calcium channel blockers. Patients with CMD have an elevated risk for coronary events and death of approximately 1.7 % per year. Moreover, there is an increased morbidity with frequent presentations in practices and emergency admissions. Clinical research efforts should aim at a better characterization of the underlying mechanisms of CMD in order to develop targeted treatment approaches.

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