Background. Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a working clinical category rather than a distinct morphological entity. In the absence of ≥50% stenosis of the major epicardial coronary arteries, infarction may be caused by plaque rupture or erosion, vasospasm, spontaneous coronary artery dissection, thromboembolism, or coronary microvascular dysfunction. Aim. To analyze which structural and functional abnormalities of the coronary microcirculation may contribute to MINOCA and which of them are supported by direct morphological evidence. Materials and methods. This narrative review is based on a targeted search of PubMed/MEDLINE, open-access full-text sources, documents of the European Society of Cardiology and the American Heart Association, Russian clinical guidelines, and Russian cardiology journals. Results. Direct pathological studies of the microvasculature in patients with clinically established MINOCA are scarce. The strongest morphological evidence concerns microvascular obstruction and microembolization, endothelial injury, arteriolar remodeling, perivascular fibrosis, and capillary rarefaction; however, much of it was obtained in other forms of ischemic heart disease, in reperfusion injury, or in conditions that mimic MINOCA. Myocarditis and takotsubo syndrome have distinct morphological features and explain troponin elevation in the absence of epicardial obstruction. Microvascular spasm is mainly a functional phenomenon and usually leaves no specific histological signature. Conclusion. Established morphological signs of infarction and microvascular injury should be distinguished from presumed functional spasm, and morphological findings should be interpreted together with clinical and imaging data.