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Epicardial coronary disease includes dynamic disorders capable of causing myocardial ischaemia without fixed obstructive stenosis. Vasospastic angina (VSA) and myocardial bridging (MB) are paradigmatic entities characterized by transient luminal narrowing and reversible flow impairment. Although traditionally viewed as distinct, they frequently overlap, sharing mechanisms such as endothelial dysfunction, smooth muscle hyperreactivity, altered shear stress, and autonomic imbalance. VSA results from episodic coronary constriction, whereas MB involves systolic compression of an intramyocardial segment with possible diastolic flow limitation. The aim of this article is to provide a mechanistic appraisal of these conditions and their clinical implications within chronic coronary syndromes.