Coronary vasospasm, affecting both epicardial arteries and the coronary microcirculation, is a significant yet frequently underdiagnosed and undertreated cause of coronary syndromes. When promptly identified, it carries a relatively benign prognosis. Recognition can be straightforward in non-cardiology settings when triggered by known spasmogenic agents such as misoprostol (obstetrics) or 5-fluorouracil (oncology). Vasospasm may also be incidentally revealed during noninvasive functional testing, typically presenting as ST-segment elevation during early recovery phases, or after administration of agents like aminophylline following dipyridamole or β-blockers following dobutamine. In patients with high clinical suspicion but negative Holter or stress test findings, targeted provocation with ergonovine or hyperventilation protocols can safely induce vasospasm and unmask regional wall motion abnormalities, indicating epicardial involvement. Hyperventilation-Doppler echocardiography enables the detection of microvascular dysfunction through reductions in coronary flow velocity in the mid-distal left anterior descending coronary artery. A multi-stress, multi-marker functional testing approach offers a noninvasive, safe, and effective diagnostic strategy. Inducible wall motion abnormalities are specific for epicardial spasm, while Doppler-detected flow reduction is more sensitive for microvascular dysfunction. Early diagnosis is essential, as coronary vasospasm, though potentially life-threatening, is highly manageable with appropriate therapy. Management of patients with proven epicardial coronary artery or microvascular vasospasm involves starting therapy with calcium channel blockers and nitrates, and avoiding β-blockers, as they can worsen vasospasm by blocking β2-mediated vasodilation and leaving α1-mediated vasoconstriction unopposed.
Varga et al. (Sun,) studied this question.