Myocardial infarction with non-obstructive coronary arteries: a focus on vasospastic angina

Abstract

Vasospastic angina (VSA) is considered a broad diagnostic category including documented spontaneous episodes of angina pectoris produced by coronary epicardial vasospasm as well as those induced during provocative coronary vasospasm testing and coronary microvascular dysfunction due to microvascular spasm. The hallmark feature of VSA is rest angina, which promptly responds to short-acting nitrates; however, VSA can present with a great variety of symptoms, ranging from stable angina to acute coronary syndrome and even ventricular arrhythmia. VSA is more prevalent in females, who can present with symptoms different from those among male patients. This may lead to an underestimation of cardiac causes of chest-related symptoms in female patients, in particular if the coronary angiogram (CAG) is normal. Evaluation for the diagnosis of VSA includes standard 12-lead ECG during the attack, Holter monitoring, exercise testing, and echocardiography. Patients suspected of having VSA with a normal CAG without a clear myocardial or non-cardiac cause are candidates for provocative coronary vasospasm testing. The gold standard method for provocative coronary vasospasm testing involves the administration of a provocative drug during CAG while monitoring patient symptoms, ECG and documentation of the coronary artery. Treatment of VSA consists of lifestyle adaptations and pharmacotherapy with calcium channel blockers and nitrates.

Keywords: Coronary artery disease; Myocardial infarction; Non-obstructive coronary atherosclerosis; Vasospastic angina.

Fig. 1

Ischaemic heart disease (CAD Coronary artery disease)

Fig. 2

Epicardial coronary spasm. Example of focal coronary spasm (upper panel) and diffuse coronary spasm (lower panel) during provocative coronary vasospasm testing with intracoronary acetylcholine (ACH)

Fig. 3

Coronary microvessel spasm. Example of coronary microvascular dysfunction. During infusion of intracoronary acetylcholine (IC ACH) there is no visible spasm of the left coronary artery (left panel). During infusion the ECG shows diffuse ST-segment elevation (mid panel). The coronary flow reserve (CFR) prior to IC ACH administration is 2.7 (right panel, A), a reduced CFR during IC ACH infusion (right panel, B), and recovery of the CFR after administration of nitroglycerin IC (right panel, C) (FFR fractional flow reserve, HSR hyperaemic stenosis resistence, HMR hyperaemic microvascular resistance)