Coronary Artery Vasospasm

Abstract

Coronary artery vasospasm (CVS) is an important mechanism of myocardial ischemia and produces any of the manifestations of coronary artery disease from silent myocardial ischemia, to effort-induced angina and variant angina, to acute coronary syndrome including myocardial infarction or sudden cardiac death. The pathogenesis, characteristic clinical features, diagnosis, and treatment of CVS are summarized. Emphasis is placed on correct diagnosis of CVS using pharmacological spasm provocation test, either during coronary angiography or with echocardiographic monitoring of ventricular wall motion. Current underutilization of pharmacologic provocative test at the time of coronary angiography cannot be justified, as there is no evidence supporting that the incidence of CVS is declining. Physicians' vigilance for objective documentation of CVS is necessary for appropriate management of patients with various clinical presentations of ischemic heart disease.

Keywords: Coronary artery vasospasm.

Figure 1. A representative case of coronary artery vasospasm documented by pharmacologic spasm provocation test during invasive coronary angiography: focal vasoconstriction (arrow, A) resulting in total occlusion of proximal left anterior descending coronary artery developed with ergonovine injection (E2, A), which was normalized with nitroglycerin administration (N, B).

Figure 2. Schematic illustrations showing relationship between angina threshold (dotted line) and daily activity in classic effort angina (A) and variant angina (B). In classic effort angina with fixed angina threshold, daily activity exceeding the angina threshold results in chest pain attack (blue), which is quite predictable and usually develops during daytime paralleling with the level of physical activity. However, in variant angina, the angina threshold itself varies significantly during a day and the level of physical activity is not associated with chest pain attack: thus, chest pain attack is quite unpredictable depending on the change of angina threshold, not on the level of physical activity (orange) (modified from reference 3).

METS = metabolic equivalents.

Figure 3. A representative Holter monitoring in a patient with spontaneous coronary vasospasm. Characteristic ST-segment elevation at early morning with rapid progression to ventricular tachyarrhythmia is well demonstrated.

Figure 4. Representative electrocardiograms showing various clinical presentations of patients with coronary artery vasospasm: acute coronary syndrome with deep T wave inversion in the precordial leads (A), prominent ST-segment elevation mimicking ST elevation myocardial infarction (B), development of ventricular fibrillation and ST elevation in aborted sudden cardiac death (C, D), and ST-segment depression during exercise treadmill test in a patient with effort-induced chest pain (E).

Figure 5. Serial coronary angiograms in a patient who developed coronary artery vasospasm after repeated interventions for fixed stenosis of the left anterior descending coronary artery.