Coronary artery spasm is a unique type of coronary artery disease. Spasms can occur in angiographically normal vessels or at sites of atherosclerotic lesions. Its clinical manifestations and treatment strategies differ significantly from those of typical coronary artery disease.
Patients with coronary artery spasm are often younger, and apart from smoking, most lack the classic risk factors for atherosclerosis. Smoking, alcohol use, and drug abuse are important triggers for coronary artery spasm.
The condition is characterized by rest angina, which occurs without physical exertion or emotional stress as triggers. Episodes typically occur between midnight and 8 a.m. Patients may experience syncope due to malignant arrhythmias. In rare cases, sustained and severe coronary artery spasm can lead to acute myocardial infarction (AMI) or even sudden cardiac death.
If the spasm causes vascular occlusion, the clinical presentation includes rest angina with transient ST-segment elevation on the electrocardiogram (ECG). These patients have distinct clinical features: rest angina differentiates them from stable angina; transient ST-segment elevation distinguishes them from stable angina, unstable angina (UA), and non-ST-segment elevation myocardial infarction (NSTEMI); and the transient nature of the ST-segment elevation differentiates them from ST-segment elevation myocardial infarction (STEMI). This allows for a direct diagnosis (previously referred to as variant angina or Prinzmetal's angina). However, non-occlusive coronary artery spasm may present with ST-segment depression or T-wave changes, making it more challenging to differentiate from typical angina. Additionally, coronary artery spasm is often self-limiting, and its transient nature makes it difficult to capture on ECG or conventional coronary angiography. Long-term ambulatory ECG monitoring can help detect ST-segment changes during symptomatic episodes. Definitive diagnosis often requires provocative testing with acetylcholine or ergonovine.
The mainstay of treatment for coronary artery spasm includes cessation of smoking and alcohol along with the use of calcium channel blockers and nitrates. For cases involving microvascular spasm, nicorandil may be considered. Beta-blockers may exacerbate or trigger spasms and should not be used alone in patients with variant angina. However, they are not contraindicated in patients with coexisting fixed stenoses.
The prognosis for coronary artery spasm is generally favorable, with a 5-year survival rate of 89%-97%. However, patients with multivessel or left main coronary artery spasm have a poorer prognosis.