Prinzmetal’s angina, also called variant angina, is a type of angina that originates from coronary vasospasm.1 Prinzmetal’s angina often produces chest pain-like symptoms precipitated by myocardial ischemia occurring almost exclusively at rest. It is often not triggered by exertion or emotional stress, and is sometimes associated with ST elevation.2 Variant angina is generally a benign disease with self-limiting symptoms. Ventricular arrhythmias such as polymorphic ventricular tachycardia that can lead to cardiac sudden death can be seen.3 Other important clinical features of variant angina include the high frequency of asymptomatic ischemic episodes and the syncope that sometimes occurs during the ischemic episodes.4
Syncope is due to severe arrhythmias, including ventricular tachycardia, ventricular fibrillation, and high-degree atrioventricular block.4
There are multiple precipitating factors that play a role in the pathophysiology of Prinzmetal’s angina. Specifically, the deficient basal release of nitric oxide (NO) due to endothelial dysfunction, and enhanced vascular smooth muscle contractility with the involvement of the Rho/Rho-kinase pathway are reported to play important roles in the pathogenesis of coronary artery spasm.4 Other precipitating factors of coronary artery spasm include imbalance in autonomic nervous activity, increased oxidative stress, chronic low-grade inflammation, magnesium deficiency, and genetic susceptibility.4 Genetics have also been found to play a role with coronary artery spasm such as gene polymorphisms of endothelial NO synthase (NOS), paraoxonase, and other genes.4
The diagnosis is often confirmed by demonstrating ST segment elevation during an episode of angina and subsequently by inducing multi-vessel coronary spasm with ergonovine.5 Most often Prinzmetal’s angina can be successfully treated with antianginal agents such as calcium channel blockers and long-acting nitrates.4
A 65-year-old male with no significant past medical history except tendonitis and hyperlipidemia presented status post out-of-hospital cardiac arrest. The patient originally had complained of chest discomfort and tightness in the chest for about one week prior to presenting to the hospital. The patient noted dizziness and diaphoresis during these episodes. The most recent of these episodes culminated with a severe episode of chest tightness, diaphoresis and syncope; the patient was given CPR by their spouse for a couple of minutes prior to the arrival of paramedics. As witnessed by the spouse, the patient turned blue and had transient seizure-like activity. EKG in the field showed less than 1 mm of ST elevation in II, III, and aVF, and some flattening of the ST segment in the anterior precordial leads. Upon arrival to the hospital, the ST changes had reverted back to normal. Serial cardiac enzymes were negative, electrolytes were within normal limits, and echocardiogram revealed normal LV function and no valvular abnormalities were noted. The patient then underwent left heart catheterization, which showed no significant occlusive coronary artery stenosis.
The patient eventually discharged home on a ZOLL LifeVest for presumed out-of-hospital cardiac arrest. The patient had one episode of similar chest pain — the LifeVest alarm was activated, and he was able to disable the device from shocking him as his arrhythmia self-terminated after 9.5 sec. He developed ST elevation, clearly seen in Figure 1, prior to initiation of polymorphic VT.
The patient was then brought to the hospital for insertion of a dual chamber ICD. The patient tolerated the procedure with no significant complications, and was later discharged from the hospital.
Shortly thereafter, the patient had two episodes of ventricular tachycardia. Both episodes were pace terminated into ventricular fibrillation, both requiring ICD shocks (Figure 2). The patient was then placed on amiodarone and metoprolol, and placed on a 30-day event monitor.
A couple of days later, he developed another episode of chest pressure associated with ST elevation just prior to development of recurrent ventricular tachycardia and ventricular fibrillation.
This finding is suggestive of Prinzmetal’s vasospasm-induced ventricular tachycardia. The patient was more aggressively treated with Imdur, L-Arginine, and beta blocker was uptitrated.
The patient’s anginal symptoms continue to improve, and his arrhythmias also have subsided with aggressive antianginal mediations.
This is a very interesting case that clearly demarcates the association of ST elevation with life-threatening ventricular arrhythmias. His ST elevation was confirmed on the scene, on the Holter monitor, and on the LifeVest monitor. It is unclear the incidence of sudden cardiac death related to this phenomenon, but this should be thought after as an etiology for patients presenting with chest pains prior to their cardiac arrest or prior to their syncope. It is likewise of great importance of the early and aggressive treatment in these patients with multiple antianginal medications until they have no more chest pains and to consider them for ICD implantation early on in their course to avoid sudden cardiac death.
- Prinzmetal M, Kennamer R, Merliss R, et al. Angina Pectoris. I. A variant form of angina pectoris; preliminary report. Am J Med 1959;27:375–388.
- Tsurukawa T, Kawabata K, Miyahara K, et al. Sudden death during Holter electrocardiogram monitoring in a patient with variant angina. Intern Med 1996;35:966–969.
- Yuksel UC, Celik T, Iyisoy A, et al. Polymorphic ventricular tachycardia induced by coronary vasospasm: A malignant case of variant angina. Int J Cardiol 2007;121:210–212.
- Kusama Y, Kodani E, Nakagomi A, et al. Variant angina and coronary artery spasm: The clinical spectrum, pathophysiology, and management. J Nihon Med Sch 2011;78:4–12.
- Chin A, Casey M. Variant angina complicated by polymorphic ventricular tachycardia. Int J Cardiol 2010;145:e47–49.