Refractory Vasospastic Angina: When Typical Medications Don't Work

Abstract

Vasospastic angina (VSA) is defined as spasm of the coronaries leading to transient constriction and eventual myocardial ischemia. VSA is treated typically with calcium-channel blockers (CCBs) and nitrates. However, there are times when the vasospasm is refractory to typical medications. When this occurs, unconventional treatment modalities may be employed for symptomatic relief. We present a case of a 48-year-old-male with a history of inferior ST-elevation myocardial infarction (STEMI) status post percutaneous coronary intervention (PCI) with drug-eluting stent (DES) to the distal right coronary artery (RCA), who presented with recurrent angina. The pain was described as pressure-like, substernal, radiating to both arms, and similar to his previous STEMI presentation. On presentation to the emergency room, he had an elevated serum troponin with no electrocardiogram (EKG) changes. He was taken to the cath lab where it was found that he revealed severe focal stenosis just proximal to the previously placed stent. Immediately after guidewire passage into the RCA, acute vasospasm developed, resulting in diffuse, severe stenosis, extending over previously normal segments to the proximal RCA, resolving with intracoronary nicardipine and nitroglycerin, including the initial focal stenosis. The patient was diagnosed with VSA. Unfortunately, despite optimal medical therapy, he developed refractory VSA, requiring the use of unconventional treatment methods. Our patient presented with a lesser-known phenomenon called refractory VSA, where intermittent vasospasm continues despite being on a combination of two medications. Treatment for VSA is well-documented, however, little data is available for refractory VSA.

Keywords: acute coronary syndrome; nstemi; prinzmetal angina; refractory vasospastic angina; stemi; vasospastic angina.

Figure 1. Electrocardiogram on presentation to the emergency room

Normal sinus rhythm of 90 beats/min with normal axis and intervals. There is poor R-wave progression but no signs of acute ST-changes. There are old T-wave inversions in lead III.

Figure 2. Left heart catheterization demonstrating RCA from LAO 30

A: Focal stenosis of 90% in the distal RCA, which was determined to be a result of vasospasm. B: Vasospasm in the distal RCA with guidewire introduction. C: Diffuse vasospasm with guidewire in place, expanding from the distal to the proximal RCA. D: Vasospasm resolved with intracoronary nitroglycerin and intracoronary nicardipine. RCA - Right Coronary Artery; LAO - Left Anterior Oblique

Figure 3. Vasospastic angina pathophysiology

As smooth muscle hyperreactivity occurs, a cycle is initiated leading to spasm of the vessel and ischemia. If this spasm does not subside, infarction, arrhythmia, or even sudden cardiac death may occur.

Figure 4. Vasospastic and refractory vasospastic angina treatment

CAD - Coronary Artery Disease; CCB - Calcium Channel Blocker; PCI - Percutaneous Intervention