Cardio Case Challenge: Syncope in a 53-Year-Old Woman With Dyspnea and Morning Chest Pain

Maria Cristina Bravi, MD, PhD


April 18, 2022


Analysis of the patient's cardiac monitoring during her cardiac arrest was diagnostic. During the episode of chest pain, which began at 7:37 am, the tracing revealed hyperacute T waves in the inferior leads, II, III, and aVF (Figure 1).

Figure 1.

Diffuse T-wave inversions in the precordial leads were also seen. The patient described an unpleasant sensation like "a brick" on her chest, with associated dyspnea. She appeared pale and diaphoretic. Twenty minutes later, at 7:57 am, the monitoring demonstrated ST-segment elevation of 2-3 mm in the inferior leads with reciprocal depressions in the anterioseptal leads (Figure 2). The ST-segment elevations increased to between 8 and 10 mm (Figure 3), and subsequently degenerated into polymorphic ventricular tachycardia (Figure 4).

Figure 2.

Figure 3.

Figure 4.

A few minutes later (at 8:01 am), she spontaneously converted to a supraventricular tachycardia with frequent premature ventricular contractions, and then to a sinus rhythm. During the ventricular arrhythmia, the patient experienced cardiac arrest but recovered spontaneous circulation and regained consciousness after 2 minutes of CPR with concomitant spontaneous cardioversion. Immediately following the event, the patient underwent coronary angiography; no evidence of coronary artery disease was noted. During angiography, vasospasm of the right coronary artery was witnessed and successfully treated with intracoronary injection of nitroglycerin. Angiographic findings lead to the diagnosis of coronary artery spasm (CAS) or Prinzmetal angina.

In 1959, Prinzmetal and colleagues described a syndrome characterized by nonexertional chest pain and ST-segment elevation.[1] The episodes of chest pain occurred in a cyclic manner, especially in the early morning hours. This syndrome was named Prinzmetal angina or variant angina. Coronary artery vasospasm without atherosclerotic lesions is hypothesized to be the pathophysiologic mechanism responsible for the associated chest pain and ST-segment elevation. Vagal withdrawal or changes in sympathetic activity may play a role in CAS.[2] Endothelial dysfunction with reduced nitric oxide synthase is a contributory factor in CAS even though it has been demonstrated that basal nitric oxide levels do not appear to be decreased during coronary spasm.[3] Another possible mechanism for CAS may be the effects of p122 protein on phospholipase C-δ1activity.[4] In a small study, investigators determined that not only does the p122 protein appear to be upregulated in patients with coronary spasm, thus enhancing vasomotility, but it also increases intracellular calcium to acetylcholine.


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