ST-segment elevation induced by coronary artery spasm during tilt-table test

A 57-year-old heavy-smoking man without prior medical history was referred for an elective tilt-table test after experiencing recurrent syncopal episodes of uncertain etiology. He denied any history of chest pain, palpitation or shortness of breath. Baseline electrocardiogram (ECG) was normal (Figure 1(a)). Ten minutes through the test, while at 70° from the horizontal plane, he started complaining of retrosternal squeezing chest pain with shortness of breath and diaphoresis during which he remained hemodynamically stable. ECG during this episode revealed ST-segment elevation (STE) in the anterolateral leads (Figure 1(b)). The patient was then laid supine and given one tablet of sublingual nitroglycerin and, 5 minutes later, chest pain and STE resolved (Figure 1(c)). Serial cardiac markers were not elevated. Coronary angiography revealed a nonocclusive 60% left anterior descending lesion. The patient did not experience further chest pain during the index hospitalization and was discharged on a calcium channel blocker and nitrate for coronary artery spasm.

Figure 1.

(a) Normal baseline ECG. (b) ECG performed 10 minutes through the test during chest pain revealing ST-segment elevation in the anterolateral leads. (c) ECG performed 5 minutes after sublingual nitroglycerin administration showing resolution of the elevated ST-segment.

The tilt-table test is generally considered a safe diagnostic tool utilized in the workup of patients with unexplained syncope. In rare instances, life-threatening complications occur as myocardial infarction [Goolamali et al. 2004], ventricular tachycardia [Yiu et al. 2011] and cardiac arrest [Wang et al. 2000] that are usually a consequence of coronary artery spasm or marked decrease in arterial blood pressure. The underlying mechanism of tilt-table test-induced coronary spasm is not clear. An accepted hypothesis is the augmented parasympathetic tone, which follows the increased sympathetic activity, provoking coronary spasm. Coronary spasm frequently occurs in an atherosclerotic lesion but can also occur in normal coronary arteries. In the presented case, the occurrence of STE that rapidly resolved after nitroglycerin therapy and the absence of occlusive coronary artery disease suggest that the underlying etiology is coronary artery spasm. A recent study showed that prior anginal symptoms were absent in 21 % of patients presenting with syncope due to coronary artery spasm [Togashi et al. 2013] and therefore coronary spasm should be ruled out in cases with unexplained syncope even without prior history of typical angina. The fact that our patient never had chest pain suggests that his prior syncopal events might be silent episodes of coronary artery spasm/ischemia. We propose that the occurrence of STE during tilt-table test should be immediately managed for probable coronary artery spasm with coronary vasodilators in addition to returning the patient to the supine position which can abort this episode and avoid complications.