Case Report

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American Journal of Emergency Medicine

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American Journal of Emergency Medicine 31 (2013) 996.e1-996.e4

Bradyarrhythmic syncope in a patient with Prinzmetal’s variant angina: a case report?

Abstract

We present the case of a 46-year-old woman with Prinzmetal’s angina and syncope due to severe bradyarrhythmias. Dynamic electrical changes were documented on 12-lead 24-hour electrocar- diographic (ECG) monitoring. We highlight the importance of continuous ECG monitoring in making the diagnosis and the indication for permanent cardiac pacing in this case.

Myron Prinzmetal first described a “variant” form of angina in his classic 1959 publication. This is a distinct clinical entity characterized by episodes of chest pain occurring at rest, associated with ST-segment elevation [1]. In some cases, vasospasm-induced ischemia causes life- threatening ventricular arrhythmias, transient high-degree atrioven- tricular (AV) block, asystole, with syncope, and even sudden cardiac death [2]. Only few reports of syncope related to bradyarrhythmias in this context exist in the literature, and the therapeutic options are still debated. These cases are mainly presented as short snap-shot of arrhythmic events and not in conjunction with the dynamics of the ST- segment changes during the whole episode. To the best of our knowledge, this is the first case when both the evolution of the ST- segment changes and bradyarrhythmic events are documented based on 12-lead ECG continuous monitoring during a typical Prinzmetal’s attack associated with syncope.

A 46-year-old woman was admitted with recurrent Atypical chest pain only at rest, never on exertion. She had similar attacks during the previous months, always during the night. She also describes 2 episodes of syncope. She was premenopausal. Her only Cardiovascular risk factor was smoking (30 pack years). She had no other medical history. Physical examination, cardiac biomarkers, resting ECG, and echocardiography were normal. An ambulatory treadmill test 1 week before admission was negative.

The patient had a typical attack during the 12-lead ECG continuous monitoring. The tracing revealed increasing ST-segment elevation in leads II, III, aVF, V₅, and V₆ (Fig. 1A and B). The ischemic attack was followed by both AV conduction disturbances and severe Sinus bradycardia (Figs. 1B andC and 2). The whole episode lasted 27 minutes and was accompanied by typical Adams-Stokes syncope. The ST-segment elevation, and reciprocal ST changes gradually disappeared. Consequent- ly, both the sinus rhythm and AV conduction progressively improved and returned to normal at the end of the aforementioned period.

Treatment with oral nitrates, nifedipine, aspirin, and atorvastatin was initiated. She was referred for coronary angiography, which

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excluded significant coronary artery stenosis (Fig. 3). In view of the severity of bradyarrhythmias and the lack of evidence for the safety of medical treatment alone, we decided on permanent cardiac pacing with a bicameral pacemaker. She was discharged with the following medication: isosorbit 5-mononitrate 40 mg/d, verapamil R 240 mg/d, and atorvastatin 80 mg/d. We advised smoking cessation and avoidance of ?-blockers. The evolution was favorable at 1 and 3 years of follow-up. The patient was free of symptoms, and the 24-hour Holter ECG monitoring revealed no abnormality.

We stress the important role of 24-hour ECG Holter monitoring in making the correct diagnosis of Prinzmetal’s variant angina (PVA) in our patient. A 24-hour or 48-hour Holter recording can be definitive in the diagnosis, but its value relies on the frequency of attacks [3]. Continuous 24-hour Holter ECG monitoring of patients with PVA could reveal serious cardiac arrhythmias, but only in 50% to 60% of cases [4]. These arrhythmias are generally associated with marked ST-segment elevation of 4 mm or more [5,6]. Bradyarrhythmias are associated with acute ST elevations in the inferior leads, whereas ventricular arrhythmias can be seen with acute ST elevations in the anterior leads [4].

Calcium-channel blockers and nitrates represent the First-line treatment for PVA. Short-acting nitrates are useful as relievers and long-acting nitrates are useful for preventing ischemic attacks [7]. A survey by Kimura and Kishida [8] showed that calcium-channel blockers were effective in 92.5% of patients. Despite these global data, we suggest that nondihydropyridine calcium-channel blockers should be avoided in a patient with documented Severe bradycardia because of the unpredictable risk of negative chronotropic effect.

The prognosis of vasospastic angina is generally good when there is no significant coronary artery stenosis [9]. However, little is known about patients with associated severe bradyarrhythmias. In 1968, Giannely first reported a case where a permanent pacing system has been implanted because of high-degree AV block and syncope during episodes of Prinzmetal’s angina [10]. There are only few cases reported in the literature since then. When medical therapy alone was considered, it was seldom helpful in preventing high-degree AV block. Thus, the effectiveness and the safety of medical treatment remain a therapeutic dilemma in patients with PVA and coexisting severe bradyarrhythmias. To avoid an unacceptable risk as syncope or even worse, sudden cardiac death, a cardiac pacemaker should be implanted as a first-line therapy.

Although the indication for cardiac pacemaker implantation in PVA is not established in latest guidelines, we propose that it should be a strong indication in high-risk patients. In our case, we considered permanent cardiac pacing very early on, given the severity of bradyarrhythmias.

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R-N. Siliste et al. / American Journal of Emergency Medicine 31 (2013) 996.e1–996.e4

Fig. 1. Twelve-lead 24-hour ECG monitoring. A, Beginning of ST elevation in inferior and lateral leads. B, A monophasic deflection including the QRS complex, the ST segment, and T waves in inferior and lateral leads with reciprocal changes in DI, aVL, and V₁ to V₃. C, Prolonged pause due to sinus dysfunction interrupted by a ventricular escape complex.

R-N. Siliste et al. / American Journal of Emergency Medicine 31 (2013) 996.e1–996.e4

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Fig. 2. Twelve-lead 24-hour ECG monitoring. D, Junctional escape rhythm followed by sinus rhythm with first-degree AV block. E, Complete suprahisian AV block. F, Type I Mobitz second-degree AV block. This was followed by first-degree AV block and finally by normalization of the AV conduction.

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Calin Siliste MD, PhD

University of Medicine and Pharmacy “Carol Davila“

Bucharest, Romania University and Emergency Hospital of Bucharest, Romania E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2013.01.024

Fig. 3. Right coronary angiogram in left anterior oblique projection showing a large vessel without significant lesions.

Roxana-Nicoleta Siliste MD, PhD Ilinca Savulescu-Fiedler MD, PhD

University of Medicine and Pharmacy “Carol Davila“

Bucharest, Romania Department of Internal Medicine and Cardiology Coltea Clinical Hospital, Bucharest, Romania

References

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