Description

A woman in her 70s was admitted to our emergency department (ED) with recurrent atypical chest pain and syncope. The episodes of chest pain occurred only at night and during sleep, lasting between 5 and 10 min, waking her up. The patient had been experiencing these episodes for the past 2 months. For this reason, she initiated a 24-hour Holter recording the day before being admitted to our ED, which she was still wearing during her first medical contact in our ED. However, what worried the patient and prompted the visit to the ED was the episode of syncope that occurred shortly after the onset of chest pain during the night, which had never occurred before. Her only cardiovascular risk factor was arterial hypertension, for which she was medicated with losartan and hydrochlorothiazide. Physical examination revealed no abnormalities, and she had a normal 12-lead ECG, a normal transthoracic echocardiogram and negative high-sensitivity troponin levels.

Since the patient experienced a chest pain episode during Holter monitoring, tracings were obtained, revealing increasing ST-segment elevation in lead II, followed shortly after by Mobitz I atrioventricular (AV) block and Mobitz II AV block (figure 1). ST-segment elevation lasted for about 5 min, and syncope occurred during this period. ST changes gradually normalised after the episode, as well as the conduction abnormalities, ending in T-wave inversion.

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Figure 1

24-hour Holter recording with ST-segment elevation in lead II, Mobitz I atrioventricular (AV) block, and Mobitz type II AV block during an episode of chest pain and syncope.

The patient was referred for coronary angiography, which showed an ectatic right coronary artery (RCA) with mild distal stenosis (figure 2). As the bradyarrhythmias were short-lived, and the patient was not taking specific medication for Prinzmetal angina (PA), we chose not to implant a pacemaker at this time. There were no further events during the hospital stay, and she was discharged with isosorbide dinitrate 40 mg two times a day, amlodipine 5 mg daily and atorvastatin 40 mg daily. As we did not implant a pacemaker, we chose not to administer non-dihydropyridine calcium channel blockers. The patient remained asymptomatic at the 3-month, 6-month and 1-year follow-up consultations, and serial Holter monitoring did not show further repolarisation or conduction abnormalities.

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Figure 2

Coronary angiography revealing ecstatic right coronary artery with mild distal stenosis.

PA is a clinical condition characterised by chest pain at rest accompanied by ST-segment elevation. In some cases, PA can result in serious complications such as ventricular arrhythmias, myocardial infarction, high-degree AV block or sudden cardiac death.1 The majority of patients with coronary artery spasm (CAS) predominantly experience symptoms at rest, primarily between 18:00 and 06:00. They also occur in a cyclical manner. CAS episodes tend to be prolonged and relatively resistant to nitrates. They also occur in a cyclical manner. Two-thirds of cases are women, and the condition is unrelated to cardiovascular risk factors. It has recently been demonstrated that CAS reflects the impairment of the vasodilator/anti-aggregatory synergy between nitric oxide and hydrogen sulphide.2 Crises of CAS are associated with inflammatory damage to the endothelial glycocalyx layer, resulting in platelet activation and aggregation: this is reversed by infusion of N-acetylcysteine, a hydrogen sulphide donor. Given that the ORBITA trial3 revealed that stenting of large coronary stenoses was ineffective for the prevention of (exercise-induced) angina, it is conceivable that overt CAS plays a role.

The diagnosis of PA can be made based on symptoms, ST-segment changes during an anginal episode or invasive provocative testing. Holter monitoring is a useful tool for diagnosing PA, as chest pain is only present in 20%–30% of cases of ischaemic ST-segment elevation.4 The mainstay of treatment for PA is medical and non-medical therapy, with calcium-channel blockers and nitrates being the primary therapies.5 Less is known about the best management of patients with PA who develop bradyarrhythmias, as there are only a handful of case reports.6 7 In both cases, pacemaker implantation was decided due to more severe presentation. In our case, ECG changes were inferior and were associated with mild stenosis in the RCA, which increases the probability of AV block (the AV nodal artery usually arises from the RCA). Nonetheless, the presence of AV block could have been complicated by development of torsade de pointes, reason of temporary pacemaker implantation prior to acetylcholine coronary reactivity testing.

However, in our case, medical therapy successfully managed coronary spasm and AV block, leading to symptom-free follow-up. Therefore, pacemaker implantation should be considered only for refractory or severe cases.