Ventricular Fibrillation in a Patient with Multi-Vessel Coronary Spasm Four Days after the Initiation of an Oral Beta-blocker
Manabu Kurabayashi, Hidetoshi Suzuki, Yasuteru Yamauchi, Kaoru Okishige
Division of Cardiology, Yokohama City Minato Red Cross Hospital, Yokohama City, Japan
Doi: 10.12890/2016_000439 - European Journal of Case Reports in Internal Medicine - © EFIM 2016
Received: 13/05/2016
Accepted: 26/05/2016
Published: 06/07/2016

How to cite this article: Kurabayashi M, Suzuki H, Shimura T, Yamauchi Y, Okishige K. Ventricular fibrillation in a patient with multi-vessel coronary spasm four days after the initiation of an oral beta-blocker. EJCRIM 2016 EJCRIM 2016;3:doi:10.12890/2016_000439

Conflicts of Interests: The authors declare there are no competing interests.

This article is licensed under a Commons Attribution Non-Commercial 4.0 License

ABSTRACT

We describe a case of ventricular fibrillation occurring in a patient with multi-vessel coronary spasm after the initiation of an oral beta-blocker. A 56-year-old man began to experience chest discomfort and his computed tomography revealed intermediate coronary stenoses. He was administered medications including an oral beta-blocker but suddenly collapsed while walking 4 days later. An automated external defibrillator detected ventricular fibrillation and delivered successful electrical cardioversion. An acetylcholine provocation test after stabilization of the status revealed triple-vessel coronary spasm. Beta-blockers may provoke exacerbation of coronary spasm and result in lethal arrhythmia.

LEARNING POINTS

KEYWORDS

Coronary spasm, ventricular fibrillation, beta-blocker, acetylcholine provocation test.

INTRODUCTION

Beta-blockers have a vasoconstrictive effect and may provoke exacerbation of coronary spasm[1]. It is known that coronary spasm can cause serious arrhythmias and consequently sudden cardiac death[2]. We herein describe a case of ventricular fibrillation occurring in a patient with multi-vessel coronary spasm 4 days after the initiation of an oral beta-blocker.

CASE REPORT

A 56-year-old man with a history of dyslipidaemia began to experience chest discomfort on effort and at rest. He presented to a local hospital where coronary computed tomography revealed intermediate stenoses in the mid portion of the left anterior descending artery (LAD) and the first diagonal branch. The patient was prescribed medications including low-dose aspirin, a statin and a beta-blocker (atenolol 25 mg once daily), but his symptoms worsened.
Four days later he took his medications and went shopping on foot. At 10 am, he suddenly collapsed while walking. Cardiac massage was immediately performed by bystanders and after 5 min of resuscitation effort, an automated external defibrillator (AED) was attached. It detected ventricular fibrillation and delivered a successful electrical cardioversion (Fig. 1A). The AED electrocardiogram (ECG) record just after successful cardioversion showed ST-segment elevation (Fig. 1B), which disappeared promptly (Fig. 1C). After the return of spontaneous circulation, the patient was brought to the emergency department of our hospital.


(click to enlarge)
Figure 1: The electrocardiogram record of the automated external defibrillator.

DISCUSSION

Beta-blockers reduce heart rate and contractility, resulting in relief of myocardial ischaemia. However, blockade of the vasodilatory β2-adrenergic effect even with β1-selective agents[3] and relative enhancement of the vasoconstrictive α1-adrenergic effect[1] can result in exacerbation of coronary spasm and provoke lethal arrhythmia. In this case, the patient had experienced ventricular fibrillation 4 days after the initiation of an oral β1-selective adrenergic blocker, and was ultimately diagnosed as having multi-vessel coronary spasm. The fact that multi-vessel spasm was provoked by intracoronary injection of low-dose acetylcholine indicates that this patient’s baseline coronary artery tone may be high. To our knowledge, there are few cases of the initiation of oral beta-blocker therapy resulting in ventricular fibrillation in patients with coronary spastic angina.
Coronary spasm can cause critical ischaemic heart disease. In particular, multi-vessel spasm is often complicated by lethal ventricular arrhythmias[4], similar to our case. A previous study reported that reperfusion after coronary spasm, rather than coronary spasm itself, correlated with the onset of ventricular arrhythmia in some cases[4]. Those patients may not be diagnosed as having coronary spasm following emergency coronary angiography just after resuscitation. Physicians should perform a spasm provocation test after the patient has stabilized and emergency coronary angiography had not revealed any likely cardiac lesions, because coronary spasm was detected in 11% of patients who survived cardiac arrest without structural heart disease[5]. Coronary spasm is a more common cause of lethal ventricular arrhythmia or cardiac arrest than one might expect.


(click to enlarge)
Figure 2: Emergency coronary angiography and elective acetylcholine provocation test
References
  1. Robertson RM, Wood AJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation 1982;65:281–285.
  2. Takagi Y, Yasuda S, Tsunoda R, Ogata Y, Seki A, Sumiyoshi T, et al. Clinical characteristics and long-term prognosis of vasospastic angina patients who survived out-of-hospital cardiac arrest: multicenter registry study of the Japanese Coronary Spasm Association. Circ Arrhythm Electrophysiol 2011;4:295–302.
  3. Kaplan NM. Kaplan’s Clinical Hypertension. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2002:261–267.
  4. Myerburg RJ, Kessler KM, Mallon SM, Cox MM, deMarchena E, Interian A Jr, et al. Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm.N Engl J Med 1992;326:1451–1455.
  5. Krahn AD, Healey JS, Chauhan V, Birnie DH, Simpson CS, Champagne J, et al. Systematic assessment of patients with unexplained cardiac arrest: Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER). Circulation 2009;120:278–285.