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Sinus node dysfunction associated with discontinuation of cilostazol in a patient taking atenolol
Editor—We wish to report a case of cardiac arrest followed by an episode of severe bradycardia associated with discontinuation of the antithrombotic agent cilostazol in a patient taking atenolol. Cilostazol is recognized to have cardiovascular effects.1A 72-yr-old man (157.6 cm, 49.2 kg) with atherosclerotic disease in arteries of his right lower leg was scheduled to undergo femorotibial reconstruction. He had a history of hypertension and diabetes mellitus. His medication included cilostazol 100 mg daily, atenolol 25 mg daily, amlodipine 5 mg twice daily, doxazosin 1 mg twice daily, and insulin 5 units three times daily. Cilostazol was discontinued five days before the operation. The heart rate gradually decreased from 75 beats min–1 to 60 beats min–1 over the next 2 days. Atenolol, amlodipine, and doxazosin were continued up to the day of surgery. Insulin was stopped on the day of operation.
Before induction of general anaesthesia, the heart rate was 60 beats min–1 and blood pressure was 140/62 mm Hg. General anaesthesia was induced with propofol. Tracheal intubation was facilitated by vecuronium. Anaesthesia was maintained with sevoflurane 0.6–0.8% and nitrous oxide 67% in oxygen and fentanyl. After induction, the patient had a heart rate of 50 beats min–1 and a blood pressure of 130/40 mm Hg. Approximately 2 h after induction of anaesthesia, the deep femoral artery was clamped to remove thrombus. The cross clamping time was 68 min. Before unclamping, heart rate and blood pressure were 50 beats min–1 and 130/40 mm Hg. Arterial blood gas analysis revealed pH 7.41, 
39 mm Hg, 
150 mm Hg, and base excess +0.7, with a serum potassium of 4.6 mmol litre–1. Four minutes after unclamping, the patient had a cardiac arrest (asystole). After 4 min of closed-chest cardiac massage, and administration of atropine 1 mg and epinephrine 1 mg, cardiac rhythm was restored. Thereafter, heart rate and blood pressure were stabilized at 80 beats min–1 and 130/40 mm Hg using dopamine 5 µg kg–1 min–1, and arterial blood gas analysis revealed a pH 7.43, 35.6 mm Hg, 373 mm Hg, and a base excess +0.4, with a serum potassium of 4.9 mmol litre–1. Electrocardiogram showed no ST segment elevation before or after the event. The patient was transferred to the intensive care unit on dopamine and a propofol infusion. Approximately 30 min later, severe bradycardia (26 beats min–1) was noted. Epinephrine 1 mg was administered and the heart rate returned to 60 beats min–1. Coronary angiography, echocardiogram, and 24 h Holter monitoring revealed no abnormalities. The patient was discharged from hospital on the 17th day after surgery without further sequelae.
Cilostazol increases heart rate,1 2 whereas atenolol decreases it. In this patient, cilostazol was stopped 5 days before surgery and atenolol was continued up to the day of operation. The heart rate gradually decreased after stopping the cilostazol. It may be that discontinuation of cilostazol combined with continuation of a ß-blocking agent impaired the balance between the tachycardiac effect of cilostazol and the bradycardic action of atenolol, leading to perioperative sinus node dysfunction.
As the base excess and serum potassium did not change after unclamping of the deep femoral artery, which was performed 4 min before the cardiac arrest, metabolic factors would have only had a minor influence on the cardiac arrest. In addition, the likelihood of myocardial infarction, coronary spasm, or sick sinus syndrome,3 occurring during general anaesthesia in this patient should be small.
As cilostazol has antiplatelet properties,1 it is commonly stopped before surgery. In contrast, ß-blocking drugs should be continued perioperatively.4 However, discontinuation of cilostazol in a patient taking ß-blocking drugs may result in sinus dysfunction. Adjustment of the dose of a ß-blocker should be considered when cilostazol is discontinued preoperatively.
Yamanashi, Japan
References
1 Woo SK, Kang WK, Kwon KI. Pharmacokinetic and pharmacodynamic modeling of the antiplatelet and cardiovascular effects of cilostazol in healthy humans. Clin Pharmacol Ther 2002; 71: 246–52[CrossRef][Medline]
2 Atarashi H, Endoh Y, Saitoh H, Kishida H, Hayakawa H. Chronotropic effects of cilostazol, a new antithrombotic agent, in patients with bradyarrhythmias. J Cardiovasc Pharmacol 1998; 31: 534–9[CrossRef][Web of Science][Medline]
3 Ishiyama T, Hanagata K, Yamaguchi T, Matsukawa T, Kashimoto S, Kumazawa T. Undiagnosed sick sinus syndrome manifest during combined general and cervical epidural anesthesia. J Anesth 2000; 14: 102–4[Medline]
4 London MJ, Zaugg M, Schaub MC, Spahn DR. Perioperative ß-adrenergic receptor blockade: physiologic foundations and clinical controversies. Anesthesiology 2004; 100: 170–5[CrossRef][Web of Science][Medline]
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