Cardiovascular Drugs and Therapy 1992;6:139 © Kluwer Academic Publishers, Boston. Printed in U.S.A.
Letter to the E d i t o r
Syncope and Recurrent Long Sinus Arrest in VasospasticAngina
tool to evaluate the intrinsic sinus node function in patients with certain types of ischemic heart disease.
Junichi Hasegawa, Hideyuki Kitamura, Hiroto Mashiba
Junichi Hasegawa, MD, DMSc Hideyuki Kitamura, MD Hiroto Mashiba, MD, DMSc Department of Internal Medicine Saihaku Hospital & Tottori University 397 Yamato, Saihaku, Tottori 683-03 Japan
Dear Sir, Recently, pharmacological autonomic nerve blockade has been applied as a tool to evaluate the intrinsic sinus node function in patients with the sick sinus syndrome . Although ischemic heart disease has been recognized as an underlying disease of sinus dysfunction, it may involve transient and reversible ischemic disease, such as vasospastic angina. In such patients, pharmacological autonomic nerve blockade using atropine and propranolol may fail to show the intrinsic sinus node function, because propranolol may induce coronary vasospasm, sometimes in patients with vasospastic angina [2-5]. We report a case of a 52-year-old man who showed anginal attacks, syncopes, and recurrent long sinus arrests (3-5 sec, Fig. 1) during Holter monitoring. The electrophysiologic study without drugs revealed a normal sinus node recovery time (1350 msec) and sinoatrial conduction time (104 msec). Coronary arteriography revealed an intact coronary artery system, and the provocation test for coronary spasm using ergonovine maleate was positive. Antianginal therapy using nitrates and a calcium antagonist (diltiazem, 30 mg four times daily), which often aggravates the symptoms in patients with sinus node dysfunction, prevented not only anginal attacks, but also sinus arrests, as confirmed in multiple records of Holder monitoring. This case suggests that transient and reversible ischemia is a cause of symptoms similar to those of sick sinus syndrome and that pharmacological autonomic nerve blockade using atropine and propranolol is not always a perfect
References 1. Jordan JL, Yamaguchi I, Mandel WJ. Studies on the mechanism of sinus node dysfunction in the sick sinus syndrome. Circulation 1978;57:217-223. 2. Yasue H, Omote S, Takizawa A, et al. Exertional angina pectoris caused by coronary arterial spasm: Effects of various drugs. Am J Cardiol 1979;43:647-652. 3. Robertson RM, Wood A J J, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation 1982;65:281-285. 4. Kagiyama K, Yasue H, Horio Y, et al. Effects of propranolol and nifedipine on exercise-induced attack in patients with variant angina: Assessment by exercise thallium-201 myocardial scintigraphy with quantitative rotational tomography. Circulation 1986;74:374-380. 5. Nanas JN, Sutton RB, Alazraki N, Tsagaris J. Acute myocardial infarction in post infarct patient possibly through beta blocker-induced coronary artery spasm. Am Heart J 1987; 113:388-391.
Fig. 1. Long sinus arrests observed in 24-hour ambulatory recording (lead: CMs). The recording gain was reduced to lh of usual recording (2.5 mm = 1 mV). Each episode (A and B) was preceded by anginal pain. 139