Syncope Due to Advanced Atrioventricular Block Despite No Demonstrable Cardiac Disease

Syncope Due to Advanced Atrioventricular Block Despite No Demonstrable Cardiac Disease DANIEL KOSINSKI and BLAIR P. GRUBB From the Eloctrophysiology Section, Division of Cardiology, Medical College of Ohio. Toledo. Ohio KOSINSKI, D., ET AL.: Syncope Due to Advanced Atrioventricular Block Despite No Demonstrable Car-

diac Disease. Cardiovascular syncope can be due to a variety of abnormalities. Often, multiple testing modalities are necessarv to obtain an accurate diagnosis. We report on a young female patient witb recurrent syncope in whom conventional evaluation was unremarkable. A diagnosis was established by prolonged ambulatory monitoring. (PACE 1997; 20[Pt. 11:997-998) cardiovascular syncope, diagnostic methods, ambulatory monitoring

Introduction Syncope of uncertain etiology can he due to a variety of causes. In the evaluation of syncope of suspected cardiovascular etiology, it is often necessary to use a variety of diagnostic modalities in order to obtain an accurate diagnosis. We describe a case of syncope due to prolonged asystole in a yoinig patient with a normal cardiovascular evaluation. We will highlight the occasional necessity of applying prolonged ambulatory monitoring to diagnose patients when necessary. The patient was a 15-year-old previously healthy female who began to experience recurrent episodes of idiopathic syncope. Some episodes of syncope were preceded by a prodrome of dizziness; however, other episodes occurred quite abruptly. Scalar ECG was unremarkable, and Holter monitoring was also nondiagnostic. Electroeucephalography was also performed and was unremarkable. The patient was referred for cardiac evaluation. Echocardiography was performed and was normal. It was felt that with no primary structural or electrical heart disease, her episodes likely represented neurocardiogenic syncope. Head-upright tilt testing was recommended. On baseline head-upright tilt test, her heart rate was 72 beats/min and blood pressure was 114/68 mmHg. She tolerated 30 minutes of tih at a 70° tilt angle. Isoproterenol (1 jjig/minj was insti-

Address for reprints: Daniel Kosinski, M.D.. Division of Cardiology, Medical Collogo of Ohio, CS 10008, Toledo, OH 43699. Fax:"(419) 381-3041. Received October 1, 1996: revision October 22, 1996; accepled October 23. 1996.

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tuted and she was retilted at 70° for 10 minutes. She remained asymptomatic and had no significant changes in heart rate or blood pressure. Despite a negative tilt test, in light of the other information, a decision was made to empirically treat her for neurocardiogenic syncope. She was placed on a serotonin reuptake inhibitor (serzone. nefazadone hydrochloride [Bristol-Myers-Squibb. Princeton, N|, USA]). In addition, she wore an event recorder monitor. Approximately 5 weeks after her tilt test, she transmitted a rhythm strip during a period of presyncope. Complete heart block was observed. Approximately 3.5 hours later, she experienced a syncopal episode that was demonstrated to be due to high grade atrioventricular block (Fig. 1). Electrophysiological study was performed. which showed normal conduction intervals. Her atrio-Hisian interval was 84 ms (nl 60-120 ms) and her infra-Hisian conduction was 37 ms [nl 35-55 ms). Sinus node function was normal and the Wenkebach period of her atrioventricular node was 171 beats/min. During removal of her sheath at electrophysiology study, she experienced a vagal reaction. She was recommended to cardiac pacing, and a dual chamber cardiac pacemaker with hysteresis capability was placed (Marathon DR. Intermedics. Inc.. Angleton, TX, USA). She was also placed on fluorohydrocortisone. She subsequently developed several episodes of presyncope that were demonstrated to be aborted by pacing. Discussion The evaluation of syncope is often formidable, and occasionally, even despite aggres-

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KOSINSKI, ETAL.

Stfip Starting at 57seconds.Includes B.O seconds at 25 mm/s. Signal Gain: 10 mm/mv.i Comment

Rate: 3 6 l

Figure 1. Advanced atrioventricular block is seen during syncope.

sive evaluation, a clear etiology for the event(s) cannot be determined.^ In general, patients without structural heart disease have a better prognosis than those with structural heart disease. In younger patients without structural heart disease, neurocardiogenic syncope is a common etiology and this can generally be diagnosed with head upright tilt testing.^ In this group of patients, electrophysiological study has a Class II indication only in those witb a negative bead-upright tilt test.^ And indeed, in our case, electrophysiological study itself was unremarkable. It has been demonstrated that in some groups of patients prolonged

ambulatory monitoring maybe necessary to establish a diagnosis.•^'^ Our case illustrates several points: 1. Each diagnostic modality has its limitations, and occasionally, multiple modalities need to be used. 2. Even in patients without structural heart disease, it is necessary to be persistent in attempting to establish a definite diagnosis. 3. Wben conventional testing fails to establish a diagnosis, prolonged ambulatory monitoring may be of benefit.

References 1. Kapoor W. Diagnostic evaluation of syncope. Am I Med 1991; 90:91-106. 2. Kosinski D, Grubb BP. Neurally mediated syncope with an npdate on indications and usefulness of head upright tilt table testing and pharmacologic therapy. Gnrr Opin Gardiol 1994; 9:53. 3. Zipes DI. et al. Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures. I Am Goll Gardiol 1995; 26:555-573.

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Kinlay S, Leitch J, Neil A, et al. Gardiac event recorders yield more diagnosis and are more cost effective than Holter monitoring in patients with palpitations. Ann Intern Med 1976; 124:16-20. Krahn A. Klein G, Norris G, et al. The etiology of syncope in patients with negative tilt table testing and electrophysiology testing. Girculation 1995; 42: 1819-1824,

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