Symptomatic swallowing-induced paroxysmal supraventricular tachycardia

DIAGNOSTIC SHELF

Symptomatic Swallowing-Induced Paroxysmal Supraventricular Tachycardia

DAVID M. MIRVIS, MD JACK P. BANDURA, MD, PhD DANIEL A. BRODY, MD, FACC

Memphis, Tennessee

A 55 year old woman with palpitations during ingestion of food or drink was

evaluated with surface, esophageal and dynamic electrocardiographic techniques. Recordings documented the consistent induction of supraventricular tachycardia by swallowing; no definable gastrointestinal or other cardiac abnormality was present. Nine previously reported cases are reviewed, with special reference to the role of vagovagal reflexes in the pathogenesis of this unusual clinical syndrome.

Physical m a n e u v e r s such as eyeball compression a n d the Valsalva m a neuver are c o m m o n l y effective in converting p a r o x y s m a l s u p r a v e n tricular tachycardia to normal sinus r h y t h m . 1 By increasing vagal tone, t h e y alter the critical relations between refractory periods and conduction velocities needed to sustain r e e n t r a n t a r r h y t h m i a s . 2 I n d u c t i o n of these t a c h y a r r h y t h m i a s by physical m a n i p u l a t i o n s is considerably less c o m m o n . One such association is swallowing-induced atrial tachycardia. Although it was first described by Sakai and Mori 3 in 1926, only a few cases T M have been reported and its origin is unclear. We r e p o r t here one such case studied with esophageal and d y n a m i c electrocardiographic techniques. C a s e Report

From the Department of Medicine, University of Tennessee Center for the Health Sciences, Memphis, Tennessee. This study was supported in part by Grants HL-01362, HL-14032 and HL09495 from the National Heart, Lung, and Blood Institute, U. S. Public Health Service, Bethesda, Maryland and by a grant from the Southern Medical Association. Manuscript received September 7, 1976; revised manuscript received October 12, 1976, accepted October 20, 1976. Address for reprints: David M. Mirvis, MD, University of Tennessee Center for the Health Sciences, 951 Court Avenue, Room 339M, Memphis, Tennessee 38163.

A 55 year old woman was referred for evaluation of palpitations. Approximately 6 months before referral she noted the onset of an irregular heartbeat and short runs of rapid regular palpitations during meals and, particularly, with the ingestion of hot coffee or tea. Palpitations were noted only rarely at other times. Apprehension accompanied each episode. She denied chest pain and symptoms of pulmonary or peripheral circulatory congestion, gastrointestinal or biliary tract dysfunction. Five years before evaluation, she had hypertension and was effectively treated with a hydralazine-thiazide combination. She consumed an average of three cups of coffee and two cups of tea a day but did not drink alcoholic beverages or use tobacco products. Physical examination demonstrated a mildly obese apprehensive patient with an intermittently irregular pulse but no other abnormal findings. Routine laboratory studies including chest roentgenograms, serum electrolyte determinations and thyroid function tests were normal as were radiographic studies of the upper gastrointestinal tract including cineesophagrams. Esophageal manometric studies were normal; esophageal distension at multiple levels did not induce arrhythmia. An echocardiographic evaluation yielded normal findings; the left atrial size and mitral valve movements were normal. Resting 12 lead electrocardiograms and a Frank lead vectorcardiogram were normal. The P-R interval measured 0.18 second, there were no delta waves and the corrected Q-T interval was normal. A 24 hour Holter dynamic electrocardiographic record revealed numerous episodes of supraventricular tachycardia (Fig. 1). Of 87,207 beats monitored, 8,629 (9.9 percent) were atrial premature beats or beats occurring within runs

May 4, 1977 The American Journal of CARDIOLOGY Volume 39

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SWALLOWING-INDUCED

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FIGURE 1. An example of supraventricular tachycardia recorded simultaneously on three channels using an esophageal electrode. Swallowing was initiated after the first QRS-T complex, as indicated by the dark bullets. Of note are the initiation of the tachycardia by an atrial premature beat different from the sinus P wave (first P wave of each panel), the prolonged P-R interval of this beat relative to that of sinus beats and the variation of P-P intervals during the paroxysm. 11= lead II; BE = bipolar recording from the esophageal electrodes, 37 cm and 36 cm distal to the nares; UE = unipolar recording from the esophageal lead placed 37 cm distal to the anterior nares. Paper speed = 50 mm/sec.

of supraventricular tachycardia. The majority occurred during the three major meals and with ingestion of coffee (Fig. 2); the sleep period was almost free of tachycardia. An esophageal lead electrocardiogram was recorded using a previously described bipolar lead. 12 Within two cardiac cycles after the onset of dry swallowing, short bursts of a supraventricular tachycardia were consistently recorded (Fig. 1). Carotid sinus massage did not induce the arrhythmia and the intravenous injection of 1.0 mg of atropine did not abolish it. A total of 78 episodes were recorded using the esophageal lead technique. In each, the tachycardia was initiated by an atrial premature depolarization falling near the end of the T wave of the preceding sinus beat, that is, with a coupling interval of 54 + 6 percent (mean + I standard deviation) of the preceding R-R interval. The P wave configuration of the initiating beat differed from that of the sinus P wave in both unipolar and bipolar esophageal records (Fig. 1); however, the initiating P wave was similar to all subsequent P waves. The atrial rate during the tachycardia varied both within a given episode and in successive runs. Each episode consisted of 5.0 4- 2.2 beats. The rate ranged from 148 to 210 beats/min

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during these paroxysms, with an interval heart rate of 75 to 105 beats/min. Therapy with digoxin (0.25 mg daily), an anticholinergic agent (Pro-Banth;ne ®, 15 mg orally, four times daily) and orally administered propranolol (160 mg daily) was without effect. Quinidine sulfate (200 mg six times daily) abolished the arrhythmia. The frequency, duration and rate of the tachycardia during therapy did not differ (P >0.2) from pretreatment values. Discussion

Since the first report of swallowing-induced tachycardia ("schlucktachykardie") by Sakai and Mori 3 in 1926, isolated cases have appeared in the European 4,6,7 and American 1,5,s-ll literature. All the reported cases were characterized by reproducible induction of paroxysmal atrial tachycardia of varying duration by swallowing in the absence of known cardiac or esophagogastric disease. A single case of swallowing-induced atrial fibrillation, an abnormality electrophysiologically akin to atrial tachycardia, has also been described. 13 Eleetrophysiologic basis of the dysrhythmia: The electrophysiologic origin of the tachycardia is unknown. Some 1°,11 suggest that an ectopic focus is operative whereas others s support a reentrant pathogenesis. Without complete invasive electrophysiologic studies, 14-16 a specific mechanism cannot be established. However, the intracardiac studies of Engle et al. 11 and the recording of upright P waves in the inferior leads in our case suggest an atrial rather than an atrioventricular (A-V) nodal or subjunctional origin of the abnormal impulses. Mechanism of tachycardia: Direct mechanical versus vagal stimulation: The mechanism for this unusual association remains speculative. Some 9,11,13 suggest a direct mechanical interaction between the distended esophagus and the adjacent left atrium. Two observations are offered as support. First, both Bajaj et al.9 and Cohen et al. 13 reported induction of arrhythmia by inflation of an intraluminal esophageal balloon at, and only at, the subcarinal level. In other cases, as in ours, atrial esophageal distension was not arrhythmogenic. Second, the intracardiac electrograms described by Engle et al. 11 suggest a left atrial origin of the atrial forces.

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FIGURE 2. Representative samples of a Holter heart rate trend recording. Six 30 minute segments are illustrated corresponding to periods of sleep (A, 3:30 to 4:00 AM), eating breakfast (B, 7:15 to 7:45 AM), eating lunch (C, 11:40 AM to 12:10 PM), drinking coffee (D and E, 1:40 to 2:10 PM and 3:05 to 3:35 PM, respectively) and eating dinner (F, 5:10 to 5:40 PM). Apparent is the temporal association of swallowing-related activity and frequent episodes of tachycardia.

SWALLOWING-INDUCED TACHYCARDIA--MIRVIS ET AL.

An alternate proposal is that a reflex arc is operative, 5,7,8,1° with the afferent limb activated by swallowing. The most commonly considered path of such a reflex is a vagovagal arc, consonant with the known predominance of vagal afferents in the alimentary tract. Although the more commonly observed result of vagotonia is suppression of supraventricular tachycardia, there are substantial experimental and clinical data demonstrating that induction of tachyarrhythmias may occur. Nahum and Hoff 17 provoked atrial fibrillation in the dog by local application of methacholine to the area of the sinus node, an effect blocked by prior atropinization. Topical application and intravenous injection of acetylcholine similarly resulted in numerous atrial extrasystoles followed by atrial fibrillation, ls-21 An increase in the vulnerability of the atria to fibrillation induced by a single appropriately timed stimulus has also been reported. 2°,22

The mechanism of this seemingly paradoxic effect of vagotonic agents is unknown 23 although it may be given an electrophysiologic basis. Vagal stimulation reduces the relative refractory periods of atrial tissue but in a nonuniform manner. 24This temporal dispersion of recovery periods may then lead to circuitous pathways resulting in abnormal beats. Acetylcholine prolongs the relative refractory period of the A-V node, 2 a site frequently included in the reentry path of supraventricular tachycardias. 16 This prolongation may also lead to circus movements by providing the requisite degree of block for reentry to o c c u r . 2 The delayed conduction permits the impulse to return to atrial tissue

after the completion of repolarization. Indeed, the combination of delayed conduction in junctional tissue and accelerated recovery in the atria may interact synergistically to sustain reentrant tachycardia. Additionally, acetylcholine-induced hyperpolarization may enhance transmission of the dominant impulse into the site of a normally shielded ectopic focus, triggering it to discharge. Clinical reports likewise support the potential ability of vagal stimulation to induce tachyarrhythmias. The induction of atrial fibrillation, supraventricular tachycardia and ventricular tachycardia by carotid sinus massage has been documented. 25-27 Therapy: Specific vagolytic therapy has been uniformly unsuccessful in reported cases. In one report 10 atropine shortened the duration of attacks but did not prevent their occurrence. Digoxin, a vagotonic agent, has likewise been of no benefit. In contrast, cardiac glycoside therapy exacerbated the tachycardia in two cases. 5,H Propranolol has reduced the duration of rate of attacks 1°,11 but has not, when used alone, abolished the arrhythmia. In our case no significant effects on the rate and duration of the tachycardia were noted with vagal or beta adrenergic blockade or with digitalis. However, this finding may relate to the wide range of rates and the short duration of the paroxysms before treatment. Quinidine, alone or with propranolol, has been the most effective agent, abolishing the arrhythmia in two previously reported cases 1°,11 and in ours. Thus, although a specific therapeutic regimen cannot be suggested, general suppressive therapy has been of value in most known cases.

References 1. Scherf D, Schott A: Extrasystoles and Allied Arrhythmias. Chicago, Year Book Medical Publishers, 1973, p 441-455 2. Cranefield PF: The Conduction of the Cardiac Impulse. Mount Kisco, New York,..Futura, 1975, p 31-73 3. Sakai D, Mori F: Uber einen Fall von sog "Schlucktacbykardie." Z Gesamte Exp Med 50:106-109, 1926 4. Gallavardin L, Froment R: Tachycardie paroxystique de dC~jlutition (avec accidents syncopaux). Lyon Med 145:456-4 9, 1930 5. Forsberg CW: Paroxysmal premature ventricula, contractions induced by swallowing: case report. Lancet 53:298-302, 1930 6. Clerc A: A propos de la tachycardie de dC=glutition.Arch Mal Coeur 34:73-80, 1941 7. Forssmann O, Stenqvist H: Paroxysmal tachycardia which the patient was momentarily able to produce himself. Acta Meal Scand 136:326-330, 1950 8. Kramer P, Harris L, Kaplan R, et ah Recurrent supraventricular paroxysmal tachycardia precipitated by swallowing. Proc N Engl Cardiovasc Soc 21:21, 1962-63 9. Bajaj SC, Ragaza EP, Silva H, et ah Deglutition tachycardia. Gastroenterology 62:632-635, 1972 10. Undsay AE: Tachycardia caused by swallowing: mechanisms and treatment. Am Heart J 85:679-684, 1973 11. Engle TR, Laporte SM, Meister SG, et al: Tachycardia upon swallowing: evidence for a left atrial automatic focus. J Electrocardiol 9:69-73, 1976 12. Copeland GD, Tullis IF, Brody DA: Clinical evaluation ot a new esophageal electrode, with particular reference to the bipolar esophageal electrocardiogram. I. Normal sinus mechanism. Am Heart J 57:862-873, 1959 13. Cohen L, Larson DW, Strandjord N: Swallowing-induced atrial fibrillation (abstr). Circulation 42:Supp1111:111-145,1970 14. Bigger JT Jr, Goldreyer BN: The mechanisms of supraventricular tachycardia. Circulation 42:673-688, 1970 15. Goldreyer BN, Gallagher JJ, Damato AN: The electrophysiologic

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demonstration of atrial ectopic tachycardia in man. Am Heart J 85:205-215, 1973 Wu D, Denes P- Mechanisms of paroxysmal supraventricular tachycardia. Arch Intern Med 135:437-442, 1975 Nahum LH, I-loft HE= Production of auricular fibrillation by application of acetyl-beta-methylcholine chloride to localized regions on the auricular surface. Am J Physiol 129:428-429, 1940 Iglauer A, Davis D, Altschule MD: Auricular fibrillation in normal, intact animals after the intravenous injection of mecholyl. Am Heart J 22:47-55, 1941 Scherf D, Chick FB: Abnormal cardiac rhythms caused by acetylcholine. Circulation 3:764-769, 1951 West TC, Turner L, Loomis TA: Effects of acetylcholine as me-. chanical and electrical properties of isolated rabbit auricles. J Pharmacol Exp Ther 3:475-482, 1954 Loomis TA, Krop S: Auricular fibrillation induced and maintained in animals by acetylcholine or vagal stimulation. Circ Res 3: 390-396, 1955 Brooks CMcM, Hoffman BF, Suckling EE, et al: Excitability of the Heart. New York, Grune & Stratton, 1955, p 209-215 Trautwein W: Generation and conduction of impulses in the heart as effected by drugs. Pharmacol Rev 15:277-332, 1963 Alessi R, Nusynowitz M, Abildskov JA, et al: Nonuniform distribution of vagal effects on the atrial refractory period. Am J Physiol 194:406-410, 1956 Wilson FN: Report of a case of auricular flutter in which vagus stimulation was followed by an increase in the rate of the circus movement. Heart 11:61-66, 1924 Cannata D, Narbonne ND: Clinical observations on the role of the vegetative nervous system in the pathogenesis of atrial fibrillation. Cardiologia 32:329-345, 1958 Scherf D, Cohen J, Rafailzedeh M: Excitatory effects of carotid sinus pressure. Am J Cardiol 17:240-252, 1966

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