Chronic accelerated ventricular rhythm

J. ELECTROCARDIOLOGY, 9 (3) 1976 249-254

Case Studies:

Chronic Accelerated Ventricular Rhythm BY ROBERTM. DAVIDSON, M.D., F.A.C.C.

for control. He subsequently developed an atrial tachycardia with intermittent 2:1 atrioventricular block during episodes of pericarditis and congestive heart failure. His rhythm converted to normal sinus with digoxin and quinidine sulfate. He recovered fully from his myocardial infarction and underwent cardiac catheterization four months later, which showed hypokinesis of the posterior and inferior walls and subtotal occlusion of the right coronary artery and partial occlusion of the circumflex coronary artery. He subsequently remained asymptomatic and was on no medication when he developed his current episode of tachycardia. His risk factors for coronary artery disease included adult onset diabetes mellitus and Type II hyperlipoproteinemia as well as a strong family history for heart disease. On admission to the hospital he was in no distress, his heart rate was 210 and regular, blood pressure 100/70. His neck veins showed intermittent cannon "a" waves. The remainder of the cardiac and general physical examination were otherwise unremarkable. His electrocardiogram (ECG) (Fig. 1) showed a rapid ventricular rate with wide QRS complexes and no identifiable atrial activity. Carotid sinus massage and intravenous lidocaine had no appreciable effect on the arrhythmia. A His bundle electrogram was then performed using standard techniques (Fig. 2). This study demonstrated an atrial rate of 140, a ventricular rate of 205 with complete atrioventricular dissociation, and His bundle potentials falling within the QRS complexes. Ventricular pacing up to rates of 150 failed to affect the arrhythmia, but mechanical stimulation of the right ventricle with the pacing catheter produced a ventricular premature beat which converted the rhythm to normal sinus. The His e l e c t r o g r a m , while in n o r m a l sinus rhythm, was completely normal. Over the next few days the patient's rhythm varied between normal sinus and another rhythm of similar rate which appeared to be an acceler-

SUMMARY T w o patients are presented with accelerated ventricular r h y t h m s of u n u s u a l l y l o n g duration. The clinical a n d electrophysiological aspects of this problem are discussed. Accelerated idioventricular rhythms have been described in association with acute myocardial infarction, digitalis toxicity, chronic forms of heart disease, and in the absence of apparent heart disease. 1-4Their benign nature and self-limited course have been repeatedly emphasized? -7 The following two cases illustrate accelerated idioventricular rhythms of unusually long durattion without apparent complications.

CASE REPORTS CASE 1: The patient was a 29 year old man who was admitted to the Malcolm Grow United States Air Force Medical Center for the first time with a complaint of a rapid heart beat for about seven hours. He had had an acute myocardial infarction of the inferior wall seven months previously. During that admission he manifested frequent ventricular premature beats in the first four hospital days which required continuous intravenous lidocaine infusion

From the Division of Cardiology, Department of Medicine, Malcolm Grow USAF Medical Center, Andrews Air Force Base, Washington, D.C. Reprint requests to: Robert M. Davidson, M.D., 436 North Roxbury Drive, Beverly Hills, CA 90210. 249

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ated ventricular rhythm of a different rate and morphology from the rapid ventricular tachycardia which he manifested initially (Fig. 3). While in this rhythm his ECG again demonstrated complete atrioventricular dissociation. This intermittent rhythm disturbance was seen on all ECGs throughout the next three years of follow-up, with the ventricular rate

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varying from 50 to 120/min. (corresponding closely to the sinus rate). During this time he had no symptoms of angina pectoris or any other manifestations of ischemic heart disease, other than this rhythm disturbance. A repeat His bundle electrogram was done during this period which confirmed that this rhythm had a ventricular origin (Fig. 4). i! !i

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Attempts to supress this rhythm with therapeutic doses of quinidine sulfate, procaine amide, propranolol, and diphenylhydantoin sodium wre all unsuccessful. Although this was felt to be a benign rhythm disturbance, he was maintained on quinidine polygalacturonate to prevent a recurrence of his rapid ventricular tachycardia. C A S E 2: The patient was a 56 year old man who was admitted to the Malcolm Grow United States Air Force Medical Center with a three day history of hemoptysis and a long history of chronic bronchitis. He had no prior history of cardiovascular disease and was on no medication. Cardiovascular findings of note included a pulse which varied between 55 and 85, intermittent cannon "a" waves in the neck, and a first heart sound of varying intensity. An ECG showed normal sinus r h y t h m at a rate of 85 with periods of ventricular r h y t h m at a rate of 55 (Fig. 5). A His bundle electrogram was done which showed intermittent atrioventricular dissociation with a normal A-H-V

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relationship d u r i n g normal sinus r h y t h m , but no His activity associated with spontaneous episodes of ventricular r h y t h m (Fig. 6). A r e v i e w of this p a t i e n t ' s p r e v i o u s ECGs showed similar intermittent atrioventricular dissociation and accelerated ventricular r h y t h m in an ECG t a k e n routinely six months previously. An ECG taken over a year before his present admission showed intermittent parasystolic ventricular premature beats with the same configuration as the ventricular b e a t s d u r i n g his a c c e l e r a t e d v e n t r i c u l a r rhythm. F u r t h e r evaluation of the patient disclosed a carcinoma of the lung requiring pneumonectomy. Post-operatively he developed atrial fibrillation and atrial flutter which required cardioversion. He was maintained on quiaidine polygalacturonate, 1.1 gr/day, and digoxin, .25 mg/day. Electrocardiograms done three months and eight months later showed sinus tachycardia at rates of 110 to 120/min without any evidence of accelerated ventricular rhythm or ventricular premature beats. He died of complications of his carcinoma nine months

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after his original admission. Autopsy showed metastatic carcinoma not involving the heart. There were several mild focal coronary artery lesions but no significant cardiac pathology was found.

DISCUSSION Both p a t i e n t s d e m o n s t r a t e d accelerated isorhythmic ventricular rhythms, but with some important clinical and electrophysiological differences. Clinically, the first patient had significant coronary artery disease as well as at least one episode of rapid ventricular tachycardia, while the second patient had no significant heart disease nor known episodes of tachycardia. In each case the rate of the abnormal ventricular r h y t h m was about the same as the rate of the underlying sinus rhythm and was, therefore, faster than the expected rate of an i d i o v e n t r i c u l a r focus b u t slower t h a n the usual rate of a ventricular tachycardia. Massumi and Ali 3 s u g g e s t e d the t e r m i n o l o g y "accelerated isorhythmic ventricular rhythms" for this particular type of arrhythmia. In Case #1 the ventricular rhythm was consistently initiated by a ventricular premature beat with fixed coupling to the previous normal beat (of 0.52 + / - 0.04 sec) and continued with atrioventricular dissociation until a ventricular capture from a normal sinus beat could occur. The inter-ectopic intervals were not constant and were not a multiple of the basic ectopic rate. The initiation of the ventricular rhythm was not typical of an accelerated idioventricular r h y t h m (idioventricular tachycardia) in that it was initiated in each case J. ELECTROCARDIOLOGY, VOL. 9, NO. 3, 1976

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by a fixed coupled premature beat and not by slowing of the sinus rate or acceleration of the v e n t r i c u l a r rate. This type of v e n t r i c u l a r rhythm might, therefore, fit under Schamroth's d e s i g n a t i o n of " e x t r a s y s t o l i c v e n t r i c u l a r tachycardia," except that the rate is much slower than the usual range of 140 to 180/min. 7 It is of interest that Massumi and Ali included several patients in their category of accelerated isorhythmic ventricular r h y t h m s who had ventricular r h y t h m s which were initiated by ventricular p r e m a t u r e beats2 In contrast to the r h y t h m disturbance in the first case, the second patient demonstrated a typical ventricular parasystolic rhythm. A constant ectopic cycle length of 1.04 sec was present throughout the ECG and the ventricular r h y t h m emerged whenever the ectopic interval occurred during an excitable period of the ventricle. Normal sinus r h y t h m resumed, as in Case #1, whenever ventricular capture could occur. The inter-ectopic intervals were an exact multiple of the ectopic cycle length and no fixed coupling to a normal sinus beat occurred. That is, there was complete entrance block and no exit block. Accelerated ventricular rhythms have been the subject of a number of reviews, all of which emphasize t h a t these r h y t h m s are usually self-limited and benign and do not require specific t h e r a p y (other t h a n withdrawal of digitalis, if digitalis toxicity is the suspected etiology). Only a few patients have been previously described with accelerated ventricular r h y t h m s of sustained duration. Chung briefly d e s c r i b e d two p a t i e n t s w i t h o u t a p p a r e n t organic heart disease who had parasystolic ventricular rhythms which lasted intermittently for at least ten years2 "9Basu and Scheinm a n TM r e c e n t l y d e s c r i b e d a p a t i e n t w i t h accelerated idioventricular r h y t h m of at least 48 hours duration which occurred following recovery from acute myocardial infarction. This arrhythmia was easily terminated with anti-arrhythmic drugs. Hill in 1936," and Heinz and Eldridge in 1957/2 each described a patient with ventricular premature beats of parasystolic origin in whom this r h y t h m was observed on two occasions about a year apart. In neither case were there more than two consecutive ventricular beats at a time; that is, they were cases o f parasystolic ventricular beats and not of ventricular rhythm. The only difference b e t w e e n i n t e r m i t t e n t p a r a s y s t o l i c v e n t r i c u l a r b e a t s and a continuous parasystolic ventricular r h y t h m is that in the latter case there is little or no exit block, and/or the ectopic cycle length is shorter or the underlying sinus rate is slower, allowing emergence of a continuous rhythm.

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Since there are so few reported examples of "chronic" accelerated ventricular r h y t h m s , the clinical significance of this a r r h y t h m i a is unclear. The fact t h a t these r h y t h m s can persist for prolonged periods without giving rise to symptoms or complications would attest to their benign nature, however. The association of a rapid and symptomatic ventricular tachycardia with a slower accelerated ventricular r h y t h m in the first case might suggest direct association between these two rhythms. This seems unlikely, however, in t h a t the QRS morphology during each of these a r r h y t h m i a s was very different, thus suggesting two different ventricular foci. In addition, the rapid ventricular tachycardia behaved like a typical r e e n t r a n t a r r h y t h m i a in t h a t it was terminated abruptly by a ventricular premature beat, while the slower accelerated ventricular r h y t h m was more typical of enhanced pacem a k e r activity. It is likely t h a t both r h y t h m s were manifestations ofischemic heart disease, but not directly associated with each other. It is of interest t h a t quinidine sulfate quickly abolished the ventricular r h y t h m in the three previously described cases of sustained accelerated ventricular rhythms, 8'~ but t h a t the r h y t h m d i s t u r b a n c e in our first case was resistant to multiple anit-arrhythmic drugs. The majority of cases of accelerated ventricular r h y t h m s have been described in association with acute myocardial infarction or digitalis toxicity, but a number of cases have been described in the absence of a p p a r e n t organic heart disease. ',3"6"9 The significance of this is just as unclear as the significance of ventricular premature beats in normal persons. Chung 8 implies t h a t patients with heart disease who developed parasystole have a poor prognosis, but it is unclear whether the parasystolic types of ventricular r h y t h m have a different significance and n a t u r a l h i s t o r y from the non-parasystolic variety. It is likely t h a t m a n y of the questions in this area will

be answered in the next few years with the availability of long term portable monitoring equipment and better anti-arrhythmic drugs. A c k n o w l e d g m e n t : The opinions expressed in this paper are those of the author and do not reflect official United States Air Force policy.

REFERENCES 1. SCHAMROTH,L: Idioventricular tachycardia. J Electrocardiol 1:205, 1968 2. NORRIS, RM AND MERCER, C J: Significance of idioventricular rhythms in acute myocardial infarction. Prog Cardiovasc Dis 16:455, 1974 3. MASSUMI, RA AND ALI, N: Accelerated isorhythmic ventricular rhythms. Am J Cardiol 26:170, 1970 4. ROTHFELD, EL, ZUCKER, I R, PARSONNET, V ET AL: Idioventricular rhythm in acute myocardial infarction. Circulation 37:203, 1968 5. SCHAMROTH,L: Idioventricular tachycardia. Dis Chest 56:466, 1969 6. GALLAGHER,JJ, DAMATO,AN AND LAU, SH: Electrophysiologic studies during accelerated idioventricular rhythms. Circulation 44:671, 1971 7. SCHAMROTH,L: The Disorders of Cardiac Rhythm. Blackwell Scientific Publications, Oxford and Edinburgh, 1971, p 120 8. CHUNG, EKY: Parasystole. Prog Cardiovasc Dis 11:64, 1968 9. CHUNG,KY, WALSH,TJ ANDMASSm, E: Ventricular parasystolic tachycardia. Br Heart J 27:392, 1965 10. BASU, D ANDSCHEINMAN,M: Sustained accelerated idioventricular rhythm. Am Heart J 89:227, 1975 11. HILL, IGW AND CAMERON, JDS: A case of parasystole showing simple interference dissociation. Am Heart J 11:140, 1936 12. HEINZ, RE AND ELDRIDGE, FL: Ventricular parasystole in a five-year-old child. Am Heart J 53:624, 1957

J. ELECTROCARDIOLOGY, VOL. 9, NO. 3, 1976