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problems during the time they were having their dysrhythmias4 The Wolff-Parkinson-White syndrome was first suggested to be a cause for SIDS when Lipsitt et a1.5 reported a case of an infant who died at 4 months of age from SIDS with autopsy findings consistent with Wolff-ParkinsonWhite syndrome, including two bundles of Kent and Maheim’s cells. Keeton et al6 reported the case of an 11-week-old girl who had a near-miss SIDS episode and was found to have type A Wolff-Parkinson-White syndrome. The prolonged QT syndrome has been implicated in a number of SIDS and near SIDS episodes. Southall et a1.7 described a case in which a neonate was known to have an irregular heartbeat in utero which reverted to normal at 9 days of age. The infant died unexpectly 2 days after leaving the hospital. A ECG reexamined after the infant’s death showed a prolonged QT interval7 One study has reported QT abnormalities in relatives of infants dying with SIDSS but a subsequent study has failed to confirm this.g Steinschneider’o performed lead IT ECGs on 30 neonates who had had a sibling die of SIDS and on 75 control neonates. He also measured the QT interval of 52 adults who had had an infant die of SIDS. There was no significant difference between either of the groups.‘” Kelly et al.” examined the ECGs of 21 near-miss SIDS victims and found no increase in the QT interval as compared to normals. In fact Haddad et alI2 reported an abbreviated QT interval in patients after near-miss SIDS. Furthermore, Montague et al. I3 have recently reported an abbreviated ventricular repolarization interval for infants at high risk of SIDS. Using 24-hour ambulatory ECG recording and 120-lead body surface potential maps in 17 infants at risk for SIDS and 17 age- and sex-matched controls, they suggested there is a difference in the autonomic activity, particularly an increased sympathetic tone, in the high-risk infants.‘” Another possible source of ventricular dysrhythmias in infancy is from myocardial tumors. Garson et a1.14reported eight patients who had electrophysiologically directed ablative surgery for medically uncontrollable ventricular tachycardia. Four of the eight patients had demonstrable tumors at the site of activation (three Purkinje cell tumors and one rhabdomyoma); four had no demonstrable gross pathology present. All eight patients were converted to sinus rhythm after tumor resection or cryoablation, and in all eight neither echocardiography nor angiography demonstrated structural abnormalities. The patient we described also had medically uncontrollable ventricular tachycardia which apparently precipitated the near SIDS episode. There was no evidence of either prolonged QT or Wolff-Parkinson-White syndromes. This infant, who had surgery after inability to control his dysrhythmia except with intravenous procainamide, was without significant ventricular ectopy for 10 days postoperatively. No histopathologic abnormalities were found in the tissue removed at that time of the operation. Because of recurrence of the ventricular tachycardia, he was placed back on a procainamide drip and eventually was weaned to oral quinidine, propranolol, and amiodarone (which has been used on an experimental basis quite effectively to control hard-to-

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treat dysrhythmias in children).15 Although the incidence of ventricular dysrhythmias caused by discrete ventricular foci is unknown at this time, these dysrhythmias do represent an important treatable etiology for the syndrome and should be considered in the differential diagnosis of such patients. REFERENCES

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2. 3.

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10. 11.

Kelly D, Shannon DC: Sudden infant death syndrome and near sudden infant death syndrome: A review of the literature, 1964 to 1982. Pediatr Clin North Am 29:1241, 1982. Emery JL: The neonatal electrocardiogram and unexpected death in infancy. Br Med J 2:833, 1977. Jones RWA, Sharp C, Rabb LR, et al: 1028 neonatal electrocardiograms. Arch DIs Child 54:427, 1979. Southall DP, Orrell MJ, Talbot JF, et al: Study of cardiac arrhythmias and other forms of conduction abnormality in newborn infants. Br Med J 2:597, 1977. Lipsitt LP, Sturner WQ, Oh W: Wolff-Parkinson-White and sudden infant death syndromes. N Engl J Med 3M):llll. 1979. Keeton BR, Southall E, Rutter N, et al: Cardiac conduction disorders in six infants with “near-miss” sudden infant deaths. Br Med J 2:600, 1977. Southall DP, Arrowsmith WA, Oakley JR, et al: Prolonged QT interval and cardiac arrhythmias in two neonates: Sudden infant death syndrome in one case. Arch Dis Child 54:776, 1979. Maron BJ, Clark CE, Goldstein RE, Epstein SE: Potential role of QT interval prolongation in sudden infant death syndrome. Circulation 54:423, 1976. Kukolich MK, Telsey A, Ott J, Motulsky AG: Sudden infant death syndrome: Normal QT interval on ECG’s of relatives. J Pediatr 60:51, 1977. Steinschneider A: Sudden infant death syndrome and prolongation of the QT interval. Am J Dis Child 132:688, 1978. Kelly DH, Shannon DC, Liberthson RR: The role of the QT interval in the sudden infant death syndrome. Circulation 55:633,

1977.

Haddad GG, Epstein MA, Epstein RA, et al: The QT interval in aborted sudden infant death syndrome infants. Pediatr Res 13:136, 1979. 13. Montague TJ, Finley JP, Mukelabai K, et al: Cardiac rhythm, rate and ventricular repolarization properties in infants at risk for sudden infant death syndrome: Comparison with age and sex matched control infants. Am J Cardiol 54:301, 1984. 14. Garson A, Gillette P, Titus JL, et al: Surgical treatment of ventricular tachycardia in infants: Infant ventricular tachycardia surgery. N Engl J Med 310~1443, 1984. 15. Garson A, Gillette P, McVey P, et al: Amiodarone treatment 12.

of critical arrhythmias in children Co11 Cardiol 4:749, 1984.

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Verapamil in parasystolic ventricular tachycardia and other wide QRS rhythms R. A. Massumi, M.D., Jairo Marin, M.D., and V. N. Udhoji, M.D., Sepulueda and Los Angeles, Calif. From Veterans Program, Reprint Medical

the

Section of Cardiology, Department of Medicine, Sepulveda Administration Medical Center, UCLA-San Fernando Valley School of Medicine, UCLA.

requests: Center,

R. A. Massumi, 16111 Plummer

M.D., Cardiology St., Sepulveda,

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1. CaseNo. 1. Top panel depicts the U-lead ECG taken in the emergencyroom, showing a wide QRS tachycardia with P waves attached to the end of the QRS. The polarity of the P wave cannot be determined with certainty. Bottom panel, After intravenous verapamil, showing a normal sinus rhythm and features of an old inferior wall myocardial infarction. The morphologic features of the QRS during tachycardia, having RBBB and extreme left axis deviation, suggestthat the focus is situated in the inferior wall of the left ventricle, presumably within or in the margins of the old inferior wall infarction.

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Fig. 2. Case No. 1. Simultaneously recorded leads 1 and V1 taken at the onset of electrophysiologic studiesand mounted in three separatepanelsshowcompetition between the ventricular tachycardia and the sinusmechanism.The sinuscycles show gradual lengthening until they reach values of 0.70 and 0.73 seconds,at which time the tachycardia becomesdominant again. The interectopic intervals spanningover the short runs of sinusrhythm are exact multiples of the tachycardia cycles, being equal to 6 cycles in A and B and 9 cycles in C, thus conforming to parasystole.

Verapamil, chronotropically the most potent calcium entry blocker, has proved eminently useful in the treatment of reentrant tachycardias which incorporate the atrioventricular (AV) node in their reentry circuit. Recently, a case of sinus node reentry tachycardia was found to respond to verapamil.’ In these arrhythmias, verapamil blocks conduction in the calcium-dependent segmentof the reentry pathways (AV node and sinoatrial node, respectively) and terminates the tachycardia. Con-

versely, ventricular tachycardias, developing in sodiumdependent Purkinje and myocardial fibers, should be unresponsive to verapamil unless certain parts of their reentry circuit have become calcium-dependent,z3 or becausetheir underlying electrophysiologic mechanismis one of triggered automacity and not reentry.‘e6Ventricular parasystolic rhythms are the result of abnormal automacity and reflect the development of spontaneousphase 4 depolarization in the fibers of the parasystolic focus. The

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Fig. 3. CaseNo. 1. His bundle recordings during persistent ventricular tachycardia (top panel) and at the time of the shifts between the ectopic and sinusrhythms (hot tom panel). Atrial activation sequenceis retrograde in the top panel, with low atrial spikesappearing before the high atria1potential. In beats6,7, and 8, the two atrial potentials becomesimultaneous(fusion P waves). In beats 9 and 10, the low atrial potentials appear after the high, and the sinusP wavesappearin a gradual fashion, before the QRS. Beats 11and 12 are the result of antegradepropagation of the sinusP wavesdown into the ventricles, fusing with ectopic discharges.Beat 13is a pure sinusbeat, while beat 14is again a fusion complex. Beats 15 and 16 are unmarred ectopic beats.

Fig. 4. CaseNo. 2. In this 66-year-old man with a history of an old anteroseptalmyocardial infarction, a ventricular parasystolewith features of RBBB and intermediate QRS axis waspresent for severalmonths (PVBs with shorter QRS complexes, top panel). The tracing taken after 5 mg of verapamil given intravenously and shown in the bottom panel demonstrate complete abolition of the ventricular parasystole. The reentry PVCs with taller QRS complexeshave also disappeared.

unexpected finding of the remarkable effectiveness of verapamil in abolishing ventricular parasystole in three casesprompted this brief communication. An example of aberrantly conducted beats in atria1 fibrillation and their disappearanceafter verapamil is included for comparison.

CaseNo. 1. This 60-year-old man with old inferior wall myocardia infarction wasseenbecauseof palpitations and mild dyspnea.His ECG showeda wide QRS tachycardia at the rate of 106 bpm (Fig. 1, top panel). The tachycardia did not respond to two consecutive bolusesof 75 mg of lidocaine given intravenously. This was taken as an indi-

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Fig. 5. CaseNo. 3. Tracings taken during electrophysiologicstudiesshow three types of PVB marked A,

B, and C, in the control tracing (top panel) and persistenceof only C type PVBs after verapamil. Type A and C PVBs depicted features of RBBB, together with RAD and LAD, respectively. Type A appearedin a parasystolic mode, while type C always occurred late in the cycle and frequently fused with normally conducted QRS complexes.Type B with LBBB-LAD morphology appearedwith a fixed coupling interval and conformed with reentry. In the bottom panel, the samerecordings were made after intravenous administration of 10 mg of verapamil. Only type A PVBs persist, and type A and B PVBs disappear.Two of the three type C PVBs have fused with the normally conducted QRS complexes.

Fig. 6. CaseNo. 3. Top panel, A run of 20-beat polymorphic ventricular tachycardias induced repeatedly through right ventricular pacing (S,-S, = 550 msce, S,-S, = 270 msec, and S,-S, = 250 msec). Bottom panel, Samepacing protocol failed to induce more than four repetitive firings despite numerousattempts. It should be noted that with intravenous injection of 75 mg of lidocaine and the use of the samepacing protocol, only two repetitive firings could be induced.

cation that the rhythm was not of ventricular origin. An intravenous injection of 5 mg of verapamil promptly slowedand then reverted the rhythm to normal sinus(Fig. 1, bottom panel). During subsequentdays of observation in the coronary care unit encompassingnumerousbouts of

the sametachycardia, intravenous drips of procainamide and bolusesof lidocaine proved totally ineffective, while intravenous verapamil regularly terminated the abnormal rhythm. During an electrophysiologicstudy performed 24 hours after the last dose of verapamil, the mechanism

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Fig. 7. In this patient with chronic atria1 fibrillation, runs of wide QRS tachycardia failed to respond to intravenous lidocaine but disappeared after intravenous verapamil. His bundle electrography demonstrated His spikes before all the wide QRS beats, thus documenting their supraventricular origin. The disappearance of the wide QRS beats after intravenous verapamil appeared to be related to a slowing of the ventricular rate, thus eliminating the conditions required for intraventricular aberrancy (bottom panel).

Fig. 8. Case No. 5. In this patient with fast ventricular rate atria1 fibrillation (top panel), the intravenous injection of 5 mg of verapamil slowed the ventricular rate and led to the emergence of a relatively fast idioventricular escape rhythm (arrows in bottom panel). This phenomenon should not be mistaken for induction of ventricular irritability.

frequently shifted between the normal sinus and the tachycardia rhythm, providing ample opportunity to study the behavior of the tachycardia (Fig. 2). The ectopic rhythm, which proved to be parasystolic, occurred whenever the sinus rate slowed to less than 86 bpm; normally conducted beats of sinus origin prevailed whenever the sinus discharge rate exceeded 100 bpm. Fluctuations in the sinus rate appeared to be related to blood pressure changes (through baroceptor reflexes) in response to the

presence or absence of atria1 preloading and its contribution to left ventricular filling. His bundle electrography showed normal A-His and His-Q intervals during sinus rhythm, and no His spikes before the QRS complexes during the parasystolic tachycardia, thus documenting its ventricular origin (Fig. 3). The RBBB-LAD morphology of the QRS during tachycardia is reminiscent of a similar configuration described by Zipes et al.,? by Lin et al.,s and by Belhassen et al. 4 9 These ventricular tachycardias,

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which had the common feature of responsivenessto verapamil, developed in otherwise normal hearts and the rhythms were not describedas parasystolic. Case No. 2. In this 66-year-old woman with a history of an old anterior infarction, two types of premature ventricular beats (PVB) with features of right bundle branch block were observed during 3 days of monitored observation. The more numerous PVBs with shorter QRS complexes followed the pattern of parasystole and disappeared completely after an intravenous injection of 5 mg of verapamil (Fig. 4). These PVBs had proved completely unresponsive to bolusesof lidocaine and to intravenous procainamide. Case No. 3. In this 65-year-old man with an old myocardial infarction, treatment with therapeutic doses of quinidine and procainamide had proved ineffective in abolishinginnumerable polymorphic PVBs and short runs of ventricular tachycardia. Dynamic monitoring showed persistenceof over 10,000PVBs/24 hours. Treatment with oral verapamil, 480 mg/day, reduced the number to 4000/ 24 hours. For this reason,an electrophysiologic study was carried out. Three types of PVB, marked A, B, and C, were observed (Fig. 5, top panel). Type A PVBs always occurred late in the sinuscycle and frequently fused with sinusbeats. Type B PVBs coupled to the preceding sinus beats at fixed intervals and were reentry in character, while type C PVBs followed the pattern of parasystole. After an intravenous injection of 10 mg of verapamil, type B and C PVBs disappearedcompletely but type A PVBs persisted (Fig. 5, bottom panel). Moreover, induction of sustained ventricular tachycardia, which was possible before verapamil, could not be achieved after verapamil (Fig. 6). Case No. 4 is presented in order to demonstrate verapamil-induced abolition of aberrantly conducted beats in atria1 fibrillation simply becauseof ventricular slowing (Fig. 7). Contrariwise, in Case No. 5, Fig. 8, verapamilinduced ventricular slowing caused the emergenceof a ventricular escapemechanismwith wide QRS complexes. These two phenomenamust be taken into consideration when differential diagnosisof wide QRS rhythms is being attempted. Addendum

Since the preparation of this manuscript, two new cases of classicand documented ventricular parasystoleat rates of 35 and 37.5 bpm have been found to be exquisitely responsive to verapamil but resistant to lidocaine and procainamide.

REFERENCES

1. Gold RL, Katz RJ, Bren GB, Varghese PJ, Ross AM: Treatment of sinus node reentrant tachycardia with verapamil. AM HEART J 109:1104, 1985. 2. Snear JF. Horowitz LN. Hodess AB. MacVaueh H. Moore E’N: Cellular electrophysiology of human myocardial infarction. Circulation 59:247, 1979. 3. Dersham GH, Han J: Actions of verapamil on Purkinje fibers from normal and infarcted heart tissues. J Pharmacol Exp Therap 261:216, 1981.

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B, Horowitz LN: Use of intravenous verapamil for 4. Belhassen ventricular tachvcardia. Am J Cardiol 54:1131, 1984. B, Rdtmensch HH, Laniado S: Response of recur5. Belhassen rent sustained ventricular tachycardia to verapamil. Br Heart J 46:679, 1981. 6. Suns RJ. Shanero WA. Shen EN. Moradv F: Effects of veraiamil on ;entricular tachycardias possibly caused by reentry, automaticity and triggered activity. J Clin Invest 72:350, 1983. 7. Zipes DP, Foster PR, Troup PJ, Pedersen DH: At,rial induction of ventricular tachycardia: Reentry versus triggered automaticity. Am J Cardiol 44:1, 1979. 8. Lin FC, Finley D, Rahimtoola SH, Wu D: Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: A unique clinical entity with specific properties. Am J Cardiol 52:95, 1983. 9. Belhassen B, Shapira I, Pelleg A, Copperman I, Kauli N, Laniados S: Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: An ECG-electrophysiologic entity. AM HEART J 108:1034, 1984.

Sudden hemodynamic collapse following relief of cardiac tamponade in aortic dissection Neil L. Coplan, M.D., Bruce Goldman, M.D., Giulia Mechanic, M.D., Fulvio Mazzucchi, M.D., and Johnathan L. Halperin, M.D. New York, N.Y.

Cardiac tamponade resulting from rupture and hemorrhageinto the pericardial spaceis the most commondirect causeof death in patients with dissectionof the ascending aorta.1,2Death usually occurs so quickly that there is no opportunity to perform pericardiocentesis,accounting for the fact that this procedure is rarely mentioned in published series reviewing clinical experiences with aortic dissection. We encountered a patient with proximal dissecting aortic aneurysm who survived for 24 hours following the onsetof symptoms,but died immediately following aspiration of a compressivehemorrhagic pericardial effusion. This clinical courseillustrates that the rise in blood pressure which follows relief of cardiac tamponade can actually have immediate deleterious effects in patients in whom tamponade hasoccurred secondaryto aortic dissection. A 77-year-old white man developed severe substernal and epigastric pain while shoveling snow. The pain was continuous, stabbing in character, and nonradiating. He had had milder pain in the past, which usually occurred about 4 hours postprandially. The severe pain persisted for 8 hours before he presentedto a local emergencyroom, where it was unrelieved by sublingual nitroglycerin or antacid medication. Physical examination on admission revealed a regular heart rate of 60 bpm and blood pressure

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