Recurrent ventricular tachycardia

Recurrent Ventricular Tachycardia* A Case Successfully Treated by Bilateral Cardiac 5ympathectomy E . HARVEY ESTES, JR ., M .D . and

H.

L . IZI .AR, JR ., M .D .

Durham, North Carolina although he had no symptoms . He was found to have a blowing systolic apical murmur with transmission to the axilla, and a short presystolic apical murmur was also described . Chest films showed a prominent pulmonary artery . The electrocardiogram was normal . He was discharged front the army in May 1944, the discharge diagnosis being valvular heart disease with mitral insufficiency, and mitral stenosis, presumably rheumatic . The patient returned to fulltime work and remained symptom free until the onset of the present illness . The patient's mother died suddenly of an unknown cause in her sixties ; his father died in his seventies of "heart dropsy ." The patient weighed 180 pounds on admission (weight prior to illness 210 to 220 pounds) . Ile was afcbrilc ; the pulse rate was 82 per minute ; the blood pressure 125/85 turn . Hg . He was alert, cooperative and comfortable on admission . The ocular fundi were normal . There was no lymphadenopathy . The lungs were normal . 'there was a basic regular heart rate of 82 heats per minute, but this was often interrupted by premature beats and runs of regular tachyeardia at a rate of 144 per minute lasting from several beats to thirty seconds . 'the heart was normal in size and a grade 1 basal systolic murmur was heard . No diastolic murmurs were made out . The peripheral vessels were normal . The remainder of the physical examination was non-contributory . During the attacks of tachyeardia the patient appeared to be in some distress and complained of a dull substernal oppression . Vagal stimulation had no effect on the tachycardia . Laboratory data were all within normal limits except for a mild elevation of white blood count to 13,900 per cu, mm . with 75 per cent polymorphomuclear leukocytes, 4 stab forms, 19 lymphocytes . 2 eosinophils . Chest film and fluoroscopy on admission revealed no cardiomegaly and no specific chamber enlargement . Initial electrocardiogram showed a right bundle branch block, a first degree A-V block, multiple premature ventricular beats and runs of ventricular tachycardia . On admission all medications were stopped, without apparent effect on the frequency or character of the

HE following case is of interest not only because of the successful employment of bilateral cardiac sympathectomy in ventricular tachyeardia, the first such case to be reported, but also because of the unusual nature of the tachycardia, its refractiveness to usual therapeutic measures, and because of the effect of the surgical procedure on intraventricular conduction .

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CASE REPORT This thirty-five year old grocery clerk was first admitted to the Durham Veterans Administration Hospital on June 23, 1953, having been transferred from another hospital with a diagnosis of recurrent paroxysmal ventricular tachycardia . The patient was well until October 1952, at which time he had a tight substernal discomfort associated with weakness and dyspnea . He was hospitalized at another hospital where a diagnosis of ventricular tachycardia was made . 'this was controlled with medications but soon recurred . Recurrences appeared without relation to activity or other events and lasted from a few seconds to seventy-two hours . The frequency and duration of these attacks necessitated his almost continuous hospitalization during the nine-month interval between the onset of symptoms and his first admission here . Medications during this period included quinidine and procaine amide given in massive doses, ACTH, rauwolfia derivatives, heavy sedation and digitalis . Between attacks of ventricular tachycardia, a heart murmur was heard which led to a diagnosis of rheumatic heart disease with mitral insufficiency. Because of the persistence of the attacks and his gradual downhill course, he was transferred to this hospital . 'fhc patient recalled no unusual childhood illnesses . He led a healthy and active childhood . He was accepted into the army in January 1944 and sent to a training camp, where he did amateur boxing . On one occasion, prior to a bout, the examining physician heard a heart murmur and cancelled the bout . The patient was referred to the hospital for further study,

From the Medical Service, Veterans Administration Hospital, Durham, North Carolina, and the Department of Medicine, Duke University Medical Center, Durham, North Carolina. Manuscript received June 27, 1960 . VOL . 31, SEPTEMBER 1961

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An electrocardiogram taken four months prior to admission (February 27, 1953) . The electrocardiogram taken on admission was identical except for the presence of multiple premature beats . FIG . 1 .

episodes of tachycardia . Since the patient had had adequate trials on quinidine and procaine amide in previous hospitals, the following drugs were tested over the next few weeks : (1) potassium chloride, 8 gm . per day given orally, (2) intravenously administered magnesium sulfate, (3) atabrine given intramuscularly in doses up to 1 gm . per day, (4) propylthiouracil, 600 mg . per day given orally . The attacks became gradually more prolongedone run lasting for 112 hours . More substernal distress began to develop during the attacks, and during attacks blood pressure dropped to 85/60 mm. Hg, the liver became palpable and basal rales appeared . Digitalization failed to relieve these signs or to influence the course of the tachycardia . The administration of mercurial diuretics and a sodium restricted diet became necessary because of fluid retention during the attacks of tachycardia . On September 27, 1953, a left dorsal sympathcctomy was performed, with removal of the stellate ganglion and the upper six thoracic ganglia . The patient had a run of tachycardia during the procedure but the following day he maintained a normal sinus rhythm . On the second postoperative day he had a sixhour run of tachycardia. Over the next three days he had recurrent episodes which became shorter in duration . After this the tachycardia ceased ; he was allowed gradually to increase his activities, and was discharged on October 30, 1953, on a regimen of quinidine, 0 .4 gm . orally four times daily . He experienced only occasional premature ventricular beats during his last few weeks of hospitalization . He returned in December 1953 at which time he was found to have occasional auricular premature

contractions . The electrocardiogram showed a reduction in QRS conduction time from 0 .14 to 0 .10 second . Incomplete right bundle branch block was present . The P-R interval was normal . In October 1954 the patient was well and had stopped taking quinidine . An electrocardiogram showed a normal QRS conduction time of 0 .08 second, the electrical axis was horizontal, the R' had disappeared in lead V, . In January 1955 he experienced a ten-hour run of tachycardia . Thereafter, he had one or two short runs per week, but these did not limit him in any way . In September 1955 he had pleuritic pain in the right side of his chest for one week . Laboratory and x-ray studies failed to establish a cause for these symptoms . In January 1956 a prolonged period of tachycardia developed with the same symptoms experienced originally and the patient was hospitalized briefly in another hospital . An electrocardiogram revealed recurrence of the right bundle branch block with a QRS duration of 0 .12 second . He was readmitted to the Durhams Veterans Administration Hospital on January 27, 1956, for re-evaluation . On February 7, 1956, a prolonged episode of tachycardia developed and ventricular tachycardia was documented electrocardiographically . On February 16, 1956, a transthoracic right dorsal sympathectoiny was performed . The postoperative course was Uneventful and he was discharged on March 1, 1956 . 'the patient was last seen in April 1960 . At this time he reported occasional short runs of tachycardia, usually about once a month, lasting for five to ten minutes, but not limiting him in any way . His only complaint was that of occasional wheezing respirations, worse with changes in weather, and mild exertional dyspnea . He was working as a ticket seller . Examination revealed him to be in good spirits, appearing well . 'there was a soft, systolic basal murmur, otherwise the physical examination was completely within normal limits .' [he heart size was normal on the chest roentgenogram . The electrocardiogram again showed a normal QRS conduction time of 0 .08 second . Electrocardiographic Findings . Electrocardiograms were forwarded by the patient's referring physician, and showed a right bundle branch block between attacks of tachycardia . (Fig. 1 .) The QRS conduction time ranged between 0 .12 and 0 .14 second . The P-R interval was 0 .20 second . The attacks of tachycardia were characterized by two distinct forms of QRS conduction . One form resembled a right bundle branch block with a ventricular rate of about 160 beats per minute ; the other a left bundle branch block with approximately the same ventricular rate . P waves could not be definitely identified on the electrocardiograms forwarded with the patient . Soon after admission to this hospital electrocardiograms were taken which again revealed a right bundle branch block between episodes of tachycardia . On AMERICAN JOURNAL OF MEDICINE



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FIG . 2 . Lead y taken on admission (.Tune 23, 1953), showing premature beats resembling each of the two types of tachyeardia in the same lead . Neither premature beat interrupts the basic auricular rhythm . admission there were frequent premature beats which varied considerably in character . These premature beats did not interrupt the auricular rhythm, and were followed by a complete compensatory pause . The P wave could often be identified in the T wave of the premature heat . On some leads premature beats were seen which resembled each of the two conduction patterns seen with the attacks of tachycardia . (Fig . 2 .) Soon after admission electrocardiograms were recorded with both of the types of paroxysmal tachyeardia . Esophageal leads revealed that both types were accompanied by complete A-V dissociation. (Fig . 3,) The QRS duration with both types of tachycardia was 0 .12 to 0 .14 second . (Figs . 4 and 5 .)

Fto . 3 . bead t (above) and simultaneous esophageal lea (below) taken during (A) normal conduction (July 3 1953), (B) the "right bundle" type tachycardia (July 7, 1953) and (C) the "left bundle" type tachycardia (July 8, 1953) . Both (B) and (C) show independent atria) and ventricular activity . The P waves arc the sharp upward spike in the esophageal lead in all tracings . VOL . 31, SEPTEMBER 1961

Subsequent preoperative electrocardiograms always revealed the findings described . Between attacks of tachyeardia there were frequent premature beats which usually had the characteristics of "main stem" exit asystoles [1], having the QRS configuration of the sinus beats, but not interrupting the auricular rhythm, and followed by a complete compensatory pause . After the first operative procedure in September 1953 there was a change in QRS conduction, the conduction time being shortened to 0 .10 second . (Fig . 6 .) There were still occasional premature ventricular contractions, which were now clearly more prolonged than die sinus beats, reaching 0 .14 second in duration . The sinus beats still showed abnormalities in conduction ; an S wave in leads i, n and in and an R' in lead V, . An electrocardiogram in January 1954 revealed a QRS conduction time of 0 .10 second. S waves were present in leads i, n and in, but these were much less striking in size than on previous records . The R' in lead V, had entirely disappeared . During 1955, coincident with the return of attacks of tachycardia, a very small R' again appeared in lead V, and QRS conduction became prolonged to 0 .12 second_ In January 1956 the electrocardiogram showed a snore prominent S wave in leads i and n and a more prominent R' in lead V, . Again "main stern" extrasystoles were seen . After the second operative procedure the electrocardiogram once more showed a reduction in QRS conduction time to 0 .10 second

Fun . 4 . Electrocardiogram showing the tachycardia resembling left bundle branch block (February 27, 1953) .

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Fm . 5 . Electrocardiogram showing the tachycardia resembling right bundle branch block (July 7, 1953) .

and again the R' began to diminish in size . It was still present on March 14, 1956 . On September 22, 1958, the electrocardiogram revealed a normal QRS conduction time, a P-R interval of 0 .16 second, a QRS duration of 0 .08 second with no evidence of R' in lead V, . COMMENTS

The difficulty in establishing a diagnosis of ventricular tachycardia is recognized . This is especially true when the tachycardia has a configuration so similar to the sinus beat, as in the runs of tachycardia in which QRS complexes resembled right bundle branch block . No fusion beats were seen and at no time could capture beats be identified, therefore the tachycardia cannot be identified with certainty as ventricular tachycardia . However, such does seem to be the case since (1) there was complete A-V dissociation with both forms of ventricular tachycardia ; (2) premature beats could be seen which resembled both types of tachycardia ; (3) the premature beats resembling the sinus beats were followed by a P wave which timed perfectly with the basic auricular rhythm . These premature beats were followed by a complete compensatory pause and can be considered "main stem" extrasystoles of high ventricular origin or low nodal extrasystoles with retrograde block . Although the ventricular origin of the tachycardia resembling left bundle branch block also cannot be proved with certainty, there is less doubt of its character because of the bizarre form of the QRS complexes, totally different from the sinus beats . Thus there is evidence in favor of ventricular tachycardia as a mechanism for both forms of

FIG . 6 . Representative strips of leads I and V, showing the

change in conduction during the course of observation . The left thoracic sympathectomy was performed between the first and second strips, the right sympathectomy between the fourth and fifth strips . tachycardia, although this cannot be proved beyond reasonable doubt . Bilateral cardiac sympathectomy has been used a number of times for treatment of tachycardia of supraventricular origin . The first such case was reported by Leriche and Fontaine in 1929 in a case of auricular tachycardia [2] . Almost all the subsequent reports have appeared in the French literature . The last and most comprehensive paper, describing six patients so treated, was that of White and Bland [3] . A number of studies in animals have shown that induced ventricular extrasystoles can be stopped by removal or blockade of the sympathetic nerve supply [4-6] . It has also been noted that adrenalin and sympathetic stimulation promote ectopic escape mechanisms [7,8] . AMERICAN JOURNAL OF MEDICINE

Recurrent Ventricular Tachycardia---Estes, Goodall and Kirshner [9] have shown that, in dogs and sheep, interruption of the sympathetic fibers to the heart by means of bilateral thoracic sympathectomy reduces the myocardial norepinephrine content to about one-sixth of its former level . This reduction was of transient nature, however, the level beginning to rise at aboutt five weeks and returning to normal at sixteen weeks . It appears that epinephrine, norepinephrinc and sympathetic stimulation are conductive to the appearance of ventricular escape beats or ventricular extrasystoles . Interruption of the sympathetic fibers reduces the tendency for ectopic beats in the experimental animal . Interruption of the sympathetic nervous system reduces the content of norepinephrine in cardiac muscle . The possible significance of such reduction in the improvement experienced by the patient is uncertain, since there is a return to control level in five to sixteen weeks . The present case illustrates the fact that bilateral cardiac sympathectomy can be a valuable therapeutic measure in treatment of paroxysmal ventricular tachycardia . It is of course recommended that more conventional methods of therapy be tried first, but if these fail cardiac sympathectomy would seem to be a reasonable next step .

Also of interest is the change in QRS conduction after each of the operative procedures in this case . This suggests that there might have been some influence of the sympathetic nervous system on the choice of conduction pathway through the A-V nodal and junctional tissue .

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SUMMARY

A patient with a refractory case of recurrent ventricular tachycardia is described, with striking improvement after bilateral cardiac sympathectomy . The operative procedure was followed by normalization of a prolonged QRS conduction time . REFERENCES

1 . MARRIOn, H . J . L . and BRADLEY, S . M. Main-stem extrasystoles . Circulation, 16 : 544, 1957 . 2 . LERICHE, R . and FONTAINE, R. Chinlrgie du sympathique . Rev . Neurol ., 1 : 1046, 1929 . 3 . WInTE, J . C . and BLAND, E . F . Contrule des tachycardies paroxystiques rebelles par sympathectomie . Lyon Chir ., 45 : 395, 1950 . 4. NAxuM, L . H . and HOFF, E . C . The influence of cardiac sympathetics and adrenin on the phenomenon of ventricular escape . Am . J . Physiol ., 113 : 101, 1935 . 5 . MALINOW, M . R ., BATTLE, F . F. and MALAMUD, B . Prevention of neurogenic ventricular arrhythmias in rat by autonomic blocking drugs . Am . J. Physiol ., 175 ; 8, 1953 . 6 . BEATTIE, J., BROW, G . R . and LONG . C. N . H . Physiologic and anatomic evidence for the existence of nerve tracts connecting the hypothalamus with spinal sympathetic centers. Pro, . Roy . Soc ., London (Series B), 106 : 253, 1930 . 7 . HOFFMAN, B . F ., SIEBENs, A . A., CRANEFIELD, P. F . and BROOKS, C . M. The effect of epinephrine and norepinephrine on ventricular vulnerability . Circulation Res., 3 : 140, 1935 . S . SIEBENs, A . A., HOFFMAN, B. F ., ENSON, Y ., FARRELL, J . EE . and BROOKS, C . M . Effects of 1-epinephrine and 1-norepinephrine on cardiac excitability . Am . J. Physiol ., 175 : 1, 1953 . 9. GOODALL, M . and KIRSHNER, N. The effect of cervico-thoracic ganglionectomy on the adrenaline and noradrcnaline content in the mammalian heart . J. Clin . Invest ., 35 : 649, 1956 .