Case Report. Aneurysmectomy for Symptomatic Supraventricular Tachycardia Associated with Ventricular Aneurysm

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1 Case Report Aneurysmectomy for Symptomatic Supraventricular Tachycardia Associated with Ventricular Aneurysm Akira TAKESHITA, M.D. and Ernest 0. THEILEN, M.D. SUMMARY A case of left ventricular aneurysm associated with repeated supraventricular tachyarrhythmias was successfully treated by ventricular aneurysmectomy. Ventricular aneurysmectomy should be considered for supraventricular tachyarrhythmia as well as ventricular tachycardia, if they are symptomatic and refractory to medical therapy. Additional Indexing Words: Left ventricular aneurysm Supraventricular tachyarrhythmia Ventricular aneurvsmectomv V ENTRICULAR aneurysm is a common complication of coronary artery disease, particularly after myocardial infarction.l)-3) A arrhythmia is a well-documented complication of aneurysm as well as congenstive heart failure or thromboembolic complications. Although serious arrhythmias are uncommon, there have been several reported cases of refractory ventricular tachycardias which could be abolished only by aneurysmectomy.4j-9) Recurrent supraventricular tachycardias have been reported also with ventricular aneurysms but they usually have been a reflection or an accompaniment of left ventricular failure.10),12) This is a report of a patient who suffered from recurrent supraventricular paroxysmal tachycardia, which were symptomatic. The arrhythmia was not controlled by drug therapy or ventricular pacing but was completely abolished by resection of the aneurysm. CASE PRESENTATION H.D., a 71-year-old man, was in good health until August, 1967, when he had an acute inferior myocardial infarction. His convalescence was uneventful until 3 months later when he began to have mild dyspnea on exertion and frequent Address for reprints: Akira Takeshita, M.D., University of Kyushu Hospitals, Fukuoka 812, Japan. Supported by Program Project Grant #HL Received for publication April 4,

2 Vol. 16 No. 1 VENTRICULAR ANEURYSMECTOMY 99 Fig.1. Electrocardiograms in May, a) 12 leads electrocardiogram during tachycardia showing a wide QRS complex of the configuration of right bundle branch block and extreme right axis. b) Lead II showing AV dissociation with a ventricular rate of 130/min and an atria] rate of 65/min. Fig.2. Roentgenogram of the chest in September, 1970.

3 100 TAKESHITA AND THEILEN Jap. Heart J January, 1975 episodes of paroxysmal tachycardia. The paroxysms tended to occur during exertion. They lasted from several minutes to hours and often caused angina, dyspnea, and occasionally even syncope. He was first seen at the University of Iowa Hospitals in November, He was found to be in mild congestive heart failure and was digitalized. He was maintained on Digoxin, 0.25mg/day, and on quinidine sulfate, 200mg q 3hrs. He continued to have recurrent tachycardia despite these medications. A number of paroxysms were terminated by electrical cardioversion at a local hospital. He was rehospitalized at the University Hospitals in May, 1968, after having tachycardia lasting for several days. The physical examination on admission revealed regular rhythm at 130/min and a blood pressure of 100/76mmHg. There was no evidence of congestive heart failure. EKG showed A-V dissociation with a ventricular rate of 130/min and an atrial rate of 65/min (Figl1). This was interpreted to be either ventricular tachycardia or A-V dissociation due to junctional tachycardia with aberrant conduction. He was cardioverted with 80 watt-sec. No premature beats were seen during the rest of his hospital stay. His basic sinus rate was noted to be rather slow at 50 or 60/min. He was discharged on quinidine sulfate, 300mg q 6hrs. He had at least 15 recurrences of similar tachycardia with electrical cardioversion at his local hospital. He tolerated the tachycardia poorly; the last 2 episodes which occurred within a month before his third admission to the University Hospitals were accompanied by symptoms of cerebral insufficiency. An excessive aphasia persisted after the last of these 2 bouts of tachycardia. In the absence of tachycardias, he was almost asymptomatic except for mild dyspnea on exertion (without angina, orthopnea, paroxysmal nocturnal dyspnea, or pedal edema). His basic sinus rate was again noted by his physician to be in the range of 46 to 56/min. At the time of his third admission to the University Hospitals in August, 1970, his apical pulse was 44/min and his blood pressure was 180/84 mmhg. The physical examination was otherwise within normal limits except for an early grade II systolic ejection murmur at the apex. No double apical impulse was present. No gallop sounds were heard. Routine laboratory studies were within normal limits, including thyroid function studies. The EKG showed changes of an old inferior myocardial infarction, but ST segments in Leads II, III, and AVF were not elevated. Radiographic examination revealed a lower mediastinal shadow which proved to be an aneurysm arising from the inferior surface of the left ventricle (Fig.2). Angiography demonstrated that the aneurysm was well demarcated and showed paradoxical motion during ventricular systole (Fig.3). The hemodynamic data at cardiac catheterization were otherwise within normal limits including a left ventricular end-diastolic pressure of 11mmHg, mean pulmonary arterial wedge pressure of 10mmHg, and a cardiac index of 2.8 L/min/M2 (Table I). The EKG recorded during paroxysms of tachycardia on this admission revealed a regular rhythm at 130/min. The QRS configurations and axis were the same as those recorded during tachycardia in the past (Fig.4). The width of the QRS complexes and the absence of discernible atrial activity suggested that the arrhythmia might be ventricular tachycardia, but esophageal electrocardiography revealed atrial activity at a rate of 260/min with 2: 1 A-V block (Fig.5). This arrhythmia was interpreted as atrial flutter. A temporary transvenous pacemaker was placed with the electrodes in the apical region of the right ventricle, on the as-

4 Vol. 16 No. 1 VENTRICULAR ANEURYSMECTOMY 101 Fig.3. a) Left ventricular angiogram at the right anterior oblique view, showing an aneurysm arising from the inferior surface of the left ventricle. b) Drawings of the systolic (dotted line) and diastolic (straight line) left ventricle, showing a paradoxical motion of the aneurysm. Table I. Hemodynamic Data in September, 1970

5 102 TAKESHITA AND THEILEN Jap. Heart J. January, 1975 Fig.4. Electrocardiograms in May 1968 and in September Fig.5. Esophageal electrocardigoram in September sumption that abolishing the sinus bradycardia by overdrive might suppress the tendency for the recurrent tachycardias; it was not successful. Furthermore, ventricular pacing produced significant hypotension accompanied by signs of poor cerebral perfusion and decreased urine output. His systolic blood pressure fell to 80-90mmHg whenever the pacemaker was turned on at a rate of 70/min. Resection of the ventricular aneurysm was subsequently carried out. There has been no recurrence of paroxysmal tachycardia, ventricular or supraventricular, for 3 years since his operation even though the patient has not received any antiarrhythmic drugs. DISCUSSION The patient was treated for numerous episodes of paroxysmal tachycardia presumed to be ventricular in origin before his last admission to our hospital. Tachycardia in 1968 can be interpreted to be either ventricular or junctional tachycardia with aberrant conduction, but he also had paroxysms of supraventricular tachycardia identified as atrial flutter with 2: 1 A-V block, during which he became significantly symptomatic. Although serious arrhythmias

6 Vol. 16 No. 1 VENTRICULAR ANEURYSMECTOMY 103 are relatively uncommon in patients with ventricular aneurysms, this complication has been well documented. Many of these have been ventricular tachycardias and have been refractory to medical therapy. There have been several cases reported in which recurrent ventricular tachycardias could be prevented only by aneurysmectomy.4)-9) The series of ventricular aneurysms reported by Schlichter, et al,10) and Dubnow, et al,11) also included supraventricular arrhythmias such as atrial flutter, atrial fibrillation and junctional tachycardias. These were apparently as frequent as ventricular arrhythmias. The supraventricular arrhythmias were usually associated with congestive heart failure, however. The mechanisms involved in the development of supraventricular arrhythmias are not fully understood. When it is associated with congestive heart failure, an elevated left atrial pressure may conceivably be an etiologic factor as postulated by Lown, et al.13) A patient may have sinus node artery disease as a facet of coronary artery disease, and this may precipitate various supraventricular arrhythmias as is said to be the case sometimes in myocardial infarction.14) It is also reported that a premature ventricular depolarization may give rise to a re-entry mechanism responsible for supraventricular tachycardia.15) It is well-established that ventricular tachycardia can be suppressed effectively with permanent pacing. The use of permanent pacing has also been reported for the suppression of supraventricular tachycardias, particularly those associated with sinus bradycardia.18),19) Ventricular pacing in our patient caused significant arterial hypotension, decreased urine output and signs of impaired cerebral circulation and did not prevent recurrence of tachycardia. It is known that ventricular pacing may decrease cardiac output because of the loss of the contribution of atrial systole to ventricular filling and therefore to stroke volume,20) but, in addition the altered ventricular depolarization during pacing may affect the integrated cardiac response unfavorably. 21),22) It may be reasonable to assume that the adverse effect of ventricular pacing in this instance was an indication of pronounced impairment of left ventricular function because of the ventricular aneurysm, which was not fully appreciated from the normal hemodynamic measurements made during normal sinus rhythm. Since sinus node recovery time was not measured with rapid atrial pacing in our patient, a brady-tachy arrhythmia syndrome was not ruled out completely,23),24) but the fact that aneurysmectomy successfully abolished the tachycardia suggests that the recurrent tachycardias in this patient were somehow related to aneurysm rather than the brady-tachy arrhythmia syndrome. This is the first case report in which symptomatic uncontrollable supra-

7 104 TAKESHITA AND THEILEN Jap. Heart J. January, 1975 ventricular tachyarrhythmia was abolished by aneurysmectomy. Currently accepted indications for ventricular aneurysmectomy include congestive heart failure, recurrent thromboembolic complications and refractory ventricular tachyarrhythmias. We suggest that aneurysmectomy should be considered for recurrent supraventricular tachyarrhythmias as well as ventricular tachycardias if they are refractory to medical therapy and produce significant hemodynamic impairment. Aneurysmectomy carries a surprisingly low surgical mortality, ranging from 6 to 10%, even though these patients have far-advanced coronary artery disease and chronic cardiac decompensation. Lillehei, et al25) reported a 6% hospital mortality in 126 patients with whom aneurysmectomy and internal mammary artery implantation were performed. Effler26) performed ventricular aneurysmectomy in 250 patients with a hospital mortality of 10%. REFERENCES 1. Chung TO: Incidence of ventricular aneurysm in coronary artery disease. Am J Med 50: 340, Gorlin R, Klein MD, Sulliran JM: Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition. Am J Med 42: 512, Abrams DL, Edelist A, Lura MH, Miller AJ: Ventricular aneurysm. A reappraisal based on a study of sixty-five consecutive autopsied cases. Circulation 27: 164, Ritter ER: Intractable ventricular tachycardia due to ventricular aneurysm with surgical cure. Ann Int Med 71: 1155, Hunt D, Slomon G, Westlake G: Case report. Ventricular aneurysmectomy for recurrent tachycardia. Brit Heart J 31: 264, Couch OA: Cardiac aneurysm with ventricular tachycardia and subsequent excision of aneurysm. Circulation 20: 251, Tind GS, Blakemore WS, Zinsser HF: Ventricular aneurysmectomy for the treatment of recurrent ventricular tachyarrhythmia. Am J Cardiol 27: 690, Magidson O: Resection of postmyocardial infarction ventricular aneurysm for cardiac arrthythmias. Dis Chest 56: 211, Maloy WC, Arrants JE, Sowell BF, Hendrix GH: Left ventricular aneurysm of uncertain etiology with recurrent ventricular arrhythmias. New Eng J Med 285: 662, Schlichter J, Hellerstein HK, Katz LN: Aneurysm of the heart. A correlative study of one hundred and two proved cases. Medicine 33: 43, Dubnow MH, Burchell HB, Titus JL: Post infarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases. Am Heart J 70: 753, Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP: Clinical diagnosis and prognosis of ventricular aneurysm. Brit Heart J 30: 497, Lown B, Klein MD, Hershberg P: Coronary and precoronary care. Am J Med 46: 705, James TN: The coronary circulation and conduction system in acute myocaridal infarction. Progr Cardiovasc Dis 10: 410, Csapb, G: Role of ventricular premature beats in initiation and termination of atrial arrhythmias. Brit Heart J 33: 105, Sowton E, Leatham A, Carson P: The suppression of arrhythmias by artificial pacemaking.

8 Vol. 16 VENTRICULAR ANEURYSMECTOMY 105 No. 1 Lancet 2: 1098, Kastor JA, DeSanctis R, Harthorne JW, Schwartz GH: Transvenous atrial pacing in the treatment of refractory ventricular irritability Ann Int Med 66: 939, Cohen HE, Kahn M, Donoso E: Treatment of supraventricular tachycardias with catheter and permanent pacemakers. Am J Cardiol 20: 735, Sowton E, Balcon P, Preston T, Leaver D, Yacoub M: Long-term control of intractable supraventricular tachycardia by ventricular pacing. Brit Heart J 31: 700, Martin RH, Cobb LA: Observations on the effect of atrial systole in man. J Lab Clin Med 68: 224, Gilmore JP, Sarnoff SJ, Mitchell JH, Linden RJ: Synchronicity of ventricular contraction. Observations comparing hemodynamic effects of atrial and ventricular pacing. Brit Heart J 25: 299, Finney JO, Jr: Hemodynamic alterations in left ventricular function consequent to ventricular pacing. Am J Physiol 208: 275, Mandel W, Hayakawa H, Danzig R, Marcus HS: Evaluation of sino-atrial node function in man by overdrive suppression. Circulation 44: 59, Narula OS, Samet P, Javier RP: Significance of the sinus-node recovery time. Circulation 45: 140, Lillehei CW, Lande AJ, Rassman WR: Surgical management of myocardial infarction. Some promising concepts utilizing revascularization, mechanical circulatory assistance, operative treatment of severe complications, and cardiac replacement. Circulation 40 (Suppl 4): 315, Effler DB: The surgical treatment of myocardial ischemia. Clin Sympos CIBA 21: 3, 1969