Unexpected, sustained ventricular tachyarrhythmia after cardiac operations

J THORAC

CARDIOVASC SURG

1991;102:883-9

Unexpected, sustained ventricular tachyarrhythmia after cardiac operations Unexpected, sustained ventricular tachyarrhythmia after cardiac operations is differentiated from sustained ventricular tachycardia and ventricular fibrillation from known antecedent causes, such as recent or perioperative myocardial infarction, low cardiac output, preoperative ventricular arrhythmia, sympathomimetic drugs, drug toxicity, and metabolic abnormalities. Sixteen of 2364 patients (0.68 %) who underwent heart operations met strict exclusion criteria for unexpected sustained ventricular tachyarrhythmia that occurred 1 hour to 12 days after operation. Recurrent ventricular tachyarrhythmias occurred in 12 patients; three died (21 % ~ despite resuscitation from the initial episode. AU patients had significant preoperative left ventricular dysfunction and 14 had ejection fractions below 30%. Fifteen of the 16 patients had monomorphic ventricular tachycardia at the initial episode. EmpiricaUy prescribed therapy was not effective in suppressing ventricular tachyarrhythmias inducible by programmed stimulation during postevent electrophysiologic studies in 10 of the 13 survivors. Inducibility was eventuaUy prevented by drugs in nine patients, three patients received automatic implantable cardiac defibrillators, and one patient underwent successful catheter ablation of ventricular tachycardia. No patient died of recurrent ventricular tachyarrhythmias during the foUow-up of 8 to 55 (mean 29) months after hospital discharge.

Stanley K -, C. Tam, MD, John M. Miller, MD, and L. Henry Edmunds, Jr., MD,

Philadelphia, Pa.

Arhythmias are common and potentially lethal complications after cardiac operations. Supraventricular arrhythmias are more common and usually better tolerated than are ventricular arrhythmias.' Postoperative sustained ventricular tachycardia and ventricular fibrillation are rare and usually have a recognizable antecedent cause. In recent years, however, we have encountered occasional patients who have experienced ventricular tachyarrhythmias without any recognizable antecedent cause. In these patients, operation appears to have either caused the arrhythmia or enhanced an unknown propensity toward the arrhythmia. In this article, we report our experience with a group of patients with unexpected, sustained postoperative ventricular tachyarrhythmias and

From the Divisions of Cardiothoracic Surgery and Cardiovascular Medicine, University of Pennsylvania, Philadelphia, Pa. Received for publication April 24, 1990. Accepted for publication Oct. 22, 1990. Address for reprints: Dr. L. Henry Edmunds, Jr., Department of Surgery, 4 Silverstein, Hospital of the University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104.

12/1/26457

our results with electrophysiologically guided therapeutic interventions.

Methods The records of all patients who underwent cardiac operations during the 46 months between June I, 1985, and March 31, 1989, at the Hospital of the University of Pennsylvania were reviewed. The criteria for unexpected, postoperative, new-onset, sustained ventricular tachyarrhythmia included the following: (I) one or more episodes of ventricular fibrillation or ventricular tachycardia of greater than \00 beats/min, lasting 30 seconds or longer or causing hypotension (mean systemic pressure less than 60 mm Hg) or low cardiac output (cardiac index less than 1.8 L/m 2/min); (2) ventricular tachyarrhythmia that occurred within I month after a cardiac operation for nonarrhythmic conditions; (3) no preoperative history of syncope, sudden death, or ventricular arrhythmias (as detected by twelve-lead electrocardiograms); (4) no history of myocardial infarction within 30 days before operation and no evidence of perioperative acute myocardial infarction or ischemia before and immediately after the onset of ventricular tachyarrhythmia, as determined by symptoms of angina pectoris, electrocardiographic evidence, and cardiac isoenzymatic criteria; (5) no indication of myocardial ischemia from hemodynamic compromise,as documented by systemic mean blood pressure of at least 70 mm Hg, absence of clinical shock, and, in patients with a Swan-Ganz catheter (Baxter Healthcare Corporation,

883

884

The Journal of Thoracic and Cardiovascular Surgery

Tam, Miller, Edmunds

Table I. Case data Patient No.

Operation

Postoperative day of initial VT

Drugs at time ofVT

No. of Treatment

recurrences

Drugs at time of recurrent VT

Early outcome

Drugs tested EPS

Proc

S

Proc, Mex, Quin

Lido

D S S S S

Proc Proc Meto Proc, Mex, Quin

CABG

3

Lido

CS, Proc

2 3 4 5 6

CABG+ ANEU CABG+ANEU CABG CABG CABG

2 4 2 I I

Dopa Dig Lido Epi Epi

CS, Lido CS, Lido CS, Proc Lido CS, Lido

>10 0 0 I 2

7 9 10 II 12 13 14 15

RedoCABG RedoCABG CABG CABG+ ANEU AVR AVR+ CABG AVR AVR Mitralrepair

5 \I 3 12 10 7 2 4 I

None Dig, Quin None None Dopa Dig Dopa None Dopa

CS, Lido CS, Lido CS, Lido CS, Lido Lido CS, Lido CS, Lido CS, Lido CS, Lido

I 2 3 0 >10 0 I I 2

Lido Proc Lido

S S S S D S S S S

16

AVR/MVR

7

None

CS, Lido

>10

Proc

D

8

None Proc Proc Lido Lido Lido

Proc, Quin, Mex Proc, Arnio Proc, Mex, Amio Quin, Mex Proc, Amio Proc Proc Proc, Amio, Mex

VT, Ventricular tachyarrhythmia; EPS, electrophysiologic study; CABG, coronary arterial bypass grafting; Lido, lidocaine; CS, direct-current countershock; Proc, procainamide; S, survived; Mex, mexiletine; Quin, quinidine; D, died; ANEU, left ventricular aneurysmectomy; Dopa, dopamine; Dig, digoxin; Amio, amiodarone; Epi, epinephrine; Meto, metoprolol; AI CD, automatic implantable cardiac defibrillator; AVR, aortic valve replacement.

Edwards Division, Irvine, Calif.) in place, thermodilution cardiac index of greater than 2.1 L/m 2/min, or mixed venousoxygen saturation of greater than 65%; (6) absence of sympathomimetic medications during the initial episode or during recurrence of ventricular tachyarrhythmias after sympathomimetic medications were stopped; (7) absence of metabolic derangements, such as hypokalemia, hypoxemia,alkalosis, and acidosis; and (8) absence of drug toxicity (such as digoxin or quinidine). Subsequent evaluation of the ventricular tachyarrhythmia includedcardiac catheterization, programmed ventricular stimulation, and autopsy of nonsurvivors. Long-term follow-up results were obtained by direct telephone communication with patients, families, or referring physicians (closing date, March 1990).

Results During the 46 months, 16 (0.68%) of 2364 patients met all of these criteria for unexpected, new-onset, sustained ventricular tachyarrhythmia 75 minutes to 12 days after operation (Fig. I). Fifty percent (8/16) of the initial episodes of ventricular tachyarrhythmia occurred within 72 hours of operation (Fig. 1). Seven initial episodes occurred after discharge from the surgical intensive care unit. The ages ofthe patients ranged from 38 to 74 years, with a mean ± standard deviation (SD) of 59 ± 10 years. Thirteen were male. Ten patients had ischemic heart disease and six had nonischemic valvular heart disease (Table I). Nine

patients with ischemic heart disease had one or more episodes of myocardial infarction at least 6 months before the operation. One patient had had a myocardial infarction within 6 months of operation (at 3 months). Four patients had had anterolateral myocardial infarctions, two had had inferior myocardial infarctions, and four had had both. Two patients had a history of coronary arterial revascularization. One to five (mean 2.9) bypass grafts had been constructed. Attempts were made to bypass all vessels with stenosis greater than 50% of the luminal diameter. Three patients with ischemic heart disease also had left ventricular aneurysms and underwent left ventricular aneurysmectomy without patches in addition to myocardial revascularization. All 10 patients had left ventricular dysfunction, with preoperative left ventricular ejection fractions ranging between 20% and 30% (mean ± SD,25.3% ± 4.3%). Six patients were in New York Heart Association (NYHA) class IV and four were in class III. Six patients had nonischemic valvular disease; two had aortic stenosis; one had aortic stenosis and insufficiency; and one patient had isolated aortic insufficiency. One patient had mitral insufficiency (degenerative valve disease) and one patient had both aortic and mitral insufficiency. All six patients with nonischemic valvular disease had a history of congestive heart failure. Two were in NYHA class IV, three were in class III, and one was in

Volume 102 Number 6 December 1991

Results EPS Suppression with Mex, Quin Inducible with Proc Inducible with Proc Suppression with Meto Suppression with Quin Inducible with all tested drugs Inducible with drugs; catheter ablation Suppression with Proc, Amio Inducible Suppression with Amio Suppression with Proc Suppression with Proc Inducible with drugs

Unexpected ventricular tachyarrhythmia

Follow-up (rno) 8 55

Maintenance therapy Quin, Mex (stroke, D)

37 20

Amio Amio Meto Quin AICD, Quin, Mex

20

No drugs

19

Recurrent syncope, AICD

12 30 21 37 49

AICD, Quin Amio Proc (cancer, D) Proc AICD; catheter ablation; Amio, Mex; AICD removed

44 22

class II. The patient in NYHA class II had aortic insufficiency. The ejection fraction in five patients ranged between 13% and 38% (mean ± SD, 25.6% ± 11.2%). Ejection fraction was not measured in one of the patients with aortic stenosis. End-diastolic ventricular volumes of the two patients with mitral disease and the single patient with isolated aortic insufficiency were 265 ml, 296 ml, and 243 ml, respectively. The initial ventricular tachyarrhythmia occurred in the surgical intensive care unit in nine patients; eight of these patients had Swan-Ganz catheters. Thermodilution cardiac indexes before the initial episodes ranged from 2.4 to 3.6 L/m 2/min (mean ± SD, 2.8 ± 0.5 L/m 2/min). Four patients were receiving dopamine infusion at 1 to 3.5 tlg/kg/min and two patients were receiving epinephrine infusion at 0.03 to 0.05 tlg/kg/min at the time of the initial arrhythmia (Table I). All of these patients had recurrent ventricular tachyarrhythmia in the absence of low cardiac output 4 to 36 hours after all sympathomimetic agents had been stopped. Two patients were receiving lidocaine infusions (2 mg/min) at the time of the initial episode. The lidocaine had been started for a nine-beat episode of nonsustained ventricular tachycardia in one patient and for recurrent ventricular couplets in the other. Serum lidocaine levels were 3.5 and 4.7 tlg/ml (therapeutic range is 1.5 to 5.0 tlg/ml) at the time of the arrhythmia. The initial arrhythmia occurred on the convalescent ward in seven cases. Four patients were not receiving any cardiac medications. Two patients were receiving digox-

885

in and another patient was receiving both digoxin and quinidine for atrial fibrillation. Digoxin levels were 1.2, 1.5, and 1.8 ngyrnl, respectively, with a therapeutic range of 0.9 to 1.9 ng/rnl, at the time of the initial episode. The QT interval of the patient receiving quinidine at the time of the initial tachyarrhythmia was 350 msec (QTc , 418 msec). Fourteen of the 16 patients had monomorphic sustained ventricular tachycardia as the initial episode. Of the two remaining, one initially had polymorphic sustained ventricular tachycardia and the other had monomorphic sustained ventricular tachycardia, which degenerated into ventricular fibrillation. All 16 patients were initially treated successfully. Fourteen patients were treated with direct-current countershock for acute hemodynamic compromise (Table I). Twelve of the 14 patients were treated additionally with intravenous lidocaine and two who were already receiving lidocaine received procainamide. Two patients who did not require countershock were treated with intravenous lidocaine alone. Despite initial treatment success, 12 patients (75%) had at least one recurrent episode of sustained or nonsustained ventricular tachyarrhythmia of at least nine beats (Table I). Seven of the nine patients with recurrent sustained ventricular tachyarrhythmia had a third episode and four patients had a fourth episode. Three of thesefour patients had further multiple recurrences (greater than 10) and died (19% of the entire sample). One died of uncontrolled ventricular tachyarrhythmia necessitating two to six countershocks per hour. This patient had undergone coronary artery bypass grafting and left ventricular aneurysmectomy; at autopsy, all bypass grafts were patent. Two other patients died of recurrent ventricular tachyarrhythmia and the myocardial suppressive effect of intravenous procainamide and bretylium. One patient had undergone aortic valve replacement for aortic stenosis and the other had undergone aortic and mitral valve replacement for aortic and mitral insufficiency. Patients with recurrent episodes of sustained ventricular tachyarrhythmias were treated with additional drugs, adjustment of drug levels, or countershock. In general, the order of preference for empiric pharmacologic therapy was a combination of lidocaine and procainamide, followed by quinidine, mexiletine, bretylium, and amiodarone. The presence of perioperative or postoperative myocardial ischemia or infarction was ruled out by retrospective analysis of all patients and laboratory data. None had evidence of ischemia by electrocardiographic or cardioenzymatic criteria immediately after operation or after the initial episode of ventricular tachyarrhythmia. None had angina. Four patients underwent postoperative cor-

886

The Journal of Thoracic and Cardiovascular Surgery

Tam, Miller, Edmunds

Patients

1

2

S

4

5

8

7

L;2 8

9

~

~

12

Postoperative Day of First Episode Fig. 1. Time of first episode of unexpected sustained ventricular tachyarrhythmia after cardiac operation in 16 patients.

onary angiograms; all grafts were patent in all patients. Thirteen survivors underwent electrophysiologic studies 9 to 22 days (mean ± SO, 14.6 ± 3.8 days) after operation. and 7 to 19 days (mean ± SO, 10.7 ± 3.2 days) after the initial episode of ventricular tachyarrhythmia. The empiric antiarrhythmic medications were stopped for a period of fivedrug half-lives before the electrophysiologic studies, except in patients who were receiving amiodarone or patients who had frequent premature ventricular beats. At the initial electrophysiologic study, sustained ventricular tachyarrhythmia was inducible in all patients except one, whose empiric pharmacologic regimen consisted of amiodarone. The empiric pharmacologic regimen failed to suppress programmed stimulated life-threatening ventricular tachyarrhythmia in 10 of 13 patients (76.9%). Successful electrophysiologic study-guided pharmacologic suppression (defined as complete suppression of inducible sustained or nonsustained ventricular tachycardia at a rate that is hemodynamically well tolerated) was achieved in nine of 13 patients (69.2%). Four patients required one electrophysiologic study and fiveneeded two studies. Ventricular tachycardia was controlled with amiodarone in three patients, with amiodarone and procainamide in one, with procainamide alone in two patients, with quinidine in one, with mexiletine and quinidine in one, and with metoprolol in one patient. Three of the four patients in whom electrophysiologic study-guided pharmacologic suppression failed underwent placement of an automatic implantable cardiac defibrillator (AICO) and were placed on the pharmaco-

logic regimen that had achieved partial suppression at the electrophysiologic study. The fourth patient underwent catheter ablation of the ventricular tachyarrhythmia focus because of the ease of inducibility of sustained lifethreatening ventricular tachyarrhythmias and because of severe intolerance for any pharmacologic suppression. The ablation was successful, with no ventricular tachyarrhythmia inducible afterward. This patient was discharged without medication. Of the three patients with an AICO, one 'also had catheter ablation of the ventricular tachyarrhythmia focus because of a malfunctioning AICO, which was subsequently removed. After catheter ablation, the ventricular tachyarrhythmia was suppressed in this patient by a combination of mexiletine and amiodarone. The remaining two patients with an AICO were treated with quinidine in one case and a combination of quinidine and mexiletine in the other. The 13 hospital survivors were followed up for 8 to 55 months (mean ± SO, 29 ± 14 months). Two patients died: one of stroke at 8 months of follow-up and the other of lung cancer at 21 months. After discharge, nine patients were in NYHA class I and four were in class II because of exertional dyspnea or angina. Ten of the 11 patients who received only drugs or who had catheter ablation remained free of ventricular tachyarrhythmias. The eleventh patient had an episode of syncope shortly after hospital discharge while on a regimen of amiodarone and procainamide. The arrhythmia was inducible at restudy and an AICO device was placed. This patient remains free of symptoms with procainamide only. The

Volume 102 Number 6 December 1991

two other patients, both of whom had AI CD devices during their initial hospitalizations, each had a syncopal episode that triggered the device, at 9 and 17 months. Discussion

The detected prevalence of postoperative ventricular arrhythmias is proportional to the criteria used and to the sensitivity of the monitoring system, but it has been observed to be as high as 38%.2Most ventricular arrhythmias are frequent premature ventricular contractions and nonsustained ventricular tachycardia, which do not contribute to the mortality rate. Life-threatening sustained ventricular tachycardia and ventricular fibrillation are comparatively rare and usually associated with perioperative myocardial ischemia from coronary artery or graft occlusion or from transient or sustained low cardiac output. Other "causes" of ventricular tachyarrhythmias include reperfusion of previously ischemic viable myocardium.r? presence of preoperative ventricular arrhythmias,2, 6, 7 sympathomimetic drugs, hypokalemiaf hypoxemia, acidosis, alkalosis, drug toxicity, mechanical excitation from an indwelling Swan-Ganz catheter, and malfunctioning pacemaker. This article reports a series of patients in whom life-threatening ventricular tachyarrhythmias developed without known antecedent causes. In 1984, Kron and coworkers?reported 18 patients (prevalence of 1.4%) who experienced unexplained postoperative ventricular tachyarrhythmias, but this series included three patients with perioperative myocardial infarctions and two patients with cardiac indexes below 2 L/m 2/min. Topol and associates I 0 reported a similar series of 12 patients (prevalence of 0,72%) who had undergone myocardial revascularization procedures; although none had detectable coronary ischemia after operation, three of seven patients studied had occluded grafts. Our series excludes all patients with detectable evidence of postoperative myocardial ischemia, but present technology cannot rule out ischemia of small islands of myocardium. II, 12 The important point is that the life-threatening arrhythmias can occur in the absence of detectable ischemia and in the absence of other known associated causes. Therefore these patients are at special risk simply because the arrhythmia is unexpected and may first occur days or weeks after opera-

tion.!" Significant left ventricular dysfunction appears to be the only common denominator in these 16 patients. The association of electrical instability and left ventricular dysfunction13-16 in patients with coronary artery disease 17 and in patients with aortic valve disease" 18 has been noted previously, but the mechanisms involved are not

Unexpected ventricular tachyarrhythmia

887

known. Preexisting scars, hypertrophy, and cardiomyopathy are also associated with spontaneous or induced ventricular tachyarrhythmias. Fifteen patients had monomorphic ventricular tachycardia as the initial arrhythmia, and arrhythmias were easily inducible in the electrophysiology laboratory in all survivors of the acute episodes except one. The electrophysiologic substrate may be different for recurrent, sustained ventricular tachycardia and ventricular fibrillation. Prior myocardial infarction, left ventricular aneurysm, and low ejection fraction tended to be more prevalent in patients with recurrent ventricular tachycardia than in patients with recurrent fibrillation. 19, 20 These characteristics suggest reentry-type tachyarrhythmias and a cause other than acute ischemia.v? Operation, reperfusion, redistribution of left ventricular wall stresses, and a long list of perioperative anatomic, dynamic, and metabolic factors influence regional oxygen supply and demand and the myocardial milieu" for reentry conduction in fibrotic, dilated, or hypertrophied ventricles. Ideally, patients at risk for unexplained, sustained tachyarrhythmias should be identified before or immediately after operation. Routine electrophysiologic testing before operation for patients with a low ejection fraction is impractical. Exercise testing and ambulatory monitoring are of questionable benefit.'? Signal-averaged electrocardiograms may be able to identify patients at risk for sudden death. This test, which averages between 100 and 400 heartbeats, permits amplification and identification of low-amplitude electrical signals by reducing random noise. Late potentials, which are low-amplitude electrical signals occurring at the terminal portion of the QRS complex on signal-averaged electrocardiograms, are associated with increased risk for spontaneous and inducible ventricular tachyarrhythmias, particularly in patients with coronary artery disease and prior myocardial infarction. 22.24 As yet, the use of signal-averaged electrocardiograms to predict surgical patients at risk for unexpected sustained ventricular tachyarrhythmias is an unproved but attractive approach. As noted in previous studies.f 25 intravenous procainamide and bretylium may have contributed to two of our three early deaths. Both agents are known negative inotropes that may have proarrhythmic effects in patients with a history of myocardial infarction or severe left ventricular dysfunction. 26-28 However, in an emergency, therapy must be empiric. Early electrophysiologic study is mandatory to prevent recurrence and to determine which drugs suppress the arrhythmias. Studies of patients who survived out-ofhospital cardiac arrest and did not undergo operation

888

Tam, Miller, Edmunds

show that inducibility by programmed electrical stimulation is a univariate predictor of recurrent cardiac arrest. 16, 29, 30 As illustrated by our experience, empirically prescribed antiarrhythmic drugs failed to prevent recurrences in 12 of 16 patients and failed to suppress inducibility in 10 of 13 survivors. We believe electrophysiologic study is needed to determine effective pharmacologic or procedural suppressive therapy. 13, 15, 16,31-33 The absence of any late deaths in this series from recurrent ventricular tachyarrhythmia supports this practice.

REFERENCES I. Ormerod OJM, McGregor CGA, Stone DL, Wisbey C,

2.

3.

4.

5.

6.

7.

8. 9.

10.

11.

12.

Petch MC. Arrhythmias after coronary bypass surgery. Br Heart J 1984;51:618-21. Michelson EL, Morganroth J, Mac Vaugh H. Postoperative arrhythmias after coronary artery and cardiac valvular surgery detected by long-term electrocardiographic monitoring. Am Heart J 1979;97:442-8. Levites R, Banka VS, Helfant RH. Electrophysiologic effects of coronary occlusion and reperfusion. Circulation 1975;52:760-5. Kaplinsky E, Ogawa S, Michelson EL, Dreifus LS. Instantaneous and delayed ventricular arrhythmias after reperfusion of acutely ischemic myocardium: evidencefor multiple mechanisms. Circulation 1981;63:333-9. Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: a marker of restoration of antegrade flowduring intracoronary thrombolysis for acute myocardial infarction. Am Heart J 1983;105:26-32. Leutenegger F, Giger G, Fuhr P, et al. Evaluation of aortocoronary venous bypass grafting for prevention of cardiac arrhythmias. Am Heart J 1979;98:15-9. Olshausen KY, Schwarz F, Apfelbach J, Rohrig N, Kramer B, Kubler W. Determinants of the incidence and severity of ventricular arrhythmias in aortic valve disease. Am J Cardiol 1983;51:1103-9. Curry P, Fitchett D, Stubbs W, Krikler D. Ventricular arrhythmias and hypokalaemia. Lancet 1976;2:231-3. Kron IL, DiMarco JP, Harman PK, et al. Unanticipated postoperative ventricular tachyarrhythmias. Ann Thorac Surg 1984;38:317-22. Topol EJ, Lerman BB, Baughman KL, Platia EV, Griffith LSC. De novo refractory ventricular tachyarrhythmias after coronary revascularization. Am J Cardiol 1986;57: 57-9. Fennell WH, Chua KG, Cohen L, et al. Detection, prediction, and significanceof perioperative myocardial infarction following aorta-coronary bypass. J THORAC CARDIOVASC SURG 1979;78:244-53. Cheng DCH, Chung F, Burns RJ, Houston PL, Feindel CM. Postoperative myocardial infarction documented by technetium pyrophosphate scan using single-photon emission computed tomography: significance of intraoperative

The Journal of Thoracic and Cardiovascular Surgery

myocardial ischemia and hemodynamic control. Anesthesiology 1989;71:818-26. 13. Josephson ME, Horowitz LN, Spielman SR, Greenspan AM. Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest. Am J Cardiol 1980;46:948-55. 14. Minardo JD, Heger JJ, Miles WM, Zipes DP, Prystowsky EN. Clinical characteristics of patients with ventricular fibrillation during antiarrhythmic drug therapy. N Engl J Med 1988;319:257-62. 15. Ritchie JL, Hallstrom AP, Troubaugh GB, Caldwell JH, Cobb LA. Out-of-hospital sudden coronary death: rest and exercise radionuclide left ventricular function in survivors. Am J CardioI1985;55:645-51. 16. Wilber DJ, Garan H, Finkelstein D, et al. Out of hospital cardiac arrest: use of electrophysiologictesting in the prediction of long-term outcome. N Engl J Med 1988;318:1924. 17. Kowey PR, Folland ED, Parisi AF, Lown B. Programmed electrical stimulation of the heart in coronary artery disease. Am J CardioI1983;51:531-6. 18. Santinga JT, Kirsh MM, Brady TJ, Thrall J, Pitt B. Left ventricular function in patients with ventricular arrhythmias and aortic valve disease. Ann Thorac Surg 1983;35: 152-5. 19. Greene HL. Sudden arrhythmic cardiac death-mechanisms, resuscitation, and classification:the Seattle perspective. Am J Cardiol 1990;65:4B-12B. 20. Adhar GC, Larson LW, Bardy GH, Greene HL. Sustained ventricular arrhythmias: differences between survivors of cardiac arrest and patients with recurrent sustained ventricular tachycardia. J Am Coli CardioI1988;12:159-65. 21. Katz AM. Cardiomyopathy of overload: a major determinant of prognosisin congestiveheart failure. N Engl J Med 1990;322:100-1O. 22. Nalos PC, Gang ES, Mandel WJ, Ladenheim ML, Lass Y, Peter T. The signal-averaged electrocardiogram as a screening test for inducibility of sustained ventricular tachycardia in high risk patients: a prospectivestudy. J Am Coli Cardiol 1987;9:539-48. 23. Gomes lA, Winters SL, Stewart D, Horowitz S, Milner M, Barreca P. A new noninvasive index to predict sustained ventricular tachycardia and sudden death in the first year after myocardial infarction: based on signal-averaged electrocardiogram, radionuclide ejection fraction, and Holter monitoring. J Am Coli CardioI1987;10:349-57. 24. Waldo AL, Henthorn RW, Carlson MD. A perspectiveon ventricular arrhythmias: patient assessment for therapy and outcome. Am J Cardiol 1990;65:30B-5B. 25. Kron IL, Nolan SP. Severe hypotension due to the use of bretylium for postcardiotomyventricular arrhythmias. Ann Thorac Surg 1983;35:271-3. 26. Moran JM. Postoperative ventricular arrhythmia. Ann Thorac Surg 1984;38:312-3. 27. RaeAP, Kay HR, Horowitz LN, Spielman SR, Greenspan AM. Proarrhythmic effects of antiarrhythmic drugs in

Volume 102 Number 6 December 1991

patients with malignant ventricular arrhythmias evaluated by electrophysiologic testing. J Am Coli CardioI1988;12: 131-9. 28. Yelebit Y, Podrid P, Lown B, Cohen BH, Graboys TB. Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs. Circulation 1982;65:886-94. 29. Freedman RA, Swerdlow CD, Soderhold-Difatte Y, Mason JW. Prognostic significance of arrhythmia indueibilityor noninducibility at initial electrophysiologic study in survivors of cardiac arrest. Am J Cardiol 1988;61:57882. 30. Zheutlin TA, Steinman RT, Mattioni TA, Kehoe RF. Long-term arrhythmic outcome in survivors of ventricular

Unexpected ventricular tachyarrhythmia

889

fibrillation with absence of inducible ventricular tachycardia. Am J CardioI1988;62:1213-7. 31. Ruskin IN, DiMarco JP, Garan H. Electrophysiologic observations and selection of long-term antiarrhythmic therapy. N Engl J Med 1980;303:607-13. 32. Lerman BB, Waxman HL, Buxton AE, Josephson ME. Disopyramide: evaluation of electrophysiologic effects and clinical efficacy in patients with sustained ventricular tachycardia or ventricular fibrillation. 1983;51:759-64. 33. DiMarco JP, Garan H, Ruskin IN. Quinidine for ventricular arrhythmias: value of electrophysiologic testing. Am J CardioI1983;51:90-5.

Bound volumes available to subscribers Bound volumes of THE JOURNAL OFTHORACIC AND CARDIOVASCULAR SURGERY are available to subscribers (only) for the 1991 issues from the Publisher, at a cost of $64.00 for domestic, $86.48 for Canadian, and $82.00 for international subscribers for Vol. 101 (JanuaryJune) and Vol. 102 (July-December). Shipping charges are included. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 60 days after publication of the last issue of the volume. The binding is durable buckram with the JOURNAL name, volume number, and year stamped in gold on the spine. Payment must accompany all orders. Contact MosbyYear Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, Missouri 63146-3318, USA; phone (800) 325-4177, ext. 4351, or (314) 453-4351. Subscriptioos must be in force to qua6fy. Bound volumes are not available in place of a regular JOURNAL subscription.