Management of Intractable Ventricular Tachyarrhythmias After Myocardial Infarction

ROBERT W. WALD, MD, FRCP(C) MENASHE B. WAXMAN, MD, FRCP(C) PAUL N. COREY, PhD JOHN GUNSTENSEN, MD, FRCS(C) BERNARD S. GOLDMAN, MD, FRCS(C), FACC Toronto, Ontario, Canada

From the Departments of Medicine and Surgery, University of Toronto, Faculty of Medicine and the Division of cardiology and Cardiovascular Surgery, Toronto General Hospital. Toronto, Ontario, Canada. This study was supported in part by grants from the Ontario Heart Foundation, Toronto, Ontario, Canada, and the Canadian Heart Foundation, Ottawa, Ontario, Canada. h4anuscript received July 18, 1977; revised manuscript received March 27. 1979, accepted April 2, 1979. Address for reprints: Menashe B. Waxman, MD, Cardiovascular Unit, Toronto General Hospital, 101 College Street, Toronto, Ontario, Canada M5G lL7.

Twenty-five patients wtth recent or old myocardlal infarctkn were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large ante&u infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterizatkn or autopsy revealed a left ventricular aneurysm in 16 of 16 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perkperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died elther in the hospital (four patients) or suddenly withln 2 months of discharge (ffve patients). Ventrkular flbrlllatlon was documented as the cause of death in five of these patients. Surgical lnterventton was found to improve significantly the survival of these patients (P 0.05).

Ventricular tachycardia and ventricular fibrillation commonly occur within the first 24 to 48 hours of acute myocardial infarction, usually as isolated incidents that can be readily terminated and that later subside. Occasionally, however, these tachyarrhythmias complicate the early or later stages, or both, of acute myocardial infarction and assume a recurrent and intractable form. These life-threatening arrhythmias fail to respond to the usual therapeutic measures including antiarrhythmic drugs, overdrive pacing and interventions aimed at reducing afterload and ongoing ischemia, thereby rendering the patient dependent on repeated direct current cardioversion. The temporal distribution of these life-threatening events is usually unpredictable and, although several days may elapse between catastrophic periods, their continuing recurrence poses a therapeutic dilemma. Surgical intervention in the form of aneurysm resection or coronary bypass, or both, has emerged more recently as a practical mode of therapy in these patients.1-27 However, it is not universally used and more experience is required to assess the balance between the benefits and the high risk of surgery in this setting. This retrospective study relates our experience with 25 patients with intractable ventricular tachyarrhythmias and was carried out to define the features that identify such patients and to assess and compare the results of medical and surgical treatment.

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Methods Patients

Twenty-five patients with intractable ventricular tachyarrhythmias after acute myocardial infarction admitted to the Toronto General Hospital between January 1973 and March 1977 were included in this retrospective analysis. Intractable ventricular tachyarrhythmia in these patients was arbitrarily defined as a requirement for two or more defibrillations daily on 3 or more consecutive days of a hospital admission while on antiarrhythmic therapy. All arrhythmias were documented as either ventricular fibrillation or ventricular tachycardia at rates that drastically compromised the patient’s immediate circulatory status. The diagnosis of ventricular tachycardia was established by the following criteria28: (1) The QRS complexes during the

tachycardia were 120 msec or greater in duration and totally different from the complexes during supraventricular rhythm (25 of 25 patients). (2) Atrioventricular (A-V) dissociation or ventriculoatrial (V-A) block was present (25 of 25 patients). (3) Intermittent fusion beats (15 of 25 patients) or normal capture beats (8 of 25 patients) were observed. (4) In 14 patients who underwent atria1 pacing at rates in excess of the tachycardia, the procedure did not produce aberrant rhythm. (5) In 10 of 14 patients who underwent intracardiac electrophysiologic studies, ventricular tachycardia was inducible with

TABLE

I

Antiarrhythmic Drugs Used in 25 Patients With Intractable Ventricular Arrhythmia Drug Lidocaine Procainamide Propranolol Quinidine sulfate Bretylium tosylate Diphenylhydantoin

330

Dose/ 24 hr (9)

Route

Frequency

3-6 4-6 6-16 mg 0.8-2.4

Intravenous Intravenous Intravenous Oral

Continuous Continuous Every 8 hours Every 6 hours

0.6-1.8

Intravenous or intramuscular Oral

Every 8 hours

0.4-0.8

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FIGURE 1. Monitor lead recordings in Patient 16, who had intractable ventricular tachyarrhythmia on 2 successive days. Repetitive episodes of ventricular tachycardia and fibrillation occurred at irregular intervals at the times (hours and minutes) indicated while the patient was receiving procainamide, 5 g/24 hr (3.5 mg/min) by continuous intravenous drip infusion. His serum levels ranged from 9 to 12 mg/liter. All episodes but one required direct current cardfoversion, one reverted spontaneously.

one to three timed premature ventricular stimuli. In these patients a His potential preceded each QRS complex during sinus rhythm, but not during tachycardia, as recorded from the same catheter position Figure 1 illustrates part of the typical course of one of our patients. Repetitive episodes of ventricular tachycardia and

fibrillation are seen on 2 consecutive days despite a high rate of intravenous procainamide administration (5 g/24 hr or 3.5 mg/min). Aside from these clusters, the remainder of these 2 days were free of tachyarrhythmias. Clinical Management

Medical: All patients with clinical evidence of heart failure received digoxin and diuretic drugs. Serum digoxin levels were maintained in the therapeutic range of 0.8 to 1.5 ng/ml. Intravenous diuretic drugs were administered to keep the pulmonary wedge pressure (as monitored through a flow-directed catheter) at 15 to 20 mm Hg. Oxygenation, acid-base and electrolyte status were closely monitored, and appropriate therapy was instituted as required. After admission, the electrocardiogram was continuously monitored and directcurrent countershock was always promptly administered along with standard resuscitative measures. Antiarrhythmic drug management consisted of successive trials of lidocaine or procainamide, or both, followed by propranolol, quinidine sulfate, bretylium tosylate and diphenylhydantoin added individually in varying combinations. During administration of procainamide, serum levels were maintained in the range of 5 to 10 mg/liter. Serum propranolol and diphenylhydantoin levels were not routinely measured. Serum quinidine levels were frequently but not consistently measured. The aim was to maintain a serum level of 3 to 6 mg/liter. The doses of drugs used were as outlined in Table I. The maximal rates of administration were as indicated unless adverse hemodynamic effects occurred (decrease in mean blood pressure of more than 10 mm Hg, oliguria) or other intolerable side effects (for example central nervous system symptoms).

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W.B., 58kg ADMITTED

ET AL.

DIED SUDDENLY

DISCHARGED )‘l

2l-

160~ 80

QUINIDINE,

g

PROPRANOLOL,

mg

1

30

40

I

1

50

60

J

70

DAYS POST INFARCTION

ED.R., 50kg ADMITTED

ANEURYSMECTOMY

6fL,DOCA,NE,Gg

l--l

a

DISCHARGED

f

+

U

i.m.

m p.0.

PRO PRANOLOL,

mg

i,,

15 EPISODES OF VT OR VF 10 5 0L

n 30

l.: il 40 50 DAYS POST INFARCTION

60

’ 70

FffiURE 2. Antiirrhythmic drug management and episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF) requiring defibrillation in two patients. Patient 2 (W.B.) (top) did not undergo surgery and died suddenly 2 days after discharge from the hospital while receiving procainamide, 500 mg orally (p.o.), every 3 hours. Serum levels during intravenous (i.v.) procainamide infusion of 4 mg/liter ranged from 9 to 12 mglliter. Patient 17 (DR.) (bottom) underwent aneurysm resection, was discharged from the hospital 2 weeks later without medication and is alive at 31 months of follow-up. Serum levels during Intravenous procainamide infusion of 3 mg/liter ranged from 8 to 11 mg/liter. i.m. = intramuscular; i.v. = intravenous.

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giograms and coronary arteriograms were interpreted by two cardiologists and a cardiac surgeon in each instance. Anatomic data in two further patients later became available from postmortem examinations. Aneurysmectomy was performed alone in 8 of the 16 patients undergoing surgical procedures and in conjunction with coronary bypass grafting in 5. All patients with significant and bypassable coronary arterial lesions (as judged by the size and runoff of the vessel distal to the lesion) underwent bypass procedures. The extent of resection at aneurysmectomy was decided intraoperatively by the operating surgeon. The border between fibrous aneurysmal tissue and the surrounding myocardium was delineated visually on the endocardial and epicardial surfaces. A rim of fibrous tissue was left at the myocardial borders to ensure a solid substrate for sutures. When the aneurysm was too large to excise completely, as much of it as possible was resected without compromising the resulting left ventricular cavity size or mitral valve apparatus. One patient underwent coronary bypass surgery in conjunction with a large circular endocardial ventriculotomy but without resection of ventricular tissue. Two patients had coronary bypass surgery alone. All but one of these procedures were performed with intraaortic balloon pump assistance.2g

Overdrive pacing was instituted from the atria in 10 and from the ventricles in 6 patients in conjunction with the drug therapy. A therapeutic trial was deemed a failure if the patient required defibrillation during the trial. Failure of all these modalities with continuing occurrence of ventricular tachycardia or fibrillation was deemed to signal the presence of intractable ventricular tachyarrhythmia. Figure 2 illustrates the antiarrhythmic drug management in two patients, one of whom underwent surgery and another who did not. The doses and pattern of drug administration are representative of those used in every patient and clearly reflect the numerous disappointments that characterized each mode of attempted treatment Surgical: Operative intervention was considered and suggested for every patient, a recommendation based on the repeated failure of aggressive antiarrhythmic drug management in this clinical situation. However, only 16 of the 25 patients underwent a surgical procedure. The nine patients who did not undergo surgery were not identifiably different from those who did. In these patients surgery was precluded by the choice of the patient or the physicians in charge of the case, or both, a decision based partly on the high expected operative mortality rate. Cardiac catheterization was performed in 18 patients as a preoperative investigative procedure. Left ventricular cineangiography was performed in the right anterior oblique projection using power injections of Renografin-76s’. Selective coronary arteriography was performed using the Judkins technique. The cinean-

Results Clinical features (Table II): The group of 25 patients with intractable ventricular tachyarrhythmia included 21 men and 4 women whose ages ranged

TABLE II Clinical Data in 25 Patients With Intractable Ventricular Arrhythmia Cardiac Catheterization Data Case No.

Age (yr) 8Sex

Ml

25

54M 54M 68F 65M 46M 46M 49M 57M 56M 65M 67M 38M 61M 53M 42M 53M 64F 58M 44F 55M 48M 72F 30M 47M 59M

Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant Ant

Peak SCOT w)

Weeks From MI to IVT

290 560 275

C/T Ratio f%)

:

LVEDP (mm H%)

ii

i&i0 820 ‘240

Apical’

.

i 5 1 16 2

Stenosed Coronary Arteries

LV Aneurysm

’ .

Ante&apical Anteroapical Apical Apical

3’ 3

29

. .

... .

:;

31

::

f

. . ‘520 620 ‘450 178 350 500 132 730 300

t 16 24 1 1

7 yr : 1

79 71 59

Apical’ lnfrapapillary Anteroapical Anteroapical Apical Anteroapical Apical Apical Anteroapical Anteroapical

59

lnfrapapillary

7

Apical’ Ant

ii

...

19

: 1‘

31 20

5”; 64

:: 35

2: 6

‘320 252 240 ..

‘19

: 2 O.l). t One patient whose time from myocardial infarction to intractable ventricular tachyarrhythmia was 7 years is not included. C/T = cardiothoracic; EF = ejection fraction; IVT = intractable ventricular tachyarrhythmia; LVEDP = left ventricular enddiastolic pressure; Ml = myocardial infarction. l

(perioperative mortality rate 31 percent). Four of the 11 survivors had transient postoperative ventricular arrhythmias, but these were responsive to standard antiarrhythmic drugs. There was no recurrence of intractable ventricular tachyarrhythmia in any patient, and in all instances the arrhythmia-free postoperative course was in sharp contrast to the stormy arrhythmia-ridden preoperative period. Ten of the 11 patients who survived operation are alive at present follow-up of 8 to 39 months (mean 26). Of these 10,2 are in New York Heart Association30 functional class I, 3 in class II and 6 in class III. Two are not taking any drugs, three are receiving digoxin and a diuretic agent and five are receiving digoxin, a diuretic drug and an antiarrhythmic agent (propranolol and quinidine in two, quinidine in

one and procainamide in two). One patient who underwent coronary bypass surgery alone and was receiving quinidine sulfate, 400 mg orally every 6 hours, and propranolol, 40 mg orally every 6 hours, died suddenly 4 months after discharge from the hospital. All nine patients

who had no operative

procedure

either succumbed to an episode of ventricular fibrillation in the hospital (four patients) or died suddenly within 2 months of discharge from the hospital (five patients). Ventricular fibrillation was documented as the cause of the four in-hospital deaths and one of the five out of hospital deaths. Figure 4 summarizes the survival and death times of the groups of medically and surgically treated patients. Statistical analysis of these data was performed

l DEATH TIME x SURGERY TIME I CENSOR TIME

I

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24

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TIME FROM IVT,

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FIGURE 4. Survival and death times from the onset of intractable ventricular tachyarrhythmia (IVT) in the medical and surgical groups.

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TABLE IV

TABLE V

Follow-Up Data*

Characteristic Clinical Features of Patients With Intractable Ventricular Tachyarrhythmia -____

Mode of

Patients

Alive

Therapy

(no.)

(no.)

Survival W)

0

0

Medical Surgical Total

1: 25

::

-

::

* Follow-up period 8 to 39 months (mean 26).

using a previously described method.31b2 The estimated mean survival times (from the time intractable ventricular tachyarrhythmia emerged) of the medical and surgical groups were 15.8 and 170 weeks, respectively. The difference between mean survival times within the two groups was statistically significant (P 200 IU Severe clinical LV dysfunction LVEDP >20 mm HG Ejection fraction