termination of ventricular tachycardia: role of tachycardia cycle length

Termination of Ventricular Tachycardia: Role of Tachycardia Cycle Length

DENIS ROY, MD,* HARVEY L. WAXMAN, MD, ALFRED E. BUXTON, MD)

FRANCIS E. MARCHLINSKI, MD,t MICHAEL E. CAIN, MD,*

MARTIN J. GARDNER, MD,5 and MARK E. JOSEPHSON, MD11

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79 % ) and cardioversion was required in 29 patients (21% ). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 82 (83%), and 7 of 18 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 8 patients (88%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (78%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35 %). The

ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30 % ) procainamide increased the tachycardia cycle length by 49 f 42 ms (p <O.Ol) and did not modify the mode of termination. In 8 patients (28%) procainamide increased cycle length by 142 f 108 ms (p <O.Ol), but termination was more difficult. In 10 patients (44 % ) procainamide increased the cycle length by 138 f 110 ms (p <O.OOl) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.

Programmed ventricular stimulation is increasingly used to evaluate the mechanisms and therapy of recurrent VT. Previous studies have shown that in the majority of patients in whom VT can be initiated by programmed ventricular stimulation, the arrhythmia can also be terminated by appropriately timed extra-

From the Clinical Electrophysiology Laboratory, Hospital of the Uni- versity of Pennsylvania, Cardiovascular Section, Department of Medi- cine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. This work was supported in part by grants from the American Heart Association, Southeastern Pennsylvania Chapter, Philadelphia, Pennsylvania, and the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. (ROl HL24278). Manuscript received April 30, 1982, accepted June 18, 1982. l Fellow of the R. Samuel McLaughlin Foundation of Canada. + Recipient of Research Service Award F32 HL07201, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. * Supported by National Institutional Training Grant HL07346, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. 5 Supported by a grant from the Canadian Heart Foundation, Ottawa, Canada. 11 Recipient of Research Career Development Award K04 HL00361, National Heart, Lung, and Blood Institute, National ln- stitutes of Health, Bethesda, Maryland. Dr. Josephson is the Robinette Foundation Associate Professor of Medicine (Cardiovascular Dis- eases).

Address for reprints: Mark E. Josephson, MD, Cardiovascular Section, Box 683, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.

stimuli or by rapid ventricular pacing.lm5 The pacing techniques employed during electrophysiologic testing may serve as a guide for chronic pacemaker therapy of drug-resistant ventricular arrhythmias.6 It has been suggested that the mode of termination of VT is related to tachycardia cycle length. However, the relation between the specific mode of termination and the tachycardia cycle length has never been systematically evaluated in a large group of patients. The aims of this study are (1) to analyze the relation of mode of termination of VT to tachycardia cycle length, and (2) to assess the influence of procainamide on tachycardia cycle length and mode of tachycardia termination.

Methods

Patients: The study population consisted of 139 patients with recurrent VT or cardiac arrest in whom sustained VT was induced by programmed ventricular stimulation. There were 104 men and 35 women ranging in age from 8 to 74 years. Coronary artery disease was present in 101 patients, miscel- laneous cardiac abnormalities (cardiomyopathy, repair of tetralogy of Fallot, hypertensive cardiovascular disease, and mitral valve prolapse) in 22, and no documented clinical or- ganic heart disease in the remaining 16.

Electrophysiologic procedures: After informed consent was obtained, the patients underwent electrophysiologic

1346 December 1982 The American Journal of CARDIOLOGY Volume 50

TERMINATION OF VENTRICULAR TACHYCARDIA-ROY ET AL

testing in the nonsedated postabsorptive state. The administration of all antiarrhythmic agents was discontinued at least 48 hours before the procedure. Three or more electrode catheters were inserted percutaneously or by venous cutdown and positioned in the heart under fluoroscopic guidance. These usually included quadripolar catheters in the right atrium and right ventricle and a tripolar catheter at the atrioventricular junction for recording His bundle electro- grams. Electrical stimulation was performed with a specially designed digital stimulator and isolated constant current source (Bloom Associates, Narberth, Pennsylvania). The stimuli were rectangular pulses 1 ms in duration at twice diastolic threshold. Intracardiac recordings were filtered at 30 to 500 Hz and simultaneously recorded with 3 electrocardio- graphic leads. Stimulation techniques for initiating VT included the introduction of single, double, triple, or quadruple ventricular extrastimuli from the right ventricle during sinus rhythm or during ventricular pacing at 2 or 3 different basic cycle lengths. The stimulation protocol during VT included the introduction of 1 ventricular extrastimulus from the right ventricle scanning diastole until ventricular refractoriness was reached. If a single stimulus did not terminate tachycardia, 2 and sometimes 3 extrastimuli were introduced; the coupling intervals of the extrastimuli were varied until refractoriness was reached. If timed extrastimuli failed to terminate the tachycardia or if hemodynamic embarassment was marked, bursts of rapid ventricular pacing for 5 to 60 seconds starting at a cycle length 10 ms shorter than the tachycardia cycle length were employed. The protocol was altered to begin with more vigorous pacing techniques if tachycardia was hemo- dynamically unstable.

The effect of procainamide on tachycardia cycle length and termination was evaluated in 23 patients in whom tachycardia could be induced after the intravenous administration of procainamide 500 to 2,000 mg at 50 mg/min.

Results

Termination of VT: The ability of programmed ventricular stimulation to terminate VT could be studied in 123 patients. In 16 patients, programmed ventricular stimulation could not be evaluated because the tachycardia caused hemodynamic deterioration and immediate cardioversion was required. VT could be terminated by some form of programmed stimulation in 110 patients (79%). In 13 patients rapid ventricular pacing caused acceleration of the tachycardia and cardioversion was ultimately employed to terminate the arrhythmia.

Effect of programmed ventricular stimulation during VT (Table I): A single ventricular premature stimulus terminated VT in 23 of the 85 patients (27%) in whom this technique was tested. Double and triple ventricular extrastimuli terminated the tachycardia in 39 of 62 patients (63%) and 7 of 16 patients (44%), respectively. Rapid ventricular pacing terminated the tachycardia in 41 of the 54 patients (76%) in whom it was attempted.

Acceleration of VT (shortening of the tachycardia cycle length by 30 ms or more) occurred in 24 (20%) of the 123 patients who underwent ventricular stimulation during VT. Single, double, and triple extrastimuli caused acceleration of VT in a total of 5 patients, none of whom needed cardioversion. Rapid ventricular pacing produced acceleration in .19 of 54 patients (35%), 13 of

TABLE I Effects of Programmed Ventricular Stimulation (PVS) During VT (123 Patients)

Mode Patients of PVS (n)

Termination

n %

Acceleration

n %

1 VES 85 23 27 1 1.2 2 VES 62 39 63 3.2 3 VES 16

4: 44

; 13

RVP 54 76 19 35

RVP = rapid ventricular pacing; VES = ventricular extrastimuli.

whom required cardioversion because of hemodynamic deterioration or degeneration to ventricular fibrillation. The mean tachycardia cycle length was 325 ms (range 315 to 330) in the 5 patients in whom single (1 patient), double (2 patients), and triple extrastimuli (2 patients) produced acceleration of the tachycardia. The mean tachycardia cycle length was 282 ms (range 240 to 400) in the 19 patients whose tachycardia was accelerated by rapid ventricular pacing.

Relation between mode of termination of VT and tachycardia cycle length (Table II): The tachycardia cycle length was longer than 300 ms in all 23 patients in whom a single ventricular extrastimulus terminated the arrhythmia, and in 16 of these patients the cycle length was longer than 400 ms. The tachycardia cycle length exceeded 300 ms in 35 of the 39 patients (90%) in whom tachycardia was terminated by 2 ventricular extrastimuli and in 6 of 7 patients (86%) in whom 3 ventricular extrastimuli terminated tachycardia. In 45 of the 50 patients who had a tachycardia cycle length <300 ms, rapid ventricular pacing (20 patients) or cardioversion (25 patients) was required to terminate tachycardia.

Effect of procainamide on mode of termination of VT (Table III): The effect of procainamide on the ability to terminate VT was studied in 23 patients in whom the drug failed to prevent initiation of VT. The mean tachycardia cycle length was 280 ms (range 180 to 390) before administration of procainamide and was 392 ms (range 200 to 670) after procainamide with a mean increase of 112 f 99 ms (range 0 to 370) (p <O.OOOOl). The average dose of procainamide was 1,595 mg (500 to 2,000), resulting in a mean plasma level of 11.4 pglml (range 4.3 to 27.2). In 7 patients (30%) the mode of termination before and after procainamide was

TABLE II Relation of Mode of Termination of VT With Cycle Length (139 Patients)

VT Cycle Length (ms) Mode of

Termination 400-500 350-400 300-350 <300 VT(n)

1 VES 2 VES :2” 1: 3 VES .

RVP 1

z 1: 1 7

Cardioversion VT (n) ‘is 3: 3:

%: 1: 50 139

Abbreviations as in Table I.

December 1982 The American Journal of CARDIOLOGY Volume 50 1347


TABLE III Effect of Procainamide on Mode of Termination of VT (23 Patients)

Effect

Patients

n %

Mean Dose (mg)

Mean Mean VT Plasma Cycle Level Increase

Wglml) (ms)

Unchanged 7 30 1,460 7.5 49 f 42 (p <O.Ol)

Harder 6 26 1,500 12.9 142 f 108 (p (0.01)

Easier 10 44 1,750 13.7 136 f 110 (p <O.OOl)

similar. The mean increase in the tachycardia cycle length in these patients was 49 f 42 ms (p <O.Ol). In 6 patients (26%) in whom procainamide produced a mean increase of 142 f 108 ms (p <O.Ol) in the tachycardia cycle length, termination was more difficult. In 2 of these patients a single premature stimulus terminated

the tachycardia before procainamide, but 2 extrastimuli were required after procainamide (Fig. 1). In 3 patients rapid ventricular pacing terminated the arrhythmia before procainamide but was no longer successful after procainamide. All 3 patients required cardioversion to sinus rhythm. In the remaining patient the cycle length increased from 275 to 600 ms after procainamide, but the arrhythmia became incessant and could not be terminated by pacing techniques or cardioversion. In 10 patients (44%) in whom procainamide increased the cycle length by 138 f 110 ms (p <O.OOl) tachycardia termination was facilitated. Tachycardia terminated spontaneously in 4 of these patients. In 4 others tachycardia was terminated by rapid pacing at cycle lengths 40 to 175 ms longer than before procainamide. In 1 patient procainamide made it possible to terminate tachycardia with 2 extrastimuli instead of rapid pacing. In the last patient rapid pacing caused degeneration to ventricular fibrillation in the baseline state, whereas after procainamide rapid pacing at a longer cycle length than that during control terminated tachycardia.

CONTROL

1

aVF ”

v1

RVA

T

PROCAINAMIDE I.V. (13.1 mg/L)

v1

B T 1

aVF

aVF

v

FIGURE 1. Control: VT with a cycle length of 350 ms is terminated by a single ventricular extrastimulus delivered at 270 ms before procainamide administration. Prooainamide (13.1 mg/liter): Panel A, afler procainamide administration the tachycardia cycle length has increased to 550 ms. A single ventricular extrastimulus introduced at 360 ms fails to terminate tachycardia. Panel B, prolongation of ventricular refractoriness by procainamide prevents a single ventricular extrastimulus delivered at 340 ms from cap- turing the ventricle. Panel C, 2 ventricular extrastimuli at 380 and 340 ms are required to terminate VT after procainamide. In each panel sprface leads I, aVF. and V, are simultaneously recorded with a right ventricular apical electrogram (RVA). T = time lines.



Discussion

Comparison with previous studies: Our data cor- roborate previous studies,-” demonstrating that pace-

maker termination of VT can be performed in ap- proximately 80% of patients. However, the mode of stimulation required to terminate VT in this study differs from that of earlier reports. In 1976 Wellens et all showed that a single ventricular extrastimulus terminated induced VT in 20 of 43 patients (47%) and 2 or 3 ventricular extrastimuli were required in 13 patients (30%). An earlier report from this institution showed that VT was terminated by a single ventricular extrastimulus in 9 of 17 patients (53%), and 2 ventricular extrastimuli or rapid ventricular pacing was required in 6 patients (35%).4

The present study demonstrates that of 123 patients who underwent programmed ventricular stimulation during tachycardia a single ventricular extrastimulus terminated the arrhythmia in only 23 patients (19%) and that more than 1 ventricular extrastimulus or rapid ventricular pacing was required in 87 patients (71%). These observations suggest that more aggressive pacing techniques are frequently required to terminate ventricular tachycardia.

The cause for this discrepancy may be related to a change in patient population. Many of our more recent patients presented with hemodynamic collapse due in large part to faster tachycardia rates. The study by Wellens et al* and our earlier study4 were largely com- posed of patients with a tachycardia cycle length 1300 ms. Neither of these studies nor previous studies care- fully analyzed t,he effect of tachycardia cycle length on various modes of termination.

Furthermore, we observed that in our patient population with VT, more aggressive stimulation is required to induce VT. Often 3 and sometimes 4 extrastimuli are required to induce tachycardia. Hence, we may be dealing with a tachycardia that has a reentrant circuit that seems more difficult to penetrate. An additional investigation on the relation between mode of initiation and mode of termination seems necessary.

Relation between tachycardia cycle length and effect of programmed stimulation: Termination of VT by single, double, or triple ventricular extrastimuli usually required a tachycardia cycle length >300 ms. Timed extrastimuli produced acceleration of VT in only a small number of patients, none of whom needed cardioversion. Rapid ventricular pacing could terminate VT in 40% of patients with cycle lengths <300 ms. However, this technique caused acceleration of the stable tachycardia in 35% of patients, a finding similar to the 43% incidence reported by Fisher et al.3 Fur- thermore, most of the patients (13 of 19) with this complication required cardioversion because of rapid hemodynamic deterioration. Although rapid ventricular pacing techniques can be useful and their complications can be rapidly corrected in the electrophysiologic laboratory, we believe that because acceleration or degeneration to ventricular fibrillation is not uncommon,

this mode of stimulation should be rarely employed, if at all, for chronic pacemaker therapy of VT.

Effect of procainamide on termination of VT: Wellens et al7 showed that drugs that can slow the tachycardia can also facilitate termination. This finding was true in 44% of our 23 patients in whom we could study the mode of termination before and after procainamide administration. However, this drug made termination more difficult in 26% of our patients. The plasma level of procainamide or tachycardia cycle length was not a useful predictor of the effects on termination. Several factors can influence the ability to terminate VT: tachycardia cycle length, site of stimulation in relation to the site of tachycardia circuit, and ventricular conduction and refractoriness.‘-” Modifications of these factors by pharmacologic agents, stimulation at different sites, or increasing the current strength can influence the ability of an impulse to reach the reentrant circuit at a critical time to terminate the arrhythmia. Although modification of tachycardia cycle length by procainamide favors facilitation of termination, the increased ventricular refractoriness and prolonged intraventricular conduction produced by the drug can make termination more difficult (Fig. 1). The interplay of these factors will determine the effect of procainamide on tachycardia termination. Previous investi- gators have shown variable effects on reentrant tachycardia and ventricular tissue with procainamide.7T8 Our demonstration of poor correlation between cycle length slowing by procainamide and termination of VT sup- ports these earlier observations and suggests that the effect of procainamide on intraventricular conduction and refractoriness may be a more important factor. Therefore, increasing the tachycardia cycle length with drugs does not necessarily assure that pacemaker termination will be facilitated. Thus, the potential value of pacemaker and drug combination requires individual evaluation.

Limitations: Although our patient population is the largest heretofore reported, it probably represents a selected subgroup of patients with more refractory ventricular arrhythmia. Extrapolation of our findings to other patient populations may not be appropriate. In addition, because of the retrospective format of this study, there are methodologic limitations such as nonuniformity of stimulation protocol. Moreover, all methods of stimulation were not studied in each patient because of the speed with which termination was required clinically and the various staff members performing the studies. Another limitation of the present study is the use of the right ventricle usually apex or low septum as the stimulating site in this study. Changing the pacing site to the right ventricular outflow tract or the left ventricle might have produced different results, particularly after procainamide. However, because most permanent pacemakers are implanted at the right ventricular apex, our observations may still have clinical relevance. Another limitation is that stimulation was performed at twice the diastolic threshold which was

December 1982 The American Journal of CARDIOLOGY Volume 50 1349


always less than 2 mA. Most permanent pacemakers deliver between 5 and 10 mA, so that our study may underestimate the ability of less aggressive stimulation to terminate the tachycardia. A recent observation from our laboratory has demonstrated that termination of VT by 1 or 2 ventricular extrastimuli can be facilitated by increasing the current strength to 5 to 10 mA.9

Conclusions: We believe that the following conclusions can be helpful to the clinician in performing electrophysiologic testing of patients with VT and in selecting a proper mode of termination when right ventricular stimulation is employed: (1) In approxi- mately 80% of patients in whom VT can be induced the arrhythmia can be terminated by programmed ventricular stimulation, (2) Termination by timed extrastimuli usually requires a tachycardia cycle length >300 ms. (3) In patients with tachycardia cycle length <300 ms, rapid ventricular pacing or cardioversion is usually required to terminate the arrhythmia. (4) When performing rapid ventricular pacing, the clinician should be alert to the possible acceleration of tachycardia which can occur in over one third of patients. Therefore, we do not recommend that this mode of stimulation be employed for chronic pacemaker therapy of VT. (5) Al- though procainamide can slow the tachycardia and facilitate termination, it can make termination more

difficult in 1 of 4 patients. This potential problem should be tested before treating a patient with a combination of drug therapy plus a pacemaker.

Acknowledgment: We thank Bettie Kaplan for secretarial assistance, the cardiology fellows and nurses in the Electro- physiology Laboratory for their cooperation, and Eileen Eckstein for preparation of the figure.

References

1. Wellens HJJ, D&en DR, Lie KI. Observations on mechanisms of ventricular tachycardia in man. Circulation 1976;54:237-244.

2. Fisher JP, Cohen HL, Metua R, Furman S. Cardiac pacing and pacemakers. II. Serial electrophysiologic-pharmacologic testing for control of recurrent tachyarrhythmias. Am Heart J 1977;93:656-666.

3. Fisher JP, Mehra R, Furman S. Termination of ventricular tachycardia with bursts of rapid ventricular pacing. Am J Cardiol 1976:41:94-102.

4. Josephson ME, Horowitz LN, Farshldl A, Kastor JA. Recurrent sustained ventricular tachycardia. I. Mechanisms. Circulation 1976;57:431-440.

5. Josephson ME, Horowitz LN. Electrophysiologic approach to therapy of recurrent sustained ventricular tachycardia. Am J Cardiol 1979;43:63t- 642.

6. Fisher JD, Kim SG, Furman S, Matos JA. Role of implantable pacemakers in control of recurrent ventricular tachycardia. Am J Cardiol 1962;49: 194-206.

7. Wellens HJJ, Bar FWHM, Lle KI, Dfiren DR, Dohmen HJ. Effects of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia. Am J Cardiol 1977. I 40579-565.

6. Kaslor JA, Josephson ME, Guss SB, Horowitz LN. Human ventricular refractoriness. Il. Effects of procainamide. Circulation 1977;56:562-567.

9. Waxman HL, Cain ME, Greenspan AM, Joeepheen ME. Termination of ventricular tachycardia with ventricular stimulation: salutary effect of increased current strength. Circulation 1962:65:600-604.


termination of ventricular tachycardia: role of tachycardia cycle length

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