Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex

Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardiai infarction (12 had inferior, and two had both inferior and anterior myocardiai infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wail motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 * 4 and 244 + 5 msec, respectively (p < 0.05, mean * SEM). induced VT had a cycle length of 229 + 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphoiogies in two patients. in 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract wlth two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex. We conclude that the very rapid rate of VT in these patients is consistent with a very short refractory period in the VT circuit and that stimulation at the right ventricular outflow tract position may have initiated VT because the right ventricular outflow tract was nearer than the right ventricular apex to the VT circuit. (AM HEART J 1991;122:464.)

Lawrence S. Klein, MD, William F. Armstrong, MD, William M. Miles, MD, James J. Heger, MD, Douglas P. Zipes, MD, and Eric N. Prystowsky, MD. Indianapolis, Ind.

Results of programmed electrical stimulation of the heart to induce ventricular tachycardia (VT) are influenced by the pacing site. Wellens et al.l showed that in some patients VT induction from the right ventricle was site-specific. Other investigators2 have stressed the importance of left ventricular stimulation for VT initiation. Experimental studies in

animals3 have also shown that the site of ventricular stimulation may affect significantly the ability to initiate ventricular arrhythmias. The purpose of this study was to investigate the anatomic correlates and electrophysiologic characteristics in patients of VT that was inducible from the right ventricular outflow tract (RVOT) but not from the right ventricular apex (RVA).

From the Krannert Institute of Cardiology, the Department of Medicine, Indiana University School of Medicine, and the Roudebush Veterans Administration Medical Center. Supported in part by the Herman C. Krannert Fund, Indianapolis, Ind.; by grants HL-06308 and HL-07182 from the National Heart, Lung, and Blood Institute of the National Institutes of Health, Bethesda, Md.; by the Attorney General of Indiana Public Health Trust; and by the Roudebush Veterans Administration Medical Center, Indianapolis, Ind. Received for publication Nov. 19.1990; accepted Dec. 28, 1990. Reprint requests: Lawrence S. Klein, MD, Krannert Institute of Cardiology, Indiana University School of Medicine, 1001 West 10th St., Indianapolis, IN 46202. 4/l/29851

METHODS

464

Of 169 patients undergoing programmed ventricular stimulation for suspected or proven ventricular arrhythmias between April 1979 and March 1982, 17 (10%) had tachycardia induced only at the right ventricular outflow tract, and they make up the population for this study. All studies were performed in the postabsorptive nonsedated state after oral and written informed consent were obtained, and no patient was taking antiarrhythmic medication at the time of testing. Multiple electrode catheters were inserted percutane-

Volume 122 Number 2

ously into the femoral vein and were advanced to the heart under fluoroscopic guidance. Catheter positions were the high right atrium, the His bundle area, and the RVA and RVOT. Intracardiac recordings filtered at 30 to 500 Hz and standard electrocardiographic (ECG) leads I, II, III, and Vi, filtered at 0.1 to 20 Hz, were displayed simultaneously on a multichannel oscilloscope (Electronics for Medicine VR12, PPG Biomedical Systems, Cardiovascular Division, Pleasantville, N.Y.) and were recorded at paper speeds of 50 to 100 mm/set. Our protocol for programmed ventricular stimulation has been described in detail elsewhere.4 Briefly, ventricular pacing to induce VT in all patients was performed first at the RVA, using stimuli of twice diastolic threshold and 2 msec pulse width. One and two ventricular extrastimuli were introduced first during sinus rhythm and then during right ventricular pacing at cycle lengths of 600,500, and 400 msec, followed by right ventricular burst pacing using three to eight complexes at cycle lengths ~250 msec. If sustained VT was not induced at the apex, programmed ventricular stimulation using the same protocol was repeated at the RVOT. This study was completed prior to the use of triple ventricular extrastimuli or left ventricular stimulation in our laboratory. Anatomic information from two-dimensional echocardiography was technically adequate in 14 of the 17 patients. Two-dimensional echocardiograms were performed within 7 days of the electrophysiologic study, using commercially available, wide-angle, two-dimensional echocardiographic equipment. The parasternal long-axis and short-axis views, and apical four- and two-chamber views were recorded for analysis. The left ventricle was divided into nine anatomically distinct segments (Fig. 1) for measurement and analysis. Wall motion was characterized as normal, hypokinetic, akinetic, or dyskinetic. Discrete aneurysms were noted as such. All echocardiograms were analyzed by one investigator (WFA), who was blinded to the clinical and electrophysiologic data. Statistical analysis was performed using the Wilcoxon signed rank test. RESULTS Patient

population. Fourteen of the 17 patients had coronary artery disease, all with inferior myocardial infarctions and two with both inferior and anterior infarctions. Two patients had a dilated cardiomyopathy and one patient had no identifiable structural heart disease at cardiac catheterization but had a localized wall motion abnormality on an echocardiogram and was considered to have a localized cardiomyopathy (Table I). The patients ranged in age from 34 to 69 years, with a mean age of 53. There were 13 men and 4 women. Sixteen of the 17 patients had suffered at least one episode of documented ventricular fibrillation, sustained VT, or both. One patient had a history of presyncope only. Electrophysiologic characterl6tics. The ventricular effective and functional refractory periods (ERP and FRP, respectively) were determined at both the RVA and RVOT in all patients. The pacing cycle length at

VT induced at RV outflou: tract

465

7

1. A diagram of the left ventricle as viewed by twodimensional echocardiography in the parasternal long-axis view, parastemal short-axis view at the mid ventricle, and parasternal short-axis view at the base of the heart. The ventricle is divided into nine segments for analysis and measurement. (Reproduced with permission from the American Heart Association Inc., from Heger JJ, Weyman AE, Wann LS, Dillon JC, Feigenbaum H. Cross-sectional echocardiography in acute myocardial infarction: detection and localization of regional left ventricular asynergy. Circulation 1979;60:531-8.)

Fig.

which tachycardia was induced from the outflow tract was selected for comparison with that at the apex. The ERP of the apex was 242 & 5 versus 237 + 4 msec for the outflow tract, mean f SEM; p < 0.05. The FRP of the apex was 266 + 5 versus 259 + 4 msec for the outflow tract; p < 0.05. Thus there was a slight, but statistically significant reduction in the EXP and FRP at the RVOT compared with those at the RVA. The characteristica of VT in these 17 patients are depicted in Table I. While there were several different pacing cycle lengths at which VT was induced, two ventricular extrastimuli during right ventricular pacing induced VT in 15 of the 17 patients. Two ventricular extrastimuli failed to induce VT in two patients, who required right ventricular burst pacing for VT induction. The average rate of VT in this patient population was quite rapid, 229 1?:4 msec (mean rt SEM). The morphology of VT was variable for the group, being of right bundle branch block pattern in 12 patients, left bundle branch block pattern in three patients, and of both right and left bundle branch block pattern in two patients. Rowever, the axis of VT was superiorly directed (-45 degrees to -135 degrees) in 15 of the 17 patients. One patient

466

Klein

et al.

Table

I. VT

characteristics

American

RV

Patient No.

Agel Sex

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

41/M 61/M 62/M 58/M 57/F 64/M 60/F 34/M 42/M 57/M 50/M 48/M 42/M 48/M 69/M 53/M 50/F’

Cardiac diagnosis CAD CAD CAD DCM CAD CAD CAD LCM DCM CAD CAD CAD CAD CAD CAD CAD CAD

(IMI) (IMI, (IMI)

Mode induction

AMI)

v93 v93 V93 VlV3

(IMI) (IMI) (IMI)

Burst VlV3 VlV3 VlV3 VlV3

(IMI) (IMI) (IMI, (IMI) (IMI) (IMI) (IMI) (IMI)

v93 VlV3

AMI)

Burst VlV3 VlV3 VlV3 VlV3 VlV3

VT, Ventricular tachycardia; RV, right ventricular; electrograms of ventricular premature complexes if ventricular tachycardia could not be induced); extrastimuli during right ventricular pacing; LB, normal axis; CAD, coronary artery disease; DCM, anterior wall myocardial infarction.

of

outfzow outflow tract

PCL (msec)

PI (msec)

VT-CL (msec)

600 500 400 600 (250) 500 500 600 600 600 600 (350) 400 400 500 400 600+ 500

250,200 260,230 260,230 270,280 250,220 240,180 270,200 290,230 270,260 250,230 295,275 270,220 250,180 240,170

220 250 230 360 200 245 250 170 210 200 230 240 200 280 270 240 220

August 1881 Heart Journal

RV apex

Morphology/ Axis LB/sup RB/sup RB/sup RB/nl RB/sup RBlsup LB/sup LB/d/sup RBlsup RB + LB/sup LB + RB/sup RBlsup RB/sup RBlsup RB/right RBlsup RBlsup

Burst No Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes No Yes Yes

PI (msec)

PCL) (msec)

250,190 260,210 275,230 250,190

(500) (400) (400) (400) -

210,160 240,160 160,140 260,190

(400) (400) (400) (400) -

270,210 300,260 280,220 230,180 220,180

(400) (400) (550) (400) (400)

Similar intervals obtained Yes Yes No Yes Yes Yes Yes Yes Yes Yes Yes Yes No Yes No Yes Yes

PCL, pacing cycle length; PI, prematurity index (the sum of the intervals, in milliseconds, between the at which either sustained ventricular tachycardia was induced, or the most premature intervals obtainable VT-CL, ventricular tachycardia cycle length; Burst, right ventricular burst pacing; Viva, two ventricular left bundle branch block morphology; RB, right bundle branch block morphology; sup, superior axis; nl, dilated cardiomyopathy; LCM, localized cardiomyopathy; IMI, inferior wall myocardial infarction; AMI,

had a rightward VT axis and another had a normal VT axis. Because of the presumed importance of the prematurity of the ventricular extrastimuli for VT induction, and because there was a slightly shorter refractory period at the RVOT than at the RVA, the data were analyzed to determine if ventricular premature intervals equal to those inducing VT at the outflow tract were obtainable at the RVA (Table I). The sum of the shortest obtainable intervals between electrograms of ventricular premature complexes (Table I) were used to define a “prematurity index” (PI) for the RVA. This was compared with the sum of the intervals between the premature complexes that induced VT from the RVOT. Fourteen patients had pacing intervals from the RVA that were equal to or shorter than those needed to initiate VT from the RVOT (PI of the apex I PI of the RVOT). In three patients this was not the case, though in two of these three patients right ventricular (RV) burst pacing (which was not required for VT induction at the RVOT) also did not induce VT from the RV apex. Fig. 2 illustrates VT induction in patient No. 2. Following a pacing train at 500 msec, two ventricular extrastimuli failed to induce tachycardia from the RVA (Fig. 2, A). Utilizing a similar pacing cadence from the RVOT, sustained VT was induced in this patient (Fig. 2, B). Of note, the coupling interval at

the RVOT that induced VT was greater than that at the RVA that failed to induce VT. Echocardiographic findings. Echocardiograms technically adequate for analysis were available in 14 of the 17 patients. Results of wall motion analysis are shown in Fig. 3, which displays all nine segments of the left ventricle in a series of concentric rings. Twelve of the 14 patients had wall motion abnormalities in areas 3 and 4 (inferoposterior wall at the base). The third most common area of wall motion abnormality was area 7 (inferior wall at the mid ventricle level). Eight patients had wall motion abnormalities at the apex. The wall motion score index5 (Fig. 3) was highest (poorest wall motion) in areas 3 and 4, followed by areas 9 and 7. The remaining areas of the heart had very low wall motion score indices (indicating better overall wall motion). Of the two cardiomyopathy patients in the study, one (patient No. 9) had maximal wall motion abnormality in areas 3 and 4, while the other (patient No. 4) had diffuse hypokinesis. Thus 12 of the 14 patients had abnormal wall motion located at the base of the heart near the atrioventricular groove and adjacent to the RVOT (junction of area 3 and 4). Six patients had wall motion abnormalities confined to this area, whereas an additional six patients had multiple areas of wall motion abnormalities; two of these latter patients had abnormalities most marked at the base, while in the re-

volume 122 Number 2

8153762

2. Recordings of an electrophysiologic study from patient No. 2 in whom sustained ventricular tachycardia was induced from the right ventricular outflow tract but not from the right ventricular apex. In panel A, two ventricular extrastimuli (the most premature obtainable) failed to induce ventricular tachycardia. In panel B, two ventricular extrastimuli (slightly less premature than those obtainable from the right ventricular apex) initiated sustained ventricular tachycardia. Shown are electrocardiographic leads I, II, III, and Vi, along with the His bundle electrogram (HBE,J and right ventricular electrograms. RVOT, right ventricular outflow tract. Fig.

maining

four patients

ANTERIOR

the major wall motion abnor-

mality was closer to the apex. In all, 8 of the 14 patients had their major or only wall motion abnormality at the base of the left ventricle. Only two patients had no abnormality at the base of the left ventricle. Fig. 4 illustrates a two-dimensional echocardiogram in patient No. 8 who had normal coronary arteries and a normal right anterior oblique ventriculogram at cardiac catheterization. Two-dimensional echocardiography, however, revealed evidence of a discrete aneurysm at the base of the septum, shown schematically at the right of Fig. 4.

MEDIAL

LATERAL

DISCUSSION

Multiple factors affect inducibility of VT by programmed ventricular stimulation, including the number of extrastimuli, the pacing cycle lengths, and the site of ventricular stimulation.2T 4, 6 7 In this study, we identified a subset of patients in whom VT could be induced from the RVOT but not from the RVA. There was a very high prevalence of basilar wall motion abnormalities noted on echocardiography in this patient subset. Anatomically the RVOT, which was the site of tachycardia induction, is more proximal to the base of the heart than to the apex. The relative ease of VT induction from the RVOT in these patients may have been due to closer proximity of the stimulus to the reentrant circuit of the VT, which presumably was adjacent to the area of echocardiographic abnormality. The role of stimulus proximity to the reentry circuit focus has previously been demonstrated in canine experiments3 Although endocardial mapping was not performed in these patients, the superior axis and the QRS morphology of VT in

POSTERIOR

3. Method used to depict location of wall motion abnormality in each patient. All nine segments depicted in Fig. 1 are displayed here in a series of concentric rings. In the parenthesis following each bold-faced number is a pair of numbers, displayed as a fraction. The numerator refers to the number of patients in whom ventricular wall motion was abnormal in this segment (out of a total of 14 patients). The denominator refers to the wall motion index.5 Each segment was assigned a number to describe wall motion, with 0 for normal; 1 if hypokinetic; 2 if akinetic; 3 if dyskinetic; and 4 if aneurysmal. The wall motion score for a given segment in all 14 patients was added and the total was divided by 14 to derive this wall motion index. A higher wall motion index indicates a greater degree of wall motion abnormality in an individual segment.

Fig.

these patients is consistent with a VT site of origin (or endocardial exit site) near the anatomic abnormality.8 Other investigators have examined site specificity

Au&~ust 1891 American Heart Journal

Fig. 4. Two-dimensional echocardiogram, in the shortaxis view at the base of the heart, in a patient with angiographically normal coronary arteries and a normal right anterior oblique left ventriculogram. Arrows point to a discrete aneurysm at the ventricular septum base. An, Aneurysm; A, anterior; L, lateral; P, posterior; M, medial.

for VT initiation. In a study of 100 patients without VT initiated from the RVA, Doherty et al9 described 22 patients who had VT or VF induced only from the RVOT. These patients tended to be younger and were more likely to have cardiac disease unrelated to coronary artery disease. The use of three ventricular extrastimuli may have affected adversely the specificity of site-specific VT induction in their patients. VT in the 22 patients was faster than that initiated in the comparison group from the RVA, though the difference was not statistically significant. Several factors were likely responsible for VT induction from the RVOT and not from the RVA in our patients. Three of the 17 patients had shorter coupling intervals achieved at the outflow tract versus the apex. Thus it is possible that the longer coupling intervals were in part responsible for the lack of VT induction at the apex in these three patients. In contrast, when similar or shorter coupling intervals were achieved at the RVA, it was probably important that the RVOT stimulation site was anatomically closer to the presumed VT circuit. Both of these factors (extrastimulus prematurity and anatomic proximity to the reentrant circuit) may have been necessary in some patients. One limitation of this study was that it was performed before the routine use of triple extrastimuli. However, the findings reported here would have been similar, since we routinely use two extrastimuli at both RV sites prior to employing triple extrastimuli at the RVA. In fact, Morady et aLlo have suggested that in patients with sustained (but undocumented) VT, a ventricular pacing protocol utilizing two RV sites and one left ventricular site, prior to the use of triple extrastimuli, may minimize uncertainty regarding the clinical significance of induced tachycar-

dia. Utilization of several pacing sites prior to triple extrastimuli increased the yield of induced clinical tachycardia from 61% to 85 % , presumably because this allowed completion of the pacing protocol prior to induction of symptomatic, nonclinical VT or fibrillation. Nonetheless, it is possible that at least some of our patients would have had VT induced at the RV apex had triple extrastimuli been utilized. In conclusion, while an explanation for the occurrence of site-specific VT induction is not always readily apparent, it appears that in our group of patients in whom VT could be initiated only from the RVOT there was a very high prevalence of echocardiographic wall motion abnormalities close to the site of catheter stimulation. The RVOT was nearer than the RVA to damaged ventricular myocardium in these patients, and therefore was most likely closer to the origin of VT, accounting for VT induction only at this site. The authors thank Elizabeth Darling, RN, for her help with the electrophysiology studies, and Sue Hennigar for her secretarial assistance. REFERENCES

1. Wellens HJJ, Duren DR, Lie KI. Observations on mechanisms of ventricular tachycardia in man. Circulation 1976;54:237-44. 2. Robertson JF, Cain ME, Horowitz LN, et al. Anatomic and electrophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation. Am J Cardiol1981;48:2638. 3. Michelson EL, Spear JF, Moore EN. Initiation of sustained ventricular tachyarrhythmias in a canine model of chronic myocardial infarction: importance of the site of stimulation. Circulation 1981;63:776-83. 4. Prystowsky EN, Miles WM, Evans JJ, et al. Induction of ventricular tachycardia during programmed electrical stimulation: analysis of pacing methods. Circulation, 1986;73(suppl 11):32-B. 5. Heger JJ, Weyman AE, Wann S, Rogers EW, Dillon JC, Feigenbaum H. Cross-sectional echocardiographic analvsis of the extent of left ventricular asynergy in acute myocardial infarction. Circulation 1980;61:1113-8. 6. Buxton AE, Waxman HL, Marchlinski FE, Unterecker WJ, Waspe LE, Josephson ME. Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias. Circulation 1984;69:53240. 7. Estes NAM III, Garan H, McGovern B, Ruskin JN. Influence of drive cycle length during programmed stimulation on induction of ventricular arrhythmias: analysis of 403 patients. Am J Cardiol 1986;57:108-12. 8. Josephson ME, Horowitz LN, Waxman HL, Cain ME, Spielman SR, Greenspan AM, Marchlinski FE, Ezri MD. Sustained ventricular tachycardia: role of the la-lead electrocardiogram in localizine site of origin. Circulation 1981:64:257-72. 9. Doherty JU, Kienzle fiG, Waxman HL, Buxton AE, Marchlinski FE, Josephson ME. Programmed ventricular stimulation at a second right ventricular site: an analysis of 100 patients, with special reference to sensitivity, specificity and characteristics of patients with induced ventricular tachycardia. Am J Cardiol 1983;52:1184-9. 10. Morady F, DiCarlo L, Winston S, Davis JC, Scheinman MM. A prospective comparison of triple extrastimuli and left ventricular stimulation in studies of ventricular tachycardia induction. Circulation 1984;70:52-7.