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Ventricular tachycardias of right ventricular origin: Markers of subclinical right ventricular disease
Ventricular tachycardias of right ventricular origin: Markers of subclinical right ventricular disease The diagnosis of subclinical myocardial disease in patients with ventricular tachycardias of right ventricular (RV) origin and no overt cardiac abnormalities is important, inasmuch as the presence of RV cardiomyopathy or arrhythmogenic dysplasia can be associated with a poor prognosis. To this end the relative value of symptoms, ECG features of ventricular tachycardia, signal-averaged ECGs, and RV echocardiograms as compared with endomyocardial biopsy findings was prospectively evaluated. Twenty-seven patients with chronic ventricular tachycardias with a left bundle branch block-like morphology, presumed to be of RV origin, were studied. Clinical examination findings, 12-lead ECGs in sinus rhythm, radiographs of the chest, coronary angiograms, and left ventricular cineangiograms were normal in all patients. RV biopsies were abnormal in 11 patients (41%) with findings suggestive of RV dysplasia or cardiomyopathy. A multivariate analysis showed a significant correlation between an abnormal biopsy and sustained ventricular tachycardia (p < 0.05), tachycardia with a superior frontal plane axis @ < O.OOl), an abnormal signal-averaged ECG (p < 0.05), and an abnormal RV echocardiogram (p < 0.001). An abnormal RV echocardiogram was both a sensitive (73%) and a specific (94%) indicator of an abnormal RV biopsy. Sustained tachycardia although sensitive (90%) had a low specificity (56%). In comparison, a superior frontal plane axis of ventricular tachycardia and an abnormal signal-averaged ECG were indicative of high specificity and low sensitivity for abnormal myocardial histologic findings. We conclude that in a patient with RV tachycardia and no overt cardiac abnormalities, sustained tachycardia, a superior frontal plane axis of ventricular tachycardia, an abnormal signal-averaged ECG, and an abnormal RV echocardiogram suggest the presence of subclinical RV disease. An abnormal RV echocardiogram is both a specific and a sensitive indicator of myocardial abnormalities and precludes the need for endomyocardial biopsy. (AM HEART J 1994;127:360-6.)
Davendra Mehta, MD, PhD, Michael J. Davies, MD, David E. Ward, MD, and A. John Camm, MD London, England
“Idiopathic” ventricular tachycardia with a left bundle branch block-like ECG morphology originates from the right ventricle.im3 Recent studies have shown that a significant proportion of patients with so-called “idiopathic” tachycardias of right ventricular (RV) origin have subclinical cardiomyopathy or RV dysplasia, which is detected either by RV biopsy or at postmortem examination.4-6 As compared with patients with normal myocardial histologic findings, who have a good long-term prognosis, patients with RV disease have potentially malignant arrhythmias, poor long-term prognosis, and might even experience From the Department thology, St George’s Received
of Cardiological Hospital Medical
for publication
accepted
June Division Center,
360
7, 1993;
and
Reprint requests: Davendra Mehta, MD, PhD, partment of Medicine, Mount Sinai Medical Place, New York, NY 10029. Copyright @ 1994 0002-8703/94/$1.00
May
Sciences School.
by Mosby-Year + .lO 4/l/51127
Book,
Inc.
Cardiovascular
Pa-
24, 1993. of Cardiology, De1 Gustave L Levy
sudden cardiac death.43 1-g Early identification of these patients and management with either appropriate antiarrhythmic drugs or implantable defibrillators is likely to improve their long-term prognosis. Right ventricular endomyocardial biopsy (EMB) is used routinely for diagnosis of subclinical myocardial disease but is associated with a risk of cardiac perforation and tamponade. lo The relative value of noninvasive parameters such as symptoms, ECG features of ventricular tachycardia, signal-averaged ECGs, and echocardiograms in the identification of subclinical myocardial disease was assessed in patients with ventricular tachycardia of RV origin who had no clinical evidence of morphologic abnormalities of the heart. METHODS
Patients with symptomatic monomorphic ventricular tachycardias with a left bundle branch block-like ECG morphology (documented on multiple ECG leads), who had no previous history suggestive of coronary artery dis-
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Fig. 1. Twelve-lead ECGs during sustained ventricular tachycardia A, Typical patient (No. 3) with normal EMB showing ventricular tachycardia with left bundle branch block-like morphology with inferior frontal plane axis. This patient had a normal EMB, a normal RV echocardiogram, and a normal signal-averaged ECG. B, Typical patient (No. 11) with abnormal EMB showing left bundle branch block-like ventricular tachycardia with superior frontal plane axis. This patient had an abnormal RV echocardiogram and an abnormal signal-averaged ECG.
ease or heart failure, were considered for inclusion in the study. Twenty-seven consecutive patients (mean age 40 years, range 19 to 64) who had no clinical evidence of an underlying cardiac abnormality were ultimately finally included. All patients had normal clinical examination findings, normal QRS and QT intervals on ECG, normal chest radiographs (cardiothoracic ratio <50 %), and normal coronary arteriograms and left ventricular cineangiograms. During exercise stress testing with the standard Bruce
protocol, none had ST segment or T wave changes suggestive of myooardial ischemia. 11 A detailed clinical history was recorded for all patients. Spontaneous (clinical) ventricular tachycardia was defined as sustained if documented arrhythmia with a uniform QRS morphology lasted 30 seconds or more or required termination because of hemodynamic compromise and nonsustained if the arrhythmia lasted less than 30 seconds. The frontal plane axis of ventricular tachycardia was con-
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sidered superior if the axis was 180 to 360 degrees with predominantly negative QRS complexes in leads III and aVF and inferior if the axis was 0 to 180 degrees with predominantly positive QRS complexes in the previously mentioned leads (Fig. 1). All investigations were performed with patients in a drug-free state after informed written consent was obtained. Signal-averaged ECGs were performed in sinus rhythm using the Arrhythmia Research Technology system (model 1200 EPX, Arrhythmia Research Technology, Inc., Austin, Texas). ECGs were recorded in sinus rhythm, and 150 to 300 beats were averaged to obtain a noise level of 0.5 pV. High band pass filter was fixed at 25 Hz. They were considered abnormal if the duration of filtered QRS complexes was 1120 msec, the duration of filtered QRS complexes after the voltage was decreased to <40 PV was ~40 msec, and the root-mean-square voltage during the last 40 msec of filtered QRS complex was 525 gV.12 Right ventricular EMBs were performed with a King bioptome via the right femoral vein. Two to five (average 2.6) specimens were obtained from each patient. Routine histopathologic techniques were used. The biopsy specimens were reviewed by an experienced cardiac histopathologist and assessment was binary, that is, normal or abnormal after detailed assessment of all specimens in each patient, and blind with no prior knowledge of any of the clinical details. Histologic findings in these patients have been reported in detail previously.6 Echocardiograms were performed by means of a protocol based on earlier studies with some modifications.13% l4 The operator was blinded to patients’ clinical data and other investigations. Echocardiograms were obtained by means of a high-resolution M-mode and cross-sectional dual-display ultrasound system with a 3.5 MHz transducer. Dual-display M-mode and two-dimensional images were simultaneously recorded on videotape and subsequently analyzed. Adequate echocardiograms were obtained from all patients. Short- and long-axis views were obtained in left parasternal, apical, and upper sternal locations with special reference to the right ventricle. From these views, measurements of the right ventricle were taken at the inflow, body, and outflow tract regions. Eight standard measurements of the right ventricle were used. These included three at the level of the RV inflow tract, one at the level of the RV cavity, and four at the level of the RV outflow tract. All echocardiographic measurements were performed independently by two investigators, and the mean of two values was used for final analysis. Echocardiographic cavity dimensions were considered abnormal if at least two of the eight measurements of the right ventricle were beyond the previously published range.15 Statistical methods. The unpaired Student’s t test was used to determine significance between continuous variables.The chi-squaretest or Fisher’s exact test, asappropriate, was used to assessthe significance of differences between groups. Standard methodswere usedto calculate the sensitivity, specificity, and predictive value of various investigations for abnormal EMBs.il A multivariate analysis wasperformed to assessthe value of each variable in
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predicting abnormal myocardial histologic findings. A p value of <0.05 was consideredstatistically significant. RESULTS
Pertinent clinical parameters, ECG features of ventricular tachycardia, results of signal-averaged ECGs, and echocardiograms from patients with normal and abnormal EMBs are shown in Table I; and grouped data are compared in Table II. All patients had been symptomatic previously, 11 patients had had one or more episodes of syncope (2 of these 11 had also experienced sudden cardiac death), and another 10 had had presyncopal episodes. In the remaining patients the dominant symptom was episodic palpitations or breathlessness. As compared with patients with normal EMBs, the incidence of syncope was higher in patients with abnormal EMBs, but the difference was not statistically significant. The two groups were similar in age, but a significantly larger proportion of male patients had abnormal EMBs (p < 0.05). Previously documented spontaneous (clinical) ventricular tachycardia was sustained in 17 patients and nonsustained in 10. The frontal plane axis of the clinical tachycardia was superior in five patients and inferior in 21. Patient 10 in the group with abnormal EMBs had ventricular tachycardia with two different morphologic features, both with a superior frontal plane axis (Table I). ECG features of ventricular tachycardia showed significant differences in the two groups (Table II). In the group with abnormal EMBs, clinical tachycardia was significantly faster and a larger proportion of these patients had sustained tachycardia and tachycardias with a superior frontal plane axis (Table II). Signal-averaged ECGs were abnormal in 5 of the 11 patients with abnormal EMBs as compared with 1 of the 17 with normal EMBs (p < 0.05 univariate analysis). Left ventricular ejection fraction was normal in all
patients, and none had left ventricular wall motion abnormalities. Two or more RV cavity dimensions were abnormal in 11 (41% ) patients. Seven of these 11 patients also had RV wall motion abnormalities (two had diffuse hypokinesis, two had abnormalities of the inferior wall, and three had abnormalities of the RV free wall). None of the patients with normal
RV cavity dimensions had wall motion abnormalities. Abnormal RV echocardiograms were seen in a significantly larger proportion of patients with abnormal as compared with normal EMBs (p < 0.01, univariate analysis). EMBs were interpreted as abnormal in 11 patients. Findings included an increase in interstitial, subendocardial, and perivascular fibrosis (nine patients),
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Table I. Demographic data, symptoms, ECG features of ventricular tachycardia, and echocardiographicand signal-averagedECG findings in patients with normal and abnormal myocardial histologic findings Patient
VT/rate in beatslmin
Age
No. Normal 1
myocardial
2
F M
3 4 5
44 39 40
M
6
F
8 9
56 51 26 38
10 11
51 48
12 13
42 32
14 15 16
44 48 36
Abnormal
F F F M F
M F M F M F F
myocardial
Dizziness,syncope Weakness Chestpain,syncope Dizziness Breathlessness Presyncope Dizziness,syncope Dizziness Dizziness+ sweating Syncope(3 episodes) Presyncope Presyncope Syncope,dizziness Presyncope
S/250
+
115 45
S/l80 NW170 NW160
90 65
NW190 s/140 NW230
75 45 90
NW180 NW215 s/220
75 90 75
NW210 s/210
60 110 95
NW250 s/190
10
62 64 29
M
11
46
M
Dizziness,chestpain
M M F
4 5
34 23
F M
6
26 37
M
9
SAE#
115 105
NW220 s/290
Syncope,SCD Breathlessness Syncope Presyncope Syncope Syncope Syncope Dizziness,sweating Dizziness Dizziness,syncope,SCD
22 28 44
8
ECHO?
+
-
-
110
-
biopsy
1 2 3
7
Axis of VT (degrees)
biopsy
55 19
7
Symptoms*
Sex
fyr)
M
M M
Axis, Frontal plane axis of clinical ventricular tachycardia; ECHO, VT, features of clinical ventricular tachycardia; NS, nonsustained *Symptoms presented are those besides palpitations. tAbnorma (+) or normal (-) ECHO with enlarged RV dimensions tAbnorma (+) or normal (-) SAE parameters.
S/230 s/200 s/300 s/190
300 110 115 105
S/250 s/zoo
250 300
s/220 s/150
330 200
NW230 S/280
175 2801 225
S/250
315
findings on right ventricular echocardiograms; SAE, findings on signal-averaged ventricular tachycardia; S, sustained tachycardia; SCD, sudden cardiac death. with
or without
wall
motion
ECGs;
abnormalities.
Table II. Comparisonof findings in patients with normal and abnormal EMBs Normal n Age History
42 of syncope
(n)
Rate
of VT
(beats/min)
Superioraxis(n) Abnormal Abnormal Ventricular abbreviations
SAE (n) ECHO (n) tachycardia as in Table I.
with
left bundle
branch
EMB
Correlation
coefficient
(p)
11
+ 11 6:lO
35 f 13 9:2
5 (31%) 7 (44%) 207 -t 36 5 (31%) 1 (6%) l(64E)
SustainedLBBB-VT (n)
other
Abnormal
16 (yr)
Sex(M:F)
LBBB-VT,
EMB
block-like
-0.16 0.43
6 (55%) 10 (91%) 264 + 49 6 (54%) 5 (45%)
0.23 0.47 0.25 0.64 0.46
8 (73%) morphology;
presence of adipose tissue in the interstitium (six patients), and variable loss of myocardium (eight patients). In five patients the histologic features were consistent with those of dilated cardiomyopathy,
Superior
(0.4) (<0.05) (0.2) (CO.05) (0.1) (
0.7 (
frontal
plane
axis between
180 and 360 degrees
on ECG;
whereas in the remainder features were indicative of RV dysplasia. l6 Because of the overlap in the histologic findings between these two conditions, distinction was difficult and was based predominantly on
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III. Value of various parametersin predicting abnormal right ventricular EMB Table
SustainedLBBB-VT Superioraxis of LBBB-VT AbnormalSAE AbnormalECHO Abbreviations
Sensitivity
Specificity
Predictive value
91% 56%
56% 100%
59% loo?,
45%
94 P-c
89%
73 SC
94 4,
83%
as in Tables I and II.
the presence of increased amounts of adipose tissue in patients with a diagnosis of RV dysplasia.6,17- l8 None of the patients had significant interstitial tissue inflammation suggestive of myocarditis. In a multivariate analysis there was a strong correlation between abnormal EMB findings and male sex (p < 0.05), sustained tachycardia (p < 0.05), tachycardia of the superior frontal plane axis (p < O.OOl), an abnormal signal-averaged ECG (p < 0.05), and an abnormal RV echocardiogram (p < 0.001). The sensitivity, specificity, and predictive value of the preceding parameters for abnormal endomyocardial histologic findings are shown in Table III. Sustained clinical tachycardia was highly sensitive (91%) but was not a very specific (56%) indicator of abnormal myocardial histology, inasmuch as a proportion of patients with normal histology also had sustained clinical tachycardia. On the contrary, a superior frontal plane axis of clinical tachycardia and an abnormal signal-averaged ECG were both specific but not sensitive predictors of myocardial disease. An abnormal RV echocardiogram was both a specific (94%) and a fairly sensitive (73 %) indicator of abnormal myocardial histology. DISCUSSION
Identification of myocardial disease in patients with RV tachycardia and no overt cardiac abnormalities is important inasmuch as both RV cardiomyopathy and arrhythmogenic dysplasia have been shown to be associated with malignant ventricular arrhythmias and a poor long-term prognosis.4j 8,lg Postmortem examination of the heart in young persons who died of ventricular arrhythmias and had no clinically overt cardiac abnormalities has shown features of RV dysplasia/cardiomyopathy.g In comparison, patients with RV tachycardias and no myocardial disease have a good long-term prognosis.7 The present data suggest that in patients with RV tachycardia, sustained tachycardia and a superior
February 1994 liearl Journal
frontal plane axis of clinical ventricular tachycardia are indicative of the presence of myocardial disease, even at an early stage when there is no clinical evidence of morphologic cardiac abnormalities. Although previous studies have shown that an underlying cardiac abnormality such as cardiomyopathic ischemic heart disease is usually identified in patients with sustained ventricular arrhythmias,20 the significance of a superior frontal plane axis of tachycardia is not well established. In the present study this was a fairly specific marker. Ventricular tachycardias with a left bundle branch block-like ECG morphology in patients with no overt cardiac abnormalities and an inferior frontal plane axis of tachycardia were seen in those originating from the RV outflow tract.23 3,6Ventricular tachycardias with such an ECG morphology, more commonly seen in female patients, have previously been reported to be associated with an absence of morphologic cardiac abnormalities and have a good long-term prognosis.7, 91 This was also seen in a subset of the present patient population. However, it must be stressed that a similar ECG morphology for clinical tachycardia can be seen in patients with generalized RV disease, which might appear predominantly in the outflow tract. Of the 11 patients with abnormal EMBs, six had ventricular tachycardias with an inferior frontal plane axis suggestive of a RV outflow tract origin. At 3 years’ follow-up the only patient who died belonged to this group. Postmortem examination of the heart in this patient showed evidence of arrhythmogenic RV dysplasia, which predominantly affected the outflow tract. On the contrary, all patients with a superior frontal plane axis of ventricular tachycardia had an abnormal EMB. Thus in a patient with a left bundle branch block-like ECG morphology of ventricular tachycardia, a superior frontal plane axis of ventricular tachycardia is a specific but not a sensitive marker for the presence of underlying myocardial disease. Few data have been published on signal-averaged ECGs in patients with nonischemic RV tachycardias. Among 30 patients with RV tachycardias and an otherwise normal heart, reported by Buxton et a1.,7 only one had a low-amplitude high-frequency signal in the terminal QRS complex. However, EMB was not performed. Fontaine et a1.22 reported signals similar to “late potentials” at the end of QRS complexes, referred to as “epsilon waves,” in patients with arrhythmogenic RV dysplasia. All patients in this study had clinically obvious arrhythmogenic RV dysplasia. It has been suggested that an abnormal signal-averaged ECG may be used as a noninvasive
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test for the presence of underlying disease.6 However, in the present population of patients with abnormal EMBs, signal-averaged ECGs were abnormal in only 45%. Only one of the 21 patients with an normal EMB had an abnormal signal-averaged ECG. Thus although very specific, an abnormal signal-averaged ECG was not a sensitive marker for the presence of primary muscle disease. Decreased sensitivity could be due to the small volume of tissue affected at an early stage of disease, low resolution of the method used for the signal-averaged ECG, or a conduction delay of such a magnitude that the high-frequency signal is lost in the main QRS complex. Furthermore, inasmuch as the presence of late potentials is regarded as a noninvasive marker for arrhythmic substrate for reentry, it is likely that in patients with normal signal-averaged ECGs other etiologic mechanisms such as triggered activity or abnormal automaticity are operational. There was a strong concordance between abnormal endomyocardial histologic findings and abnormal echocardiograms with a fair degree of specificity and sensitivity. Detailed assessment of the right ventricle, as described by Foale et a1.,4 Simson,r2 and the American Society of Echocardiography,13 in patients with ventricular tachycardias of RV origin and no overt cardiac abnormalities, is therefore the most important noninvasive investigation in the diagnosis of myocardial disease. Because histologic findings are nonspecific and do not by themselves alter management, in the presence of an abnormal RV echocardiogram one could question the need to perform an EMB unless acute myocarditis is suspected. One of the possible limitations of this study is the use of an abnormal EMB as the “gold standard” for the diagnosis of RV disease. This technique has potential limitations, inasmuch as specimens are obtained from the right side of the interventricular septum or proximal parts of the right ventricle. Areas with relatively thin ventricular walls such as the apex and outflow tract are not biopsied because of the risk of cardiac perforation. Localized involvement of the apical region or outflow tract as can occur in arhythmogenic RV dysplasia could thus be overlooked.
derlying pathologic conditions such as cardiomyopathy or arrhythmogenic dysplasia. Furthermore, it is an early indicator since abnormal RV echocardiograms were seen in patients with no clinically overt cardiac abnormalities. An abnormal signal-averaged ECG is also a specific indicator of myocardial disease but compared with an abnormal RV echocardiogram it has a lower sensitivity.
CONCLUSIONS
13.
In patients with ventricular tachycardias of RV origin and no overt cardiac abnormalities, ECG features of tachycardia such as sustained clinical tachycardia and ventricular tachycardia with a superior frontal plane axis suggest the presence of underlying myocardial disease. An abnormal RV echocardiogram is the most useful noninvasive indicator of un-
14.
REFERENCES
1. Besteni A, Sodi-Pallares D, Medran OGA, Pileggi F. A new approach for the recognition of ventricular premature beats. Am J Cardiol 1960;5:358-69. 2. Josephson ME, Horowitz LN, Waxman HL, Cain ME, Spielman SR, Greenspan AM, Marchlinski FE, Ezri M. Sustained ventricular tachycardia: role of the 12-lead electrocardiograms in localizing site of origin. Circulation 1981;64:257-72. 3. Josephson ME, Waxman HL, Cain ME, Gardner MJ, Buxton AE. Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia. Am J Cardiol 1982;50:11-22. 4. Foale RA, Nihoyannopoulos P, Ribeiro P, Mckenna WJ, Oaklev CM. Krikler DM. Rowland E. Rieht ventricular abnormalitiesin ventricular tachycardias of right ventricular origin: relation to electrophysiologic abnormalities. Br Heart J 1986;56:45-54. 5. Pietras RJ, Lam W, Bauernfeind R, Sheikh A, Palileo E, Strasberg B, Swiryn S, Rosen KM. Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: clinical, hemodynamic, and angiographic findings. AM
HEART J 1983;105:357-66. 6. Mehta D, McKenna WJ, Ward
7.
8. 9. 10.
11. 12.
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DE, Davies MJ, Camm AJ. Significance of signal-averaged electrocardiography in relation to endomyocardial biopsy and ventricular stimulation studies in patients with ventricular tachycardia without clinically apparent heart disease. J Am Co11 Cardiol1989;14:372-9. Buxton AE, Waxman HL, Marchlinsky FE, Simson MB, Cassidy D, Josephson ME. Right ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation 1983;68: 917-27. Thiene G, Nava A, Corrado D, Rossi L, Pennelli N. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med 1988;318:129-33. Maron BJ. Right ventricular cardiomyopathy: another cause of sudden death in the young. N Engl J Med 1988;318:178-80. Deckers JW, Hare JM, Baughman KL. Complications of transvenous right ventricular endomyocardial biopsy in adult patients with cardiomyopathy: a seven-year survey of 546 consecutive procedures in a tertiary referral center. J Am Co11 Cardiol 1992;19:43-7. Sheffield LT. Exercise stress testing. In: Braunwald E, ed. Heart disease: A textbook of cardiovascular medicine. Philadelphia: WB Saunders, 1988223-41. Simson MB. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulation 1981;64:235-42. Weyman AE. Cross-sectional echocardiography. Philadelphia: Lee & Febiger, 1982:497-504. Report of the American Society of Echocardiography Committee on Nomenclature and Standards in Two-Dimentional Imaging. Circulation 198&62:212-g. Foale RA, Nihoyannopoulos P, Mckenna WJ, Klienebenne A, Nadazdin A, Rowlands E, Smith G. Echocardiographic measurements of the normal adult right ventricle. Br Heart J 1986;56:33-44. Olsen EGJ. Pathological recognition of cardiomyopathy. Postgrad Med J 1975;51:277-81.
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17. Marcus FI, Fontaine GH, Guiraudon G, Frank R, Laurenceau JL, Malergue C, Grosgogeat Y. Right ventricular dvsnlasia: a report of 24 adult cases: Circulat& 1982;65:384-98. 18. Manyari DE, Klein GJ, Gulamhusein S, Boughner D, Guiraudon GM, Wyse G, Mitchell B, Kostuk W. Arrhythmogenic right ventricular dysplasia: a generalized cardiomyopathy? Circulation 1983;68:251-7. 19. Dungan WT, Garson A Jr, Gillette PC. Arrhythmogenic right ventricular dysplasia: a cause of ventricular tachycardia in children with apparently normal hearts. AM HEART J 1981;102:745-50. 20. Buxton AE, Waxman HL, Marchlinski FE, Josephson ME.
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Electrophysiologic studies in nonsustained ventricular tachycardia: relation to underlying heart disease. Am J Cardiol 1983;52:985-91. 21. Palileo EV, Ashley WW, Swiryn S, Bauernfeind RA, Stasberg B, Petropoulos AT, Rosen KM. Exercise provocable right ventricular outflow tract tachycardia. AM HEART d 1982; 104:185-93. 22. Fontaine G, Frank R, Gallais Hammonno F, Allali I, Phan-Tut H, Grosgogeat Y. Electrocardiographic des potentials tardifs du syndrome de post-excitation. Arch Ma1 Coeur 1978;71:85464.
Pronounced increase in defibrillation associated with pacing-induced cardiomyopathy in the dog
threshold
Progressive changes in myopathology after implantation of an automatic defibrillator could compromise device efficacy. The influence of heart failure development on the defibrillation threshold was evaluated by means of a rapid ventricular pacing model of heart failure in dogs. After transvenous pacemaker lead implantation, adult mongrel dogs were randomly assigned to either the control (n = 7) or rapidly paced group (240 beatslmin, n = 6). Seventeen days after implantation, triplicate determinations of the defibrillation threshold were made with three epicardial electrodes. The average defibrillation threshold was four times higher in the rapidly paced group, 13.3 t 2.0 joules (mean t SEM), than in the control group, 3.3 ? 0.7 joules (p < O.Oi), and was significantly correlated with ventricular weight (r = 0.70, p < 0.01). Both defibrillation threshold energy per gram of ventricle and ventricular weight corrected for body weight were significantly higher in rapidly paced dogs compared with control dogs. It was concluded that myocardial hypertrophy and heart failure may profoundly increase defibrillation energy requirements. (AM HEART J 1994;127:366-76.)
S. Deborah Lucy, BSc, MCISc, MSc, Douglas L. Jones, BSc(H), MSc, PhD, and George J. Klein, MD London, Ontario, Canada
Estimates of defibrillation efficacy are made at the time of implantation of automatic defibrillators. The expectation is that once electrode geometry and size have been optimized,le5 the maximum output of the
From the Departments of Physiology and Medicine, University of Western Ontario, and the Heart and Circulation Group, The John P. Robarts Research Institute. Supported by the Medical Research Council of Canada and the Heart and Stroke Foundation of Ontario and by a Distinguished Research Professor award from the Heart and Stroke Foundation of Ontario (Dr. Klein). Received for publication Aug. 3, 1992; accepted June 1, 1992. Reprint requests: Dr. D. L. Jones, Departments of Medicine and Physiology, University of Western Ontario, London, Ontario N6A 5Cl. Copyright ?’ 1994 by Mosby-Year Book, Inc. 000%8703/94/$1.00 + .lO 4/l/51056
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device will provide a sufficient margin of safety for effective defibrillation. Nonetheless, failure to defibrillate has been observed in apparently normally functioning devices.6 A potential mechanism for this defibrillation failure may be an increase in the defibrillation energy requirement as a result of changing myocardial status, such as acute ischemia or heart failure. Heart failure after myocardial infarction is a common complication in the population of patients who are candidates for automatic defibrillators.7 Heart failure may result in hypertrophy, and a relationship between heart size and defibrillation has been demonstrated.8 Therefore we used a rapid ventricular pacing model of heart failure in the dogg-ll to test the hypothesis that heart failure increases the energy requirements for defibrillation.
Davendra Mehta, MD, PhD, Michael J. Davies, MD, David E. Ward, MD, and A. John Camm, MD London, England
“Idiopathic” ventricular tachycardia with a left bundle branch block-like ECG morphology originates from the right ventricle.im3 Recent studies have shown that a significant proportion of patients with so-called “idiopathic” tachycardias of right ventricular (RV) origin have subclinical cardiomyopathy or RV dysplasia, which is detected either by RV biopsy or at postmortem examination.4-6 As compared with patients with normal myocardial histologic findings, who have a good long-term prognosis, patients with RV disease have potentially malignant arrhythmias, poor long-term prognosis, and might even experience From the Department thology, St George’s Received
of Cardiological Hospital Medical
for publication
accepted
June Division Center,
360
7, 1993;
and
Reprint requests: Davendra Mehta, MD, PhD, partment of Medicine, Mount Sinai Medical Place, New York, NY 10029. Copyright @ 1994 0002-8703/94/$1.00
May
Sciences School.
by Mosby-Year + .lO 4/l/51127
Book,
Inc.
Cardiovascular
Pa-
24, 1993. of Cardiology, De1 Gustave L Levy
sudden cardiac death.43 1-g Early identification of these patients and management with either appropriate antiarrhythmic drugs or implantable defibrillators is likely to improve their long-term prognosis. Right ventricular endomyocardial biopsy (EMB) is used routinely for diagnosis of subclinical myocardial disease but is associated with a risk of cardiac perforation and tamponade. lo The relative value of noninvasive parameters such as symptoms, ECG features of ventricular tachycardia, signal-averaged ECGs, and echocardiograms in the identification of subclinical myocardial disease was assessed in patients with ventricular tachycardia of RV origin who had no clinical evidence of morphologic abnormalities of the heart. METHODS
Patients with symptomatic monomorphic ventricular tachycardias with a left bundle branch block-like ECG morphology (documented on multiple ECG leads), who had no previous history suggestive of coronary artery dis-
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Fig. 1. Twelve-lead ECGs during sustained ventricular tachycardia A, Typical patient (No. 3) with normal EMB showing ventricular tachycardia with left bundle branch block-like morphology with inferior frontal plane axis. This patient had a normal EMB, a normal RV echocardiogram, and a normal signal-averaged ECG. B, Typical patient (No. 11) with abnormal EMB showing left bundle branch block-like ventricular tachycardia with superior frontal plane axis. This patient had an abnormal RV echocardiogram and an abnormal signal-averaged ECG.
ease or heart failure, were considered for inclusion in the study. Twenty-seven consecutive patients (mean age 40 years, range 19 to 64) who had no clinical evidence of an underlying cardiac abnormality were ultimately finally included. All patients had normal clinical examination findings, normal QRS and QT intervals on ECG, normal chest radiographs (cardiothoracic ratio <50 %), and normal coronary arteriograms and left ventricular cineangiograms. During exercise stress testing with the standard Bruce
protocol, none had ST segment or T wave changes suggestive of myooardial ischemia. 11 A detailed clinical history was recorded for all patients. Spontaneous (clinical) ventricular tachycardia was defined as sustained if documented arrhythmia with a uniform QRS morphology lasted 30 seconds or more or required termination because of hemodynamic compromise and nonsustained if the arrhythmia lasted less than 30 seconds. The frontal plane axis of ventricular tachycardia was con-
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sidered superior if the axis was 180 to 360 degrees with predominantly negative QRS complexes in leads III and aVF and inferior if the axis was 0 to 180 degrees with predominantly positive QRS complexes in the previously mentioned leads (Fig. 1). All investigations were performed with patients in a drug-free state after informed written consent was obtained. Signal-averaged ECGs were performed in sinus rhythm using the Arrhythmia Research Technology system (model 1200 EPX, Arrhythmia Research Technology, Inc., Austin, Texas). ECGs were recorded in sinus rhythm, and 150 to 300 beats were averaged to obtain a noise level of 0.5 pV. High band pass filter was fixed at 25 Hz. They were considered abnormal if the duration of filtered QRS complexes was 1120 msec, the duration of filtered QRS complexes after the voltage was decreased to <40 PV was ~40 msec, and the root-mean-square voltage during the last 40 msec of filtered QRS complex was 525 gV.12 Right ventricular EMBs were performed with a King bioptome via the right femoral vein. Two to five (average 2.6) specimens were obtained from each patient. Routine histopathologic techniques were used. The biopsy specimens were reviewed by an experienced cardiac histopathologist and assessment was binary, that is, normal or abnormal after detailed assessment of all specimens in each patient, and blind with no prior knowledge of any of the clinical details. Histologic findings in these patients have been reported in detail previously.6 Echocardiograms were performed by means of a protocol based on earlier studies with some modifications.13% l4 The operator was blinded to patients’ clinical data and other investigations. Echocardiograms were obtained by means of a high-resolution M-mode and cross-sectional dual-display ultrasound system with a 3.5 MHz transducer. Dual-display M-mode and two-dimensional images were simultaneously recorded on videotape and subsequently analyzed. Adequate echocardiograms were obtained from all patients. Short- and long-axis views were obtained in left parasternal, apical, and upper sternal locations with special reference to the right ventricle. From these views, measurements of the right ventricle were taken at the inflow, body, and outflow tract regions. Eight standard measurements of the right ventricle were used. These included three at the level of the RV inflow tract, one at the level of the RV cavity, and four at the level of the RV outflow tract. All echocardiographic measurements were performed independently by two investigators, and the mean of two values was used for final analysis. Echocardiographic cavity dimensions were considered abnormal if at least two of the eight measurements of the right ventricle were beyond the previously published range.15 Statistical methods. The unpaired Student’s t test was used to determine significance between continuous variables.The chi-squaretest or Fisher’s exact test, asappropriate, was used to assessthe significance of differences between groups. Standard methodswere usedto calculate the sensitivity, specificity, and predictive value of various investigations for abnormal EMBs.il A multivariate analysis wasperformed to assessthe value of each variable in
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predicting abnormal myocardial histologic findings. A p value of <0.05 was consideredstatistically significant. RESULTS
Pertinent clinical parameters, ECG features of ventricular tachycardia, results of signal-averaged ECGs, and echocardiograms from patients with normal and abnormal EMBs are shown in Table I; and grouped data are compared in Table II. All patients had been symptomatic previously, 11 patients had had one or more episodes of syncope (2 of these 11 had also experienced sudden cardiac death), and another 10 had had presyncopal episodes. In the remaining patients the dominant symptom was episodic palpitations or breathlessness. As compared with patients with normal EMBs, the incidence of syncope was higher in patients with abnormal EMBs, but the difference was not statistically significant. The two groups were similar in age, but a significantly larger proportion of male patients had abnormal EMBs (p < 0.05). Previously documented spontaneous (clinical) ventricular tachycardia was sustained in 17 patients and nonsustained in 10. The frontal plane axis of the clinical tachycardia was superior in five patients and inferior in 21. Patient 10 in the group with abnormal EMBs had ventricular tachycardia with two different morphologic features, both with a superior frontal plane axis (Table I). ECG features of ventricular tachycardia showed significant differences in the two groups (Table II). In the group with abnormal EMBs, clinical tachycardia was significantly faster and a larger proportion of these patients had sustained tachycardia and tachycardias with a superior frontal plane axis (Table II). Signal-averaged ECGs were abnormal in 5 of the 11 patients with abnormal EMBs as compared with 1 of the 17 with normal EMBs (p < 0.05 univariate analysis). Left ventricular ejection fraction was normal in all
patients, and none had left ventricular wall motion abnormalities. Two or more RV cavity dimensions were abnormal in 11 (41% ) patients. Seven of these 11 patients also had RV wall motion abnormalities (two had diffuse hypokinesis, two had abnormalities of the inferior wall, and three had abnormalities of the RV free wall). None of the patients with normal
RV cavity dimensions had wall motion abnormalities. Abnormal RV echocardiograms were seen in a significantly larger proportion of patients with abnormal as compared with normal EMBs (p < 0.01, univariate analysis). EMBs were interpreted as abnormal in 11 patients. Findings included an increase in interstitial, subendocardial, and perivascular fibrosis (nine patients),
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Table I. Demographic data, symptoms, ECG features of ventricular tachycardia, and echocardiographicand signal-averagedECG findings in patients with normal and abnormal myocardial histologic findings Patient
VT/rate in beatslmin
Age
No. Normal 1
myocardial
2
F M
3 4 5
44 39 40
M
6
F
8 9
56 51 26 38
10 11
51 48
12 13
42 32
14 15 16
44 48 36
Abnormal
F F F M F
M F M F M F F
myocardial
Dizziness,syncope Weakness Chestpain,syncope Dizziness Breathlessness Presyncope Dizziness,syncope Dizziness Dizziness+ sweating Syncope(3 episodes) Presyncope Presyncope Syncope,dizziness Presyncope
S/250
+
115 45
S/l80 NW170 NW160
90 65
NW190 s/140 NW230
75 45 90
NW180 NW215 s/220
75 90 75
NW210 s/210
60 110 95
NW250 s/190
10
62 64 29
M
11
46
M
Dizziness,chestpain
M M F
4 5
34 23
F M
6
26 37
M
9
SAE#
115 105
NW220 s/290
Syncope,SCD Breathlessness Syncope Presyncope Syncope Syncope Syncope Dizziness,sweating Dizziness Dizziness,syncope,SCD
22 28 44
8
ECHO?
+
-
-
110
-
biopsy
1 2 3
7
Axis of VT (degrees)
biopsy
55 19
7
Symptoms*
Sex
fyr)
M
M M
Axis, Frontal plane axis of clinical ventricular tachycardia; ECHO, VT, features of clinical ventricular tachycardia; NS, nonsustained *Symptoms presented are those besides palpitations. tAbnorma (+) or normal (-) ECHO with enlarged RV dimensions tAbnorma (+) or normal (-) SAE parameters.
S/230 s/200 s/300 s/190
300 110 115 105
S/250 s/zoo
250 300
s/220 s/150
330 200
NW230 S/280
175 2801 225
S/250
315
findings on right ventricular echocardiograms; SAE, findings on signal-averaged ventricular tachycardia; S, sustained tachycardia; SCD, sudden cardiac death. with
or without
wall
motion
ECGs;
abnormalities.
Table II. Comparisonof findings in patients with normal and abnormal EMBs Normal n Age History
42 of syncope
(n)
Rate
of VT
(beats/min)
Superioraxis(n) Abnormal Abnormal Ventricular abbreviations
SAE (n) ECHO (n) tachycardia as in Table I.
with
left bundle
branch
EMB
Correlation
coefficient
(p)
11
+ 11 6:lO
35 f 13 9:2
5 (31%) 7 (44%) 207 -t 36 5 (31%) 1 (6%) l(64E)
SustainedLBBB-VT (n)
other
Abnormal
16 (yr)
Sex(M:F)
LBBB-VT,
EMB
block-like
-0.16 0.43
6 (55%) 10 (91%) 264 + 49 6 (54%) 5 (45%)
0.23 0.47 0.25 0.64 0.46
8 (73%) morphology;
presence of adipose tissue in the interstitium (six patients), and variable loss of myocardium (eight patients). In five patients the histologic features were consistent with those of dilated cardiomyopathy,
Superior
(0.4) (<0.05) (0.2) (CO.05) (0.1) (
0.7 (
frontal
plane
axis between
180 and 360 degrees
on ECG;
whereas in the remainder features were indicative of RV dysplasia. l6 Because of the overlap in the histologic findings between these two conditions, distinction was difficult and was based predominantly on
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III. Value of various parametersin predicting abnormal right ventricular EMB Table
SustainedLBBB-VT Superioraxis of LBBB-VT AbnormalSAE AbnormalECHO Abbreviations
Sensitivity
Specificity
Predictive value
91% 56%
56% 100%
59% loo?,
45%
94 P-c
89%
73 SC
94 4,
83%
as in Tables I and II.
the presence of increased amounts of adipose tissue in patients with a diagnosis of RV dysplasia.6,17- l8 None of the patients had significant interstitial tissue inflammation suggestive of myocarditis. In a multivariate analysis there was a strong correlation between abnormal EMB findings and male sex (p < 0.05), sustained tachycardia (p < 0.05), tachycardia of the superior frontal plane axis (p < O.OOl), an abnormal signal-averaged ECG (p < 0.05), and an abnormal RV echocardiogram (p < 0.001). The sensitivity, specificity, and predictive value of the preceding parameters for abnormal endomyocardial histologic findings are shown in Table III. Sustained clinical tachycardia was highly sensitive (91%) but was not a very specific (56%) indicator of abnormal myocardial histology, inasmuch as a proportion of patients with normal histology also had sustained clinical tachycardia. On the contrary, a superior frontal plane axis of clinical tachycardia and an abnormal signal-averaged ECG were both specific but not sensitive predictors of myocardial disease. An abnormal RV echocardiogram was both a specific (94%) and a fairly sensitive (73 %) indicator of abnormal myocardial histology. DISCUSSION
Identification of myocardial disease in patients with RV tachycardia and no overt cardiac abnormalities is important inasmuch as both RV cardiomyopathy and arrhythmogenic dysplasia have been shown to be associated with malignant ventricular arrhythmias and a poor long-term prognosis.4j 8,lg Postmortem examination of the heart in young persons who died of ventricular arrhythmias and had no clinically overt cardiac abnormalities has shown features of RV dysplasia/cardiomyopathy.g In comparison, patients with RV tachycardias and no myocardial disease have a good long-term prognosis.7 The present data suggest that in patients with RV tachycardia, sustained tachycardia and a superior
February 1994 liearl Journal
frontal plane axis of clinical ventricular tachycardia are indicative of the presence of myocardial disease, even at an early stage when there is no clinical evidence of morphologic cardiac abnormalities. Although previous studies have shown that an underlying cardiac abnormality such as cardiomyopathic ischemic heart disease is usually identified in patients with sustained ventricular arrhythmias,20 the significance of a superior frontal plane axis of tachycardia is not well established. In the present study this was a fairly specific marker. Ventricular tachycardias with a left bundle branch block-like ECG morphology in patients with no overt cardiac abnormalities and an inferior frontal plane axis of tachycardia were seen in those originating from the RV outflow tract.23 3,6Ventricular tachycardias with such an ECG morphology, more commonly seen in female patients, have previously been reported to be associated with an absence of morphologic cardiac abnormalities and have a good long-term prognosis.7, 91 This was also seen in a subset of the present patient population. However, it must be stressed that a similar ECG morphology for clinical tachycardia can be seen in patients with generalized RV disease, which might appear predominantly in the outflow tract. Of the 11 patients with abnormal EMBs, six had ventricular tachycardias with an inferior frontal plane axis suggestive of a RV outflow tract origin. At 3 years’ follow-up the only patient who died belonged to this group. Postmortem examination of the heart in this patient showed evidence of arrhythmogenic RV dysplasia, which predominantly affected the outflow tract. On the contrary, all patients with a superior frontal plane axis of ventricular tachycardia had an abnormal EMB. Thus in a patient with a left bundle branch block-like ECG morphology of ventricular tachycardia, a superior frontal plane axis of ventricular tachycardia is a specific but not a sensitive marker for the presence of underlying myocardial disease. Few data have been published on signal-averaged ECGs in patients with nonischemic RV tachycardias. Among 30 patients with RV tachycardias and an otherwise normal heart, reported by Buxton et a1.,7 only one had a low-amplitude high-frequency signal in the terminal QRS complex. However, EMB was not performed. Fontaine et a1.22 reported signals similar to “late potentials” at the end of QRS complexes, referred to as “epsilon waves,” in patients with arrhythmogenic RV dysplasia. All patients in this study had clinically obvious arrhythmogenic RV dysplasia. It has been suggested that an abnormal signal-averaged ECG may be used as a noninvasive
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test for the presence of underlying disease.6 However, in the present population of patients with abnormal EMBs, signal-averaged ECGs were abnormal in only 45%. Only one of the 21 patients with an normal EMB had an abnormal signal-averaged ECG. Thus although very specific, an abnormal signal-averaged ECG was not a sensitive marker for the presence of primary muscle disease. Decreased sensitivity could be due to the small volume of tissue affected at an early stage of disease, low resolution of the method used for the signal-averaged ECG, or a conduction delay of such a magnitude that the high-frequency signal is lost in the main QRS complex. Furthermore, inasmuch as the presence of late potentials is regarded as a noninvasive marker for arrhythmic substrate for reentry, it is likely that in patients with normal signal-averaged ECGs other etiologic mechanisms such as triggered activity or abnormal automaticity are operational. There was a strong concordance between abnormal endomyocardial histologic findings and abnormal echocardiograms with a fair degree of specificity and sensitivity. Detailed assessment of the right ventricle, as described by Foale et a1.,4 Simson,r2 and the American Society of Echocardiography,13 in patients with ventricular tachycardias of RV origin and no overt cardiac abnormalities, is therefore the most important noninvasive investigation in the diagnosis of myocardial disease. Because histologic findings are nonspecific and do not by themselves alter management, in the presence of an abnormal RV echocardiogram one could question the need to perform an EMB unless acute myocarditis is suspected. One of the possible limitations of this study is the use of an abnormal EMB as the “gold standard” for the diagnosis of RV disease. This technique has potential limitations, inasmuch as specimens are obtained from the right side of the interventricular septum or proximal parts of the right ventricle. Areas with relatively thin ventricular walls such as the apex and outflow tract are not biopsied because of the risk of cardiac perforation. Localized involvement of the apical region or outflow tract as can occur in arhythmogenic RV dysplasia could thus be overlooked.
derlying pathologic conditions such as cardiomyopathy or arrhythmogenic dysplasia. Furthermore, it is an early indicator since abnormal RV echocardiograms were seen in patients with no clinically overt cardiac abnormalities. An abnormal signal-averaged ECG is also a specific indicator of myocardial disease but compared with an abnormal RV echocardiogram it has a lower sensitivity.
CONCLUSIONS
13.
In patients with ventricular tachycardias of RV origin and no overt cardiac abnormalities, ECG features of tachycardia such as sustained clinical tachycardia and ventricular tachycardia with a superior frontal plane axis suggest the presence of underlying myocardial disease. An abnormal RV echocardiogram is the most useful noninvasive indicator of un-
14.
REFERENCES
1. Besteni A, Sodi-Pallares D, Medran OGA, Pileggi F. A new approach for the recognition of ventricular premature beats. Am J Cardiol 1960;5:358-69. 2. Josephson ME, Horowitz LN, Waxman HL, Cain ME, Spielman SR, Greenspan AM, Marchlinski FE, Ezri M. Sustained ventricular tachycardia: role of the 12-lead electrocardiograms in localizing site of origin. Circulation 1981;64:257-72. 3. Josephson ME, Waxman HL, Cain ME, Gardner MJ, Buxton AE. Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia. Am J Cardiol 1982;50:11-22. 4. Foale RA, Nihoyannopoulos P, Ribeiro P, Mckenna WJ, Oaklev CM. Krikler DM. Rowland E. Rieht ventricular abnormalitiesin ventricular tachycardias of right ventricular origin: relation to electrophysiologic abnormalities. Br Heart J 1986;56:45-54. 5. Pietras RJ, Lam W, Bauernfeind R, Sheikh A, Palileo E, Strasberg B, Swiryn S, Rosen KM. Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: clinical, hemodynamic, and angiographic findings. AM
HEART J 1983;105:357-66. 6. Mehta D, McKenna WJ, Ward
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DE, Davies MJ, Camm AJ. Significance of signal-averaged electrocardiography in relation to endomyocardial biopsy and ventricular stimulation studies in patients with ventricular tachycardia without clinically apparent heart disease. J Am Co11 Cardiol1989;14:372-9. Buxton AE, Waxman HL, Marchlinsky FE, Simson MB, Cassidy D, Josephson ME. Right ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation 1983;68: 917-27. Thiene G, Nava A, Corrado D, Rossi L, Pennelli N. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med 1988;318:129-33. Maron BJ. Right ventricular cardiomyopathy: another cause of sudden death in the young. N Engl J Med 1988;318:178-80. Deckers JW, Hare JM, Baughman KL. Complications of transvenous right ventricular endomyocardial biopsy in adult patients with cardiomyopathy: a seven-year survey of 546 consecutive procedures in a tertiary referral center. J Am Co11 Cardiol 1992;19:43-7. Sheffield LT. Exercise stress testing. In: Braunwald E, ed. Heart disease: A textbook of cardiovascular medicine. Philadelphia: WB Saunders, 1988223-41. Simson MB. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulation 1981;64:235-42. Weyman AE. Cross-sectional echocardiography. Philadelphia: Lee & Febiger, 1982:497-504. Report of the American Society of Echocardiography Committee on Nomenclature and Standards in Two-Dimentional Imaging. Circulation 198&62:212-g. Foale RA, Nihoyannopoulos P, Mckenna WJ, Klienebenne A, Nadazdin A, Rowlands E, Smith G. Echocardiographic measurements of the normal adult right ventricle. Br Heart J 1986;56:33-44. Olsen EGJ. Pathological recognition of cardiomyopathy. Postgrad Med J 1975;51:277-81.
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17. Marcus FI, Fontaine GH, Guiraudon G, Frank R, Laurenceau JL, Malergue C, Grosgogeat Y. Right ventricular dvsnlasia: a report of 24 adult cases: Circulat& 1982;65:384-98. 18. Manyari DE, Klein GJ, Gulamhusein S, Boughner D, Guiraudon GM, Wyse G, Mitchell B, Kostuk W. Arrhythmogenic right ventricular dysplasia: a generalized cardiomyopathy? Circulation 1983;68:251-7. 19. Dungan WT, Garson A Jr, Gillette PC. Arrhythmogenic right ventricular dysplasia: a cause of ventricular tachycardia in children with apparently normal hearts. AM HEART J 1981;102:745-50. 20. Buxton AE, Waxman HL, Marchlinski FE, Josephson ME.
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Electrophysiologic studies in nonsustained ventricular tachycardia: relation to underlying heart disease. Am J Cardiol 1983;52:985-91. 21. Palileo EV, Ashley WW, Swiryn S, Bauernfeind RA, Stasberg B, Petropoulos AT, Rosen KM. Exercise provocable right ventricular outflow tract tachycardia. AM HEART d 1982; 104:185-93. 22. Fontaine G, Frank R, Gallais Hammonno F, Allali I, Phan-Tut H, Grosgogeat Y. Electrocardiographic des potentials tardifs du syndrome de post-excitation. Arch Ma1 Coeur 1978;71:85464.
Pronounced increase in defibrillation associated with pacing-induced cardiomyopathy in the dog
threshold
Progressive changes in myopathology after implantation of an automatic defibrillator could compromise device efficacy. The influence of heart failure development on the defibrillation threshold was evaluated by means of a rapid ventricular pacing model of heart failure in dogs. After transvenous pacemaker lead implantation, adult mongrel dogs were randomly assigned to either the control (n = 7) or rapidly paced group (240 beatslmin, n = 6). Seventeen days after implantation, triplicate determinations of the defibrillation threshold were made with three epicardial electrodes. The average defibrillation threshold was four times higher in the rapidly paced group, 13.3 t 2.0 joules (mean t SEM), than in the control group, 3.3 ? 0.7 joules (p < O.Oi), and was significantly correlated with ventricular weight (r = 0.70, p < 0.01). Both defibrillation threshold energy per gram of ventricle and ventricular weight corrected for body weight were significantly higher in rapidly paced dogs compared with control dogs. It was concluded that myocardial hypertrophy and heart failure may profoundly increase defibrillation energy requirements. (AM HEART J 1994;127:366-76.)
S. Deborah Lucy, BSc, MCISc, MSc, Douglas L. Jones, BSc(H), MSc, PhD, and George J. Klein, MD London, Ontario, Canada
Estimates of defibrillation efficacy are made at the time of implantation of automatic defibrillators. The expectation is that once electrode geometry and size have been optimized,le5 the maximum output of the
From the Departments of Physiology and Medicine, University of Western Ontario, and the Heart and Circulation Group, The John P. Robarts Research Institute. Supported by the Medical Research Council of Canada and the Heart and Stroke Foundation of Ontario and by a Distinguished Research Professor award from the Heart and Stroke Foundation of Ontario (Dr. Klein). Received for publication Aug. 3, 1992; accepted June 1, 1992. Reprint requests: Dr. D. L. Jones, Departments of Medicine and Physiology, University of Western Ontario, London, Ontario N6A 5Cl. Copyright ?’ 1994 by Mosby-Year Book, Inc. 000%8703/94/$1.00 + .lO 4/l/51056
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device will provide a sufficient margin of safety for effective defibrillation. Nonetheless, failure to defibrillate has been observed in apparently normally functioning devices.6 A potential mechanism for this defibrillation failure may be an increase in the defibrillation energy requirement as a result of changing myocardial status, such as acute ischemia or heart failure. Heart failure after myocardial infarction is a common complication in the population of patients who are candidates for automatic defibrillators.7 Heart failure may result in hypertrophy, and a relationship between heart size and defibrillation has been demonstrated.8 Therefore we used a rapid ventricular pacing model of heart failure in the dogg-ll to test the hypothesis that heart failure increases the energy requirements for defibrillation.