- Email: [email protected]
Effects of left ventricular hypertrophy on the signal-averaged electrocardiogram
cerebrovascular and peripheral embolic events. Stroke /987;18:856-862. 3. Hanley PC, Tajik AJ, Hynes JK, Edwards WD, Reeder GS, Ha&r DJ, Seward JB. Diagnosis and classilication of atria1 septal aneurysm by two-dimensional echocardiography: report of 80 consecutive cases. J Am Coil Cardiol 1985.6:1370-1382. 4. Grosgogeat Y, Lhermitte F, Carpentier A, Faynet J, Alhomme P, Tran T. Aneurysme de la cloison interauriculaire revele par une embolie cerebrale. Arch Mal Coeur 1973.66:169-l 77. 5. Thompson Jl, Phillips LA, Melmon KL. Pseudotumor of the right atrium. Report of a case and review of its etiology. Ann Intern Med 1966,64:665-667.
Effects of Left Ventricular Hypertrophy Signal-Averaged Electrocardiogram Thomas C. Hilton, MD, Terry Greenwalt, and Thomas A. Buckingham, MD
Chalapathirao
6. Silver MD, Dorsey JS. Aneurysms of the septum primum in adults. Arch Pathol Lab Med 1978:/02:62-65. 7. Iliceto S, Papa A, Sorino M, Rizzon P. Combined atrial septal aneurysm and mitral valve prolapse: detection by two-dimensional echocardiography. Am J Cardiol 1984;54:1151-1153. 9. Roberts WC. Aneurysm (redundancy) of the atria1 septum (fossa ovale membrane) and prolapse (redundancy) of the mitral valve. Am J Cardiol 1984.34: 1153-1154. 9. Belkin RN, Waugh R.4, Kisslo J. Interatrial shunting in atrial septal aneurysm. Am J Cardiol 1986:S7:310-312.
on the V. Gudipati,
MD, Anthony
C. Pearson,
MD,
1,000 Hz. Ectopic or noisy beats were rejected by a recognition template generatedfrom thefirst 8 beats.At least I.50 beats were averaged in each recording with a rhythmias.leg Late potentials have been shown to predict noise level 25 31f21 37f27 NS digital form at l&bit accuracy with a sampling rate of
ignal-averaged electrocardiography (SAECG) has made possible the identification of late potentials in S patients at risk of developing malignant ventricular ar-
RMS QRS (uV)
From the Division of Cardiology/Department of Internal Medicine, St. Louis University Medical Center, 3635 Vista at Grand, Box 15250, St. Louis, Missouri 63110. Manuscript received January 5, 1990; revised manuscript received and accepted May 3, 1990.
764
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
66
(8 to 98) 60f29 (25 to 137)
(7 to 103) 63*24 (21 to 140)
NS
*p=o.us LAS duration = duration of low amplitude slgnal (GO mV) ln terminal QRS: LVH = left ventricular hypertrophy: NS = not slgnlfrcant; QRS duration = duration of flltered QRS: RMS LAS = root-mean-square amplitude of last 40 ms of QRS; RMS QRS = root-mean-square amplitude of flltered QRS.
rABl.E II Baseline Clinical Characteristics Echocardiographic Left Ventricular Mass Wrth LVH (%) Number Age Ws) Men Women Myocardral rnfarctron by hrstory Anterior myocardral infarction lnfenor myocardial Infarctron Both LV mass(g) Sudden cardiac death Clrnical ventrwlar tachycardra lnducrbilrty
and
Wrthout LVH (%)
TABLE Ill Statistical Association Between Individual and Combined Signal-Averaged Parameters with Clinical Events Patients With and Without Left Ventricular Hypertrophy p Value
21 61il5 16 (76) 5 (24) 15(71)
37 58~x15 29 (78) 5 (22) 19 (51)
8 (38)
9 (24)
NS
7 (33)
9 (24)
NS
0 176f68
6 (29) 8/ 19 (42) 14 (66)
Without
Wrth LV Hypertrophy
NS NS NS
QRSDuratron* LAS Duration* RMS4O(ms)” RMS QRS” Combined late potentrals+
NS
in
LV Hypertrophy
IND
CVT
SCD
IND
CVT
SCD
NS NS NS NS NS
NS NS NS NS NS
NS NS NS NS 004
0.062 OOMI OOOO 0.002 0.001
NS 0.111 0.016 0.016 0.025
NS
NS NS NS NS
* Compared to clinical events wng analyw of var!ance. t compared to cllnlcal events us,ng chl-square test. CVT = clinical ventrscular tachycardiaIND = inducible ventricular tachycardia. NS = not s,@cant. SCD = sudden cardiac death Other abbrevlatlons as I” Table II
l(3) 91i22 7 (1% 16/35 (46)
NS 0.00001 NS
1
NS
20 (54)
NS
tally significant differences in the QRS duration, LAS duration, RMS LAS or the RMS QRS (Table l). However, the QRS duration was slightly longer in patients with LVH (I22 f 22 ms us 103 f 16 ms, p = 0.09). No individual SAECG parameter was significantly associated with inducible ventricular tachycardia in patients with LV hypertrophy (Table IIl). However, 3 of the 4 individual SAECG parameters (LAS duration, RMS LAS and RMS QRS) were significantly associated with inducible ventricular tachycardia in patients with no LV hypertrophy, and the association of QRS duration to inducible ventricular tachycardia was close to statistical significance (p = 0.06). Late potentials were not associated with inducible ventricular tachycardia (p = 0.2) in patients with LV hypertrophy, but in patients without LV hypertrophy, late potentials were significantly associated with inducibility @ = O.OOI). Similarly, no individual SAECG parameter was significantly associated with clinical ventricular tachycardia in patients with LV hypertrophy (Table IIl). However, in patients with no LV hypertrophy, the RMS LAS and RMS QRS were significantly associated with clinical ventricular tachycardia @ <0.02). QRS duration and LAS duration also tended to correlate with clinical ventricular tachycardia @ = 0.19, p = 0.11, respectively). Late potentials showed no association with clinical ventricular tachycardia in patients with LV hypertrophy, but they were significantly associated with clinical ven-
*
present if L V mass was > 134 g/m2 for men or > 1 IO g/m’ for women. Electrophysiologic testing was performed in using a previously described protocol.R The endpoint of the stimulation protocol was the reproducible induction of a sustained monomorphic ventricular tachycardia. In patients with polymorphic ventricular tachycardia or ventricularfibrillation, stimulation was stopped if countershock was required. Continuous data is expressed as the mean f standard deviation and compared with one-way analysis of variance. Proportions were compared with the chi-square statistic. A p value 10.05 was considered statistically significant. Fifty-eight patients had SAECG, M-mode echocardiography and programmed electrical stimulation. Twenty-one patients had echocardiographic LV hypertrophy; 37 patients did not (Table Il). The 2 patient groups were similar in age, sex, incidence of myocardial infarction, inducible ventricular tachycardia, clinical ventricular tachycardia, and sudden cardiac death. When comparing patients with LV hypertrophy to patients without LV hypertrophy there were no statisti-
FIGURE 1. An example of a recording with a late potential. The measurements mod in this analysis are shown. The RIMS QRS is the area (unshaded and shaded) undsr the QRS curve. (Reproduced with permission from Am ./ Cardio/.23)
Duratlom
(ms)
Total ORS 140 Under 40,~N 54
THE AMERICAN
JOURNAL
OF CARDIOLOGY
SEPTEMBER
15, 1990
765
tricular tachycardia in patients with no LV hypertrophy (p = 0.025). No individual SAECG parameter had a statistically significant association with sudden cardiac death in either group (Table III). Late potentials were associated with sudden cardiac death inpatients with LV hypertrophy (p = 0.04) but not in patients without LV hypertrophy (difference not signijicant). SAECG has made possible the identification of patients at high risk of developing ventricular arrhythmia; however, clinical use of SAECG has been limited by borderline sensitivity, specificity and predictive value of this test as a predictor of serious clinical events.3 The clinical use of SAECG testing might be improved if highrisk populations are tested. Patients with LV hypertrophy represent such a high-risk population’1-‘9; however, our results show that LV hypertrophy may interfere with and subtract from the association between SAECG parameters and ventricular arrhythmias. Previous studies have shown the ability of SAECG to predict clinical ventricular tachycardia,3-6 inducible ventricular tachycardia8-lo and sudden cardiac death.3 However, no previous studies have separately analyzed patients with LV hypertrophy. Based on our findings, the exclusion of patients with LV hypertrophy may improve the ability of SAECG to predict inducible ventricular tachycardia and clinical ventricular tachycardia, but not sudden cardiac death. The fact that combined abnormal SAECG parameters (late potentials) were associated with sudden cardiac death only in patients with LV hypertrophy and not in patients without LV hypertrophy may reflect the higher incidence of sudden cardiac death in patients with echocardiographic’ 1,19and electrocardiographic’2 LV hypertrophy. Positive late potentials in patients with LV hypertrophy may identify a subgroup of these patients at higher risk for sudden cardiac death. Prospective studies will be needed to confirm this. The inducibility of sustained monomorphic ventricular tachycardia by programmed electrical stimulation is a reliable clinical endpoint for guiding antiarrhythmic therapy. Moreover, we feel that the high degree of association between individual and combined SAECG parameters and inducible ventricular tachycardia in patients without LV hypertrophy and the absence of such an association in patients with LV hypertrophy is the most significant finding in this study. The most important limitations of our study relate to the small size and highly selected nature of the study population. Data derived from a small population of patients who have undergone programmed electrical stimulation cannot be extrapolated to the population at large. Our findings may be most useful in the interpretation of SAECGs on patients being considered for programmed electrical stimulation. Thus, individual and combined SAECG parameters are significantly associated with inducible ventricular tachycardia and clinical ventricular tachycardia in patients without echocardiographic LV hypertrophy but not in patients with echocardiographic LV hypertrophy. These data suggest that LV hypertrophy interferes with 766
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
66
the usefulness of this test for identifying patients at risk for ventricular arrhythmia. Further work will be required to determine the mechanism for this interference and to see if the findings are consistent in more general patient populations. 1. Buckingham TA, Ghosh G, Homan SM. Thessen CC, Redd RM, Stevens LL, Chaitman BR, Kennedy HL. Independent value of signal-averaged electrocardiography and left ventricular function in identifying patients with sustained ventricular tachycardia in coronary artery disease. Am J Curdjo/ /986;59:568-572, 2. Buckingham TA, Thessen CC, Hertweck D. Janosik DL. Kennedv HL. Sienalaveraged &ctrocardiography in the time and frequency domains. .&I J &diol 1989:63:820-825. 3. Kuchar DL, Thorburn CS, Sammel NL. Prediction of serious arrhythmic events after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring, and radionuclide ventriculography. J Am Co11 Cardiol /987:9:53/L 538. 4. Denniss
AR, Richards DA, Cody DV. Russell PA, Young AA, Cooper MJ, Ross DL, Uther JB. Prognostic significance of ventricular tachycardia and tibrillation induced at programmed stimulation and delayed potentials detected on the signal-averaged electrocardiograms of survivors of acute myocardial infarction. Circulation 1986;74:73/L745. 5. Cain ME, Ambos HD, Witowski FX. Sobel BE. Fast-Fourier transform analysis of signal-averaged electrocardiograms for identification of patients prone to sustained ventricular tachycardia. Cimdarion /984,69:7//L720. 6. Kuchar DL, Thorburn CW, Sammel NL. Late potentials detected after myocardial infarction: natural history and prognostic significance. Circulation
1986;74:1280-1289. 7. Simson MB. The use of signals
in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulotian 1982,64:235-240. 8. Buckingham TA, Thessen CC, Stevens L, Redd RM, Janosik DL. Kennedy HL. Relation of signal-averaged late potentials to inducible ventricular arrhythmias. J Electrophysiol 1988:2:424-436. 9. Breithardt G, Borggrefe M, Quantius B, Karbenn J, Seipel L. Ventricular vulnerability assessed by programmed ventricular stimulation in patients with and without late potentials. Cimdation 1983,68:275-28/. 10. Winters SL, Stewart D, Games JA. Signal averaging of the surface QRS complex predicts inducibility of ventricular tachycardia in patients with syncope of unknown origin: a prospective study. J Am Coll Cardiol 1987:10:775-778. 11. Casale PN, Devereux RB, Milner M. Zullo C, Harshfield GA, Pickering TG, Laraah JH. Value of echocardiozraohic measurement of left ventricular mass in predi&g cardiovascular morbid &nts in hypertensive men. Ann fntern Med
1986:105:173-178. 12. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram. Prevalence, incidence, and mortality in the Framingham Study. Ann Intern Ued 1969;71:89~101. 13. Lavie CJ, Nunez BD, Garavaglia GE, Mess4 FH. Hypertensive concentric left ventricular hypertrophy: when is ventricular ectopic activity increased? South Medical J I 988;81:696m700. 14. Messerli FH, Ventura HO, Elizardi DJ. Dunn FG, Frohlich ED. Hypertension and sudden death. Increased ventricular ectopic activity in left ventricular hypertrophy. Ant J Med 1984;77:18-22. 15. Kannel WB. Prevalence and natural history of electrocardiographic left ventricular hypertrophy. Am J Med 1983;75:4-11. 16. Levy D, Anderson KM, Savage DD, Balkus SA, Kannel WB, Castelli WP. Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol 1987:60:560-565. 17. Borhani NO. Left ventricular hypertrophy, arrhythmias and sudden death in systemic hypertension. Am J Cardiol 198760:l31-181. 18. McLenachan JM, Henderson E, Morris Kl, Dargie JH. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Eng/ J %cd
1987;3/7:787-792. 19. Aronow WS, Epstein S, Koenigsberg M, Schwartz KS. Usefulness of echocardiographic left ventricular hypertrophy, ventricular tachycardia and complex ventricular arrhythmias in predicting ventricular fibrillation or sudden cardiac death in elderly patients. Am J Cardiol 1988.62:1124-1125. 20. Sahn DJ, DeMaria A, Kisslo J, Weyman A, the Committee on M-Mode Standardization of the American Society of Echocardiography. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. J Am Coil Cardiol 1978;58:1072-1083. 21. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Circulation 1977:55:613m618, 22. Woythaler JN. Singer SL, Kwan 0, Meltzer RS, Reubner B, Bommer W, DaMaria A. Accuracy of echocardiography versus electrocardiography in detecting left ventricular hypertrophy: comparison of postmortem mass measurements. J Am Cot! Cardiol 1983;2:305-3/l. 23. Buckingham TA, Thessen CC, Stevens LL, Redd RM, Kennedy HL. The effect of conduction defect on the signal-averaged electrocardiographic determination of late potentials. Am J Cardiol 1988;6/:1265-1271.
Effects of Left Ventricular Hypertrophy Signal-Averaged Electrocardiogram Thomas C. Hilton, MD, Terry Greenwalt, and Thomas A. Buckingham, MD
Chalapathirao
6. Silver MD, Dorsey JS. Aneurysms of the septum primum in adults. Arch Pathol Lab Med 1978:/02:62-65. 7. Iliceto S, Papa A, Sorino M, Rizzon P. Combined atrial septal aneurysm and mitral valve prolapse: detection by two-dimensional echocardiography. Am J Cardiol 1984;54:1151-1153. 9. Roberts WC. Aneurysm (redundancy) of the atria1 septum (fossa ovale membrane) and prolapse (redundancy) of the mitral valve. Am J Cardiol 1984.34: 1153-1154. 9. Belkin RN, Waugh R.4, Kisslo J. Interatrial shunting in atrial septal aneurysm. Am J Cardiol 1986:S7:310-312.
on the V. Gudipati,
MD, Anthony
C. Pearson,
MD,
1,000 Hz. Ectopic or noisy beats were rejected by a recognition template generatedfrom thefirst 8 beats.At least I.50 beats were averaged in each recording with a rhythmias.leg Late potentials have been shown to predict noise level 25 31f21 37f27 NS digital form at l&bit accuracy with a sampling rate of
ignal-averaged electrocardiography (SAECG) has made possible the identification of late potentials in S patients at risk of developing malignant ventricular ar-
RMS QRS (uV)
From the Division of Cardiology/Department of Internal Medicine, St. Louis University Medical Center, 3635 Vista at Grand, Box 15250, St. Louis, Missouri 63110. Manuscript received January 5, 1990; revised manuscript received and accepted May 3, 1990.
764
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
66
(8 to 98) 60f29 (25 to 137)
(7 to 103) 63*24 (21 to 140)
NS
*p=o.us LAS duration = duration of low amplitude slgnal (GO mV) ln terminal QRS: LVH = left ventricular hypertrophy: NS = not slgnlfrcant; QRS duration = duration of flltered QRS: RMS LAS = root-mean-square amplitude of last 40 ms of QRS; RMS QRS = root-mean-square amplitude of flltered QRS.
rABl.E II Baseline Clinical Characteristics Echocardiographic Left Ventricular Mass Wrth LVH (%) Number Age Ws) Men Women Myocardral rnfarctron by hrstory Anterior myocardral infarction lnfenor myocardial Infarctron Both LV mass(g) Sudden cardiac death Clrnical ventrwlar tachycardra lnducrbilrty
and
Wrthout LVH (%)
TABLE Ill Statistical Association Between Individual and Combined Signal-Averaged Parameters with Clinical Events Patients With and Without Left Ventricular Hypertrophy p Value
21 61il5 16 (76) 5 (24) 15(71)
37 58~x15 29 (78) 5 (22) 19 (51)
8 (38)
9 (24)
NS
7 (33)
9 (24)
NS
0 176f68
6 (29) 8/ 19 (42) 14 (66)
Without
Wrth LV Hypertrophy
NS NS NS
QRSDuratron* LAS Duration* RMS4O(ms)” RMS QRS” Combined late potentrals+
NS
in
LV Hypertrophy
IND
CVT
SCD
IND
CVT
SCD
NS NS NS NS NS
NS NS NS NS NS
NS NS NS NS 004
0.062 OOMI OOOO 0.002 0.001
NS 0.111 0.016 0.016 0.025
NS
NS NS NS NS
* Compared to clinical events wng analyw of var!ance. t compared to cllnlcal events us,ng chl-square test. CVT = clinical ventrscular tachycardiaIND = inducible ventricular tachycardia. NS = not s,@cant. SCD = sudden cardiac death Other abbrevlatlons as I” Table II
l(3) 91i22 7 (1% 16/35 (46)
NS 0.00001 NS
1
NS
20 (54)
NS
tally significant differences in the QRS duration, LAS duration, RMS LAS or the RMS QRS (Table l). However, the QRS duration was slightly longer in patients with LVH (I22 f 22 ms us 103 f 16 ms, p = 0.09). No individual SAECG parameter was significantly associated with inducible ventricular tachycardia in patients with LV hypertrophy (Table IIl). However, 3 of the 4 individual SAECG parameters (LAS duration, RMS LAS and RMS QRS) were significantly associated with inducible ventricular tachycardia in patients with no LV hypertrophy, and the association of QRS duration to inducible ventricular tachycardia was close to statistical significance (p = 0.06). Late potentials were not associated with inducible ventricular tachycardia (p = 0.2) in patients with LV hypertrophy, but in patients without LV hypertrophy, late potentials were significantly associated with inducibility @ = O.OOI). Similarly, no individual SAECG parameter was significantly associated with clinical ventricular tachycardia in patients with LV hypertrophy (Table IIl). However, in patients with no LV hypertrophy, the RMS LAS and RMS QRS were significantly associated with clinical ventricular tachycardia @ <0.02). QRS duration and LAS duration also tended to correlate with clinical ventricular tachycardia @ = 0.19, p = 0.11, respectively). Late potentials showed no association with clinical ventricular tachycardia in patients with LV hypertrophy, but they were significantly associated with clinical ven-
*
present if L V mass was > 134 g/m2 for men or > 1 IO g/m’ for women. Electrophysiologic testing was performed in using a previously described protocol.R The endpoint of the stimulation protocol was the reproducible induction of a sustained monomorphic ventricular tachycardia. In patients with polymorphic ventricular tachycardia or ventricularfibrillation, stimulation was stopped if countershock was required. Continuous data is expressed as the mean f standard deviation and compared with one-way analysis of variance. Proportions were compared with the chi-square statistic. A p value 10.05 was considered statistically significant. Fifty-eight patients had SAECG, M-mode echocardiography and programmed electrical stimulation. Twenty-one patients had echocardiographic LV hypertrophy; 37 patients did not (Table Il). The 2 patient groups were similar in age, sex, incidence of myocardial infarction, inducible ventricular tachycardia, clinical ventricular tachycardia, and sudden cardiac death. When comparing patients with LV hypertrophy to patients without LV hypertrophy there were no statisti-
FIGURE 1. An example of a recording with a late potential. The measurements mod in this analysis are shown. The RIMS QRS is the area (unshaded and shaded) undsr the QRS curve. (Reproduced with permission from Am ./ Cardio/.23)
Duratlom
(ms)
Total ORS 140 Under 40,~N 54
THE AMERICAN
JOURNAL
OF CARDIOLOGY
SEPTEMBER
15, 1990
765
tricular tachycardia in patients with no LV hypertrophy (p = 0.025). No individual SAECG parameter had a statistically significant association with sudden cardiac death in either group (Table III). Late potentials were associated with sudden cardiac death inpatients with LV hypertrophy (p = 0.04) but not in patients without LV hypertrophy (difference not signijicant). SAECG has made possible the identification of patients at high risk of developing ventricular arrhythmia; however, clinical use of SAECG has been limited by borderline sensitivity, specificity and predictive value of this test as a predictor of serious clinical events.3 The clinical use of SAECG testing might be improved if highrisk populations are tested. Patients with LV hypertrophy represent such a high-risk population’1-‘9; however, our results show that LV hypertrophy may interfere with and subtract from the association between SAECG parameters and ventricular arrhythmias. Previous studies have shown the ability of SAECG to predict clinical ventricular tachycardia,3-6 inducible ventricular tachycardia8-lo and sudden cardiac death.3 However, no previous studies have separately analyzed patients with LV hypertrophy. Based on our findings, the exclusion of patients with LV hypertrophy may improve the ability of SAECG to predict inducible ventricular tachycardia and clinical ventricular tachycardia, but not sudden cardiac death. The fact that combined abnormal SAECG parameters (late potentials) were associated with sudden cardiac death only in patients with LV hypertrophy and not in patients without LV hypertrophy may reflect the higher incidence of sudden cardiac death in patients with echocardiographic’ 1,19and electrocardiographic’2 LV hypertrophy. Positive late potentials in patients with LV hypertrophy may identify a subgroup of these patients at higher risk for sudden cardiac death. Prospective studies will be needed to confirm this. The inducibility of sustained monomorphic ventricular tachycardia by programmed electrical stimulation is a reliable clinical endpoint for guiding antiarrhythmic therapy. Moreover, we feel that the high degree of association between individual and combined SAECG parameters and inducible ventricular tachycardia in patients without LV hypertrophy and the absence of such an association in patients with LV hypertrophy is the most significant finding in this study. The most important limitations of our study relate to the small size and highly selected nature of the study population. Data derived from a small population of patients who have undergone programmed electrical stimulation cannot be extrapolated to the population at large. Our findings may be most useful in the interpretation of SAECGs on patients being considered for programmed electrical stimulation. Thus, individual and combined SAECG parameters are significantly associated with inducible ventricular tachycardia and clinical ventricular tachycardia in patients without echocardiographic LV hypertrophy but not in patients with echocardiographic LV hypertrophy. These data suggest that LV hypertrophy interferes with 766
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
66
the usefulness of this test for identifying patients at risk for ventricular arrhythmia. Further work will be required to determine the mechanism for this interference and to see if the findings are consistent in more general patient populations. 1. Buckingham TA, Ghosh G, Homan SM. Thessen CC, Redd RM, Stevens LL, Chaitman BR, Kennedy HL. Independent value of signal-averaged electrocardiography and left ventricular function in identifying patients with sustained ventricular tachycardia in coronary artery disease. Am J Curdjo/ /986;59:568-572, 2. Buckingham TA, Thessen CC, Hertweck D. Janosik DL. Kennedv HL. Sienalaveraged &ctrocardiography in the time and frequency domains. .&I J &diol 1989:63:820-825. 3. Kuchar DL, Thorburn CS, Sammel NL. Prediction of serious arrhythmic events after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring, and radionuclide ventriculography. J Am Co11 Cardiol /987:9:53/L 538. 4. Denniss
AR, Richards DA, Cody DV. Russell PA, Young AA, Cooper MJ, Ross DL, Uther JB. Prognostic significance of ventricular tachycardia and tibrillation induced at programmed stimulation and delayed potentials detected on the signal-averaged electrocardiograms of survivors of acute myocardial infarction. Circulation 1986;74:73/L745. 5. Cain ME, Ambos HD, Witowski FX. Sobel BE. Fast-Fourier transform analysis of signal-averaged electrocardiograms for identification of patients prone to sustained ventricular tachycardia. Cimdarion /984,69:7//L720. 6. Kuchar DL, Thorburn CW, Sammel NL. Late potentials detected after myocardial infarction: natural history and prognostic significance. Circulation
1986;74:1280-1289. 7. Simson MB. The use of signals
in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulotian 1982,64:235-240. 8. Buckingham TA, Thessen CC, Stevens L, Redd RM, Janosik DL. Kennedy HL. Relation of signal-averaged late potentials to inducible ventricular arrhythmias. J Electrophysiol 1988:2:424-436. 9. Breithardt G, Borggrefe M, Quantius B, Karbenn J, Seipel L. Ventricular vulnerability assessed by programmed ventricular stimulation in patients with and without late potentials. Cimdation 1983,68:275-28/. 10. Winters SL, Stewart D, Games JA. Signal averaging of the surface QRS complex predicts inducibility of ventricular tachycardia in patients with syncope of unknown origin: a prospective study. J Am Coll Cardiol 1987:10:775-778. 11. Casale PN, Devereux RB, Milner M. Zullo C, Harshfield GA, Pickering TG, Laraah JH. Value of echocardiozraohic measurement of left ventricular mass in predi&g cardiovascular morbid &nts in hypertensive men. Ann fntern Med
1986:105:173-178. 12. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram. Prevalence, incidence, and mortality in the Framingham Study. Ann Intern Ued 1969;71:89~101. 13. Lavie CJ, Nunez BD, Garavaglia GE, Mess4 FH. Hypertensive concentric left ventricular hypertrophy: when is ventricular ectopic activity increased? South Medical J I 988;81:696m700. 14. Messerli FH, Ventura HO, Elizardi DJ. Dunn FG, Frohlich ED. Hypertension and sudden death. Increased ventricular ectopic activity in left ventricular hypertrophy. Ant J Med 1984;77:18-22. 15. Kannel WB. Prevalence and natural history of electrocardiographic left ventricular hypertrophy. Am J Med 1983;75:4-11. 16. Levy D, Anderson KM, Savage DD, Balkus SA, Kannel WB, Castelli WP. Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol 1987:60:560-565. 17. Borhani NO. Left ventricular hypertrophy, arrhythmias and sudden death in systemic hypertension. Am J Cardiol 198760:l31-181. 18. McLenachan JM, Henderson E, Morris Kl, Dargie JH. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Eng/ J %cd
1987;3/7:787-792. 19. Aronow WS, Epstein S, Koenigsberg M, Schwartz KS. Usefulness of echocardiographic left ventricular hypertrophy, ventricular tachycardia and complex ventricular arrhythmias in predicting ventricular fibrillation or sudden cardiac death in elderly patients. Am J Cardiol 1988.62:1124-1125. 20. Sahn DJ, DeMaria A, Kisslo J, Weyman A, the Committee on M-Mode Standardization of the American Society of Echocardiography. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. J Am Coil Cardiol 1978;58:1072-1083. 21. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Circulation 1977:55:613m618, 22. Woythaler JN. Singer SL, Kwan 0, Meltzer RS, Reubner B, Bommer W, DaMaria A. Accuracy of echocardiography versus electrocardiography in detecting left ventricular hypertrophy: comparison of postmortem mass measurements. J Am Cot! Cardiol 1983;2:305-3/l. 23. Buckingham TA, Thessen CC, Stevens LL, Redd RM, Kennedy HL. The effect of conduction defect on the signal-averaged electrocardiographic determination of late potentials. Am J Cardiol 1988;6/:1265-1271.