528
functions. Over 1000 such devices have been
implanted already, and with Food and Drug Administration approval of several such devices expected soon this number will increase dramatically. By providing rescue defibrillation or cardioversion in the event of tachycardia acceleration, these devices overcome many of the earlier objections. Initial reports have been favourable,s indicating a high success rate with infrequent induction of ventricular fibrillation. With this technique, acceleration of tachycardia remains a hazard,66 especially when the original ventricular rate is fast;7 and electrophysiological testing does not reliably indicate its likelihood.8 Subthreshold pacing may offer a means to terminate ventricular tachycardia without the risk of acceleration, but its efficacy has yet to be confirmed and it is not specifically available in current ICDs. Lest enthusiam for these combined devices should reach excessive heights, Johnson and Marchlinski9 have sounded a cautionary note in their account of two patients with these devices. One patient with mitral valve disease and a history of atrial fibrillation had an ICD inserted for ventricular tachycardia. A postoperative episode of atrial fibrillation triggered antitachycardia pacing, which induced ventricular tachycardia; after a further series of pacing interventions, a defibrillating shock successfully restored sinus rhythm. In a second patient sinus tachycardia triggered postoperative and induction of ventricular antitachycardia pacing tachycardia which then triggered a 500-V shock. Thus inappropriate delivery of antitachycardia pacing can be arrhythmogenic and may lead to progressively more aggressive intervention. Inappropriate delivery of therapy results from erroneous detection of a tachyarrhythmia and the highlights diagnostic limitations of existing ICDs which, without exception, use heart rate as their primary means of arrhythmia detection. When defibrillators were used only to treat ventricular fibrillation or very fast ventricular tachycardia, difficulties with this approach were infrequent. Since antitachycardia pacing is now used for slower ventricular tachycardias problems with sinus tachycardia or atrial fibrillation exceeding the heart rate threshold for arrhythmia detection have become more common. Some ICDs offer rate stability criteria to exclude inappropriate detection of atrial fibrillation and sudden-onset criteria to exclude sinus tachycardia, but their use has been limited, partly because of concerns that they may lessen the sensitivity of detection of ventricular tachycardia and partly because clinical data are lacking. Development of pressure sensing leadsl° or signal morphology processingll may eventually improve diagnostic capability. Thus, although the implantable defribillator has largely overcome concerns about the safety of antitachycardia pacing for ventricular arrhythmias,
still have reservations about widespread use. Antitachycardia pacing should always be "tuned" to suit the individual patient. Antiarrhythmic drug therapy to control the frequency of attacks, to reduce the risk of overlap with sinus tachycardia, and to inhibit atrial tachyarrhythmias is likely to be needed in we must
many
patients.
Ryan GF, Easley RM, Zaroff LI, Goldstein S. Paradoxical use of a demand pacemaker in treatment of supraventricular tachycardia due to the Wolff-Parkinson-White syndrome. Observation on termination of reciprocal rhythm. Circulation 1968; 38: 1037-43. 2. Lau CP, Cornu E, Camm AJ. Fatal and nonfatal cardiac arrest in patients with an implanted antitachycardia device for the treatment of supraventricular tachycardia. Am J Cardiol 1988; 61: 919-21. 3. Griffith MJ, Paul V, Garratt CJ, Ward J, Ward DE, Camm AJ. Two forms of back up defibrillation for antitachycardia pacing in ventricular tachycardia. Br Heart J 1990; 64: 97. 4. Kappenberger L, Valin H, Sowton E, et al. Multicenter long-term results of antitachycardia pacing for supraventricular tachycardia. Am J Cardiol 1989; 64: 191-93. 5. Fromer M, Schlapfer J, Fischer A, Kappenberger L. Experience with a new implantable pace-cardioverter-defibrillator for the therapy of recurrent sustained ventricular tachyarrhythmias: a step towards a universal tachyarrhythmia control device. PACE 1991; 14: 1288-98. 6. Schneider MAE, Siebels J, Duckeck W, Geiger M, Kuck KH. Antitachycardia pacing by pacer/defribillator devices in ventricular tachycardia: superior to low-energy cardioversion. Eur Heart J 1991; 1.
12: 364 (abstr). 7. Schöls W, Brachmann J, Schmitt
C, Kübler W. Relation of tachycardia
pacing. Eur Heart J 1991; 12: 418 (abstr). 8. Rankin AC, Zaim S, Powell A, et al. Anti-tachycardia pacemaker/ implantable cardioverter defibrillator in patients with drug-refractory ventricular tachycardia. Eur Heart J 1991; 12: 364 (abstr). 9. Johnson NJ, Marchlinski FE. Arrhythmias induced by device antitachycardia therapy due to diagnostic nonspecificity. JACC 1991; rate to success
of antitachycardia
18: 1418-25. 10. Sharma AD, Bennett TD, Erickson M, Klein GJ, Wee R, Guiraudon G. Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices. JACC 1990; 15: 648-55. 11. Tooley MA, Davies DW, Nathan AW, Camm AJ. Recognition of multiple tachyarrhythmias by rate-independent means using a small microcomputer. PACE 1991; 14: 337-40.
The heart in myotonic dystrophy Myotonic dystrophy is the commonest muscular dystrophy of adult life with a prevalence of about 5 per 100 000.1 Apart from the neuromuscular manifestations, this disorder has multiple systemic effects including cataract, mental retardation, and cardiac involvement. A study and extensive review2 of 1967 showed that published work in electrocardiographic (ECG) abnormalities occurred in 202 of 236 patients; only 16% had cardiac symptoms,
half of which
were
attributed
to
arrhythmias. Although the reports may have been biased towards positive findings, prospective studies showed a similarly high prevalence of abnormal ECGs in symptom-free patients,3,4 mainly impaired conduction and supraventricular arrhythmias. Intracardiac electrophysiological studies revealed abnormalities in all areas of the conducting system, most commonly in the His-Purkinje system;3,5 this distribution correlates with the appearance of prolonged PR and QRS intervals. Overt primary myocardial involvement in
529
Occasional cases of subacute dilating cardiomyopathy and focal myocarditis have been reported6,7 but most of the abnormalities are subclinical. Of 10 patients investigated by Hartwig et al,8 9 had abnormalities of ventricular wall motion during exercise as assessed by radionuclide angiography. Mitral valve prolapse 9 occurs in at least 30% of patients.9 The histological features of the heart reflect the clinical abnormalities. There is fibrosis and fatty infiltration, especially of conducting tissue, and also patchy involvement of other regions of the myocardium.5,lO Ultrastructural analysis shows myofibrillary degeneration and prominent I-bands, similar to those in skeletal muscle. 11 Sudden death is well recognised in myotonic dystrophy, with one report suggesting that as many as 30% of patients may die in this way.13 This complication is commonly attributed to conduction block, but has also been reported in patients with pacemakers.5,11,12 In 2 cases11.13 the patients had had spontaneous ventricular tachycardia previously, so ventricular arrhythmias may be important. Results of two studies from a group in Washington may help in planning cardiac management of patients with myotonic dystrophy. In the first study Hawley and colleagues14 looked at the rate and nature of progression of cardiac disease in a group of patients without cardiac symptoms. 37 patients were followed for a mean of 6 years. At entry, 9 had first-degree atrioventricular block, 2 had left anterior hemiblock, and 1 had complete left bundle branch block. By the end of follow-up, 6 had a new bundle branch block (2 right bundle branch, 3 left, and 1 intraventricular), 4 had a new left anterior hemiblock, and 10 more had first-degree block. Additionally, 1 manifested complete heart block and needed a permanent pacemaker; another had evidence of progressive first-degree heart block and an increasing QRS interval and died suddenly. Atrial flutter or fibrillation developed in 2 patients. The PR interval increased in 90% and the QRS interval in 74%. All patients showed gradual and predictable impairment of conduction with no sudden deteriorations. second In the study, 15 signal-averaged electrocardiography was used to look for ventricular late potentials. With this procedure, advanced signal processing and filtering techniques allow analysis of the terminal part of the QRS complex and detection of small "late potential" deflections. In a study of patients after myocardial infarction,16 the presence of late potentials on the surface ECG correlated with an increased number of "fragmented electrograms" on direct endocardial mapping. These electrogram abnormalities electrical represent delayed transmission through damaged areas of myocardium, which may then form re-entry circuits and predispose to re-entrant arrhythmias. The finding of ventricular late potentials has proved helpful in prediction of ventricular tachyarrhythmias after myocardial
myotonic dystrophy
is
rare.
infarction. 17,18 In the myotonic dystrophy study the researchers selected a group of 24 patients with no cardiac symptoms and no ECG evidence of bundle branch block. 75% met at least one criterion for the presence of late potentials vs 5% of controls, and 29% met all three criteria vs no controls. These findings cannot establish the predictive value of the technique in myotonic dystrophy, but the analogy with results in ischaemic heart disease is worrying. In particular, the patchy myocardial involvement, while causing little clinical impairment of contractile function, may provide the anatomical substrate for re-entrant
arrhythmias. How should
manage the heart in patients with myotonic dystrophy? All patients with this condition warrant annual review including a twelve-lead ECG and they should be asked about symptoms such as syncope, feeling faint, and palpitations. Patients with we
such symptoms should undergo 24-hour ECG monitoring, and if there is also evidence of conducting system disease from the surface ECG they should be considered for intracardiac electrophysiological studies and pacing. 1. Harper PS. Myotonic dystrophy. 2nd ed. London: WB Saunders, 1989. 2. Church SC. The heart in myotonia atrophica. Arch Intern Med 1967; 119: 176-81. 3. Perloff JK, Stevenson WG, Roberts NK, Cabeen W, Weiss J. Cardiac involvement in myotonic muscular dystrophy (Steinert’s disease): a prospective study of 25 patients. Am J Cardiol 1984; 54: 1074-81. 4. Olofsson B-O, Forsberg H, Andersson S, Bjerle P, Henrikson A, Wedin I. Electrocardiographic findings in myotonic dystrophy. Br Heart J 1988; 59: 47-52. 5. Motta J, Guilleminault C, Billingham M, Barry W, Mason J. Cardiac abnormalities in myotonic dystrophy: electrophysiologic and histopathologic studies. Am J Med 1979; 67: 467-73. 6. Holt JM, Lambert EHN. Heart disease as the presenting feature in myotonia atrophica. Br Heart J 1964; 26: 433-36. 7. Rausing A. Focal myocarditis in familial dystrophia myotonica. Br Heart J 1972; 34: 1292-94. 8. Hartwig GB, Rao KR, Radoff FM, Coleman RE, Jones RH, Roses AD. Radionuclide angiocardiographic analysis of myocardial function in myotonic muscular dystrophy. Neurology 1983; 33: 657-60. 9. Streib EW, Meyers DG, Sun SF. Mitral valve prolapse in myotonic dystrophy. Muscle Nerve 1985; 8: 650-53. 10. Nguyen HH, Wolfe JT, Holmes DR Jr, Edwards WD. Pathology of the cardiac conduction system in myotonic dystrophy: a study of 12 cases. JACC 1988; 11: 662-71. 11. Grigg LE, Chan W, Mond HG, Vohra JK, Downey WF. Ventricular tachycardia and sudden death in myotonic dystrophy: clinical, electrophysiologic and pathologic features. JACC 1985; 6: 254-56. 12. Cannom DS, Wyman MG, Goldreyer BN. Clinical and induced ventricular tachycardia in a patient with myotonic dystrophy. JACC 1984; 4: 625-28. 13. Hiromasa S, Ikeda T, Kubota K, et al. Ventricular tachycardia and sudden death in myotonic dystrophy. Am Heart J 1988; 115: 914-15. 14. Hawley RJ, Milner MR, Gottdiener JS, Cohen A. Myotonic heart disease: a clinical follow-up. Neurology 1991; 41: 259-62.
15. Milner MR, Hawley RJ, Jachim M, Lindsay J Jr, Fletcher RD. Ventricular late potentials in myotonic dystrophy. Ann Intern Med 1991; 115: 607-13. 16. Simson MB, Untereker WJ, Spielman SR, et al. Relation between late potentials on the body surface and directly recorded fragmented electrogram in patients with ventricular tachycardia. Am J Cardiol
1983; 51: 105-12. 17. Kuchar DL, Thorburn CW, Sammel NL. Prediction of serious arrhythmic events after myocardial infarction: signal-averaged Holter and radionuclide electrocardiogram, monitoring ventriculography. JACC 1987; 9: 531-38. 18. Nalos PC, Gang ES, Mandel WJ, Ladenheim ML, Lass Y, Peter T. The signal-averaged electrocardiogram as a screening test for inducibility of sustained ventricular tachycardia in high risk patients: a prospective study. JACC 1987; 9: 537-48.
functions. Over 1000 such devices have been
implanted already, and with Food and Drug Administration approval of several such devices expected soon this number will increase dramatically. By providing rescue defibrillation or cardioversion in the event of tachycardia acceleration, these devices overcome many of the earlier objections. Initial reports have been favourable,s indicating a high success rate with infrequent induction of ventricular fibrillation. With this technique, acceleration of tachycardia remains a hazard,66 especially when the original ventricular rate is fast;7 and electrophysiological testing does not reliably indicate its likelihood.8 Subthreshold pacing may offer a means to terminate ventricular tachycardia without the risk of acceleration, but its efficacy has yet to be confirmed and it is not specifically available in current ICDs. Lest enthusiam for these combined devices should reach excessive heights, Johnson and Marchlinski9 have sounded a cautionary note in their account of two patients with these devices. One patient with mitral valve disease and a history of atrial fibrillation had an ICD inserted for ventricular tachycardia. A postoperative episode of atrial fibrillation triggered antitachycardia pacing, which induced ventricular tachycardia; after a further series of pacing interventions, a defibrillating shock successfully restored sinus rhythm. In a second patient sinus tachycardia triggered postoperative and induction of ventricular antitachycardia pacing tachycardia which then triggered a 500-V shock. Thus inappropriate delivery of antitachycardia pacing can be arrhythmogenic and may lead to progressively more aggressive intervention. Inappropriate delivery of therapy results from erroneous detection of a tachyarrhythmia and the highlights diagnostic limitations of existing ICDs which, without exception, use heart rate as their primary means of arrhythmia detection. When defibrillators were used only to treat ventricular fibrillation or very fast ventricular tachycardia, difficulties with this approach were infrequent. Since antitachycardia pacing is now used for slower ventricular tachycardias problems with sinus tachycardia or atrial fibrillation exceeding the heart rate threshold for arrhythmia detection have become more common. Some ICDs offer rate stability criteria to exclude inappropriate detection of atrial fibrillation and sudden-onset criteria to exclude sinus tachycardia, but their use has been limited, partly because of concerns that they may lessen the sensitivity of detection of ventricular tachycardia and partly because clinical data are lacking. Development of pressure sensing leadsl° or signal morphology processingll may eventually improve diagnostic capability. Thus, although the implantable defribillator has largely overcome concerns about the safety of antitachycardia pacing for ventricular arrhythmias,
still have reservations about widespread use. Antitachycardia pacing should always be "tuned" to suit the individual patient. Antiarrhythmic drug therapy to control the frequency of attacks, to reduce the risk of overlap with sinus tachycardia, and to inhibit atrial tachyarrhythmias is likely to be needed in we must
many
patients.
Ryan GF, Easley RM, Zaroff LI, Goldstein S. Paradoxical use of a demand pacemaker in treatment of supraventricular tachycardia due to the Wolff-Parkinson-White syndrome. Observation on termination of reciprocal rhythm. Circulation 1968; 38: 1037-43. 2. Lau CP, Cornu E, Camm AJ. Fatal and nonfatal cardiac arrest in patients with an implanted antitachycardia device for the treatment of supraventricular tachycardia. Am J Cardiol 1988; 61: 919-21. 3. Griffith MJ, Paul V, Garratt CJ, Ward J, Ward DE, Camm AJ. Two forms of back up defibrillation for antitachycardia pacing in ventricular tachycardia. Br Heart J 1990; 64: 97. 4. Kappenberger L, Valin H, Sowton E, et al. Multicenter long-term results of antitachycardia pacing for supraventricular tachycardia. Am J Cardiol 1989; 64: 191-93. 5. Fromer M, Schlapfer J, Fischer A, Kappenberger L. Experience with a new implantable pace-cardioverter-defibrillator for the therapy of recurrent sustained ventricular tachyarrhythmias: a step towards a universal tachyarrhythmia control device. PACE 1991; 14: 1288-98. 6. Schneider MAE, Siebels J, Duckeck W, Geiger M, Kuck KH. Antitachycardia pacing by pacer/defribillator devices in ventricular tachycardia: superior to low-energy cardioversion. Eur Heart J 1991; 1.
12: 364 (abstr). 7. Schöls W, Brachmann J, Schmitt
C, Kübler W. Relation of tachycardia
pacing. Eur Heart J 1991; 12: 418 (abstr). 8. Rankin AC, Zaim S, Powell A, et al. Anti-tachycardia pacemaker/ implantable cardioverter defibrillator in patients with drug-refractory ventricular tachycardia. Eur Heart J 1991; 12: 364 (abstr). 9. Johnson NJ, Marchlinski FE. Arrhythmias induced by device antitachycardia therapy due to diagnostic nonspecificity. JACC 1991; rate to success
of antitachycardia
18: 1418-25. 10. Sharma AD, Bennett TD, Erickson M, Klein GJ, Wee R, Guiraudon G. Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices. JACC 1990; 15: 648-55. 11. Tooley MA, Davies DW, Nathan AW, Camm AJ. Recognition of multiple tachyarrhythmias by rate-independent means using a small microcomputer. PACE 1991; 14: 337-40.
The heart in myotonic dystrophy Myotonic dystrophy is the commonest muscular dystrophy of adult life with a prevalence of about 5 per 100 000.1 Apart from the neuromuscular manifestations, this disorder has multiple systemic effects including cataract, mental retardation, and cardiac involvement. A study and extensive review2 of 1967 showed that published work in electrocardiographic (ECG) abnormalities occurred in 202 of 236 patients; only 16% had cardiac symptoms,
half of which
were
attributed
to
arrhythmias. Although the reports may have been biased towards positive findings, prospective studies showed a similarly high prevalence of abnormal ECGs in symptom-free patients,3,4 mainly impaired conduction and supraventricular arrhythmias. Intracardiac electrophysiological studies revealed abnormalities in all areas of the conducting system, most commonly in the His-Purkinje system;3,5 this distribution correlates with the appearance of prolonged PR and QRS intervals. Overt primary myocardial involvement in
529
Occasional cases of subacute dilating cardiomyopathy and focal myocarditis have been reported6,7 but most of the abnormalities are subclinical. Of 10 patients investigated by Hartwig et al,8 9 had abnormalities of ventricular wall motion during exercise as assessed by radionuclide angiography. Mitral valve prolapse 9 occurs in at least 30% of patients.9 The histological features of the heart reflect the clinical abnormalities. There is fibrosis and fatty infiltration, especially of conducting tissue, and also patchy involvement of other regions of the myocardium.5,lO Ultrastructural analysis shows myofibrillary degeneration and prominent I-bands, similar to those in skeletal muscle. 11 Sudden death is well recognised in myotonic dystrophy, with one report suggesting that as many as 30% of patients may die in this way.13 This complication is commonly attributed to conduction block, but has also been reported in patients with pacemakers.5,11,12 In 2 cases11.13 the patients had had spontaneous ventricular tachycardia previously, so ventricular arrhythmias may be important. Results of two studies from a group in Washington may help in planning cardiac management of patients with myotonic dystrophy. In the first study Hawley and colleagues14 looked at the rate and nature of progression of cardiac disease in a group of patients without cardiac symptoms. 37 patients were followed for a mean of 6 years. At entry, 9 had first-degree atrioventricular block, 2 had left anterior hemiblock, and 1 had complete left bundle branch block. By the end of follow-up, 6 had a new bundle branch block (2 right bundle branch, 3 left, and 1 intraventricular), 4 had a new left anterior hemiblock, and 10 more had first-degree block. Additionally, 1 manifested complete heart block and needed a permanent pacemaker; another had evidence of progressive first-degree heart block and an increasing QRS interval and died suddenly. Atrial flutter or fibrillation developed in 2 patients. The PR interval increased in 90% and the QRS interval in 74%. All patients showed gradual and predictable impairment of conduction with no sudden deteriorations. second In the study, 15 signal-averaged electrocardiography was used to look for ventricular late potentials. With this procedure, advanced signal processing and filtering techniques allow analysis of the terminal part of the QRS complex and detection of small "late potential" deflections. In a study of patients after myocardial infarction,16 the presence of late potentials on the surface ECG correlated with an increased number of "fragmented electrograms" on direct endocardial mapping. These electrogram abnormalities electrical represent delayed transmission through damaged areas of myocardium, which may then form re-entry circuits and predispose to re-entrant arrhythmias. The finding of ventricular late potentials has proved helpful in prediction of ventricular tachyarrhythmias after myocardial
myotonic dystrophy
is
rare.
infarction. 17,18 In the myotonic dystrophy study the researchers selected a group of 24 patients with no cardiac symptoms and no ECG evidence of bundle branch block. 75% met at least one criterion for the presence of late potentials vs 5% of controls, and 29% met all three criteria vs no controls. These findings cannot establish the predictive value of the technique in myotonic dystrophy, but the analogy with results in ischaemic heart disease is worrying. In particular, the patchy myocardial involvement, while causing little clinical impairment of contractile function, may provide the anatomical substrate for re-entrant
arrhythmias. How should
manage the heart in patients with myotonic dystrophy? All patients with this condition warrant annual review including a twelve-lead ECG and they should be asked about symptoms such as syncope, feeling faint, and palpitations. Patients with we
such symptoms should undergo 24-hour ECG monitoring, and if there is also evidence of conducting system disease from the surface ECG they should be considered for intracardiac electrophysiological studies and pacing. 1. Harper PS. Myotonic dystrophy. 2nd ed. London: WB Saunders, 1989. 2. Church SC. The heart in myotonia atrophica. Arch Intern Med 1967; 119: 176-81. 3. Perloff JK, Stevenson WG, Roberts NK, Cabeen W, Weiss J. Cardiac involvement in myotonic muscular dystrophy (Steinert’s disease): a prospective study of 25 patients. Am J Cardiol 1984; 54: 1074-81. 4. Olofsson B-O, Forsberg H, Andersson S, Bjerle P, Henrikson A, Wedin I. Electrocardiographic findings in myotonic dystrophy. Br Heart J 1988; 59: 47-52. 5. Motta J, Guilleminault C, Billingham M, Barry W, Mason J. Cardiac abnormalities in myotonic dystrophy: electrophysiologic and histopathologic studies. Am J Med 1979; 67: 467-73. 6. Holt JM, Lambert EHN. Heart disease as the presenting feature in myotonia atrophica. Br Heart J 1964; 26: 433-36. 7. Rausing A. Focal myocarditis in familial dystrophia myotonica. Br Heart J 1972; 34: 1292-94. 8. Hartwig GB, Rao KR, Radoff FM, Coleman RE, Jones RH, Roses AD. Radionuclide angiocardiographic analysis of myocardial function in myotonic muscular dystrophy. Neurology 1983; 33: 657-60. 9. Streib EW, Meyers DG, Sun SF. Mitral valve prolapse in myotonic dystrophy. Muscle Nerve 1985; 8: 650-53. 10. Nguyen HH, Wolfe JT, Holmes DR Jr, Edwards WD. Pathology of the cardiac conduction system in myotonic dystrophy: a study of 12 cases. JACC 1988; 11: 662-71. 11. Grigg LE, Chan W, Mond HG, Vohra JK, Downey WF. Ventricular tachycardia and sudden death in myotonic dystrophy: clinical, electrophysiologic and pathologic features. JACC 1985; 6: 254-56. 12. Cannom DS, Wyman MG, Goldreyer BN. Clinical and induced ventricular tachycardia in a patient with myotonic dystrophy. JACC 1984; 4: 625-28. 13. Hiromasa S, Ikeda T, Kubota K, et al. Ventricular tachycardia and sudden death in myotonic dystrophy. Am Heart J 1988; 115: 914-15. 14. Hawley RJ, Milner MR, Gottdiener JS, Cohen A. Myotonic heart disease: a clinical follow-up. Neurology 1991; 41: 259-62.
15. Milner MR, Hawley RJ, Jachim M, Lindsay J Jr, Fletcher RD. Ventricular late potentials in myotonic dystrophy. Ann Intern Med 1991; 115: 607-13. 16. Simson MB, Untereker WJ, Spielman SR, et al. Relation between late potentials on the body surface and directly recorded fragmented electrogram in patients with ventricular tachycardia. Am J Cardiol
1983; 51: 105-12. 17. Kuchar DL, Thorburn CW, Sammel NL. Prediction of serious arrhythmic events after myocardial infarction: signal-averaged Holter and radionuclide electrocardiogram, monitoring ventriculography. JACC 1987; 9: 531-38. 18. Nalos PC, Gang ES, Mandel WJ, Ladenheim ML, Lass Y, Peter T. The signal-averaged electrocardiogram as a screening test for inducibility of sustained ventricular tachycardia in high risk patients: a prospective study. JACC 1987; 9: 537-48.
