International Journal of Cardiology, 33 (1991) 351-355 0 1991 Elsevier Science Publishers B.V. All rights reserved 0167-5273/91/$03.50

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CARD10 01375

Review

Clinical cardiac electrophysiology: the last 10 years *

Janet M. McComb

Regional Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne, U.K.

Key words: Catheter ablation; Anti-tachycardia pacemakers; Surgery for arrhythmias; Implantable car- dioverter defibrillator

Cardiac electrophysiologic techniques were in- troduced into clinical practice over 20 years ago, when it was shown that tachycardia could be induced and terminated by critically timed ex- trastimuli in the Wolff-Parkinson-White syn- drome [l]. Scherlag et al. [2] then described a simple and reliable method by which His poten- tials could be recorded in man. Application of these methods to the study of patients with ar- rhythmias has added much to our understanding of the interpretation of the surface ECG during arrhythmias, to the elucidation of the mecha- nisms of arrhythmias, and to the development of new methods of treatment. These techniques have had particular application to the study of tachy- cardias.

Many of the advances within recent years have been the result of invasive electrophysiologic techniques. Other methods which allow assess- ment of arrhythmias have also been developed,

Correspondence to: J.M. McComb, Regional Cardiotho- racic Centre, Freeman Hospital, Freeman Road, High Heaton, Newcastle-upon-Tyne, U.K.

* This review was commissioned for the 10th Anniversary of the Journal.

using the surface electrocardiogram. These in- clude signal averaging [3], QT analysis [4], etc.

Investigation of arrhythmias

The narrow complex supraventricular tachy- cardia of the Wolff-Parkinson-White syndrome was shown to involve a macro re-entrant circuit over 20 years ago [l]. More recently accurate mapping of the site of the accessory pathway has been possible, using either multiple electrode catheters positioned transvenously, or epicar- dially and endocardially at operation. Such map- ping has allowed definition of multiple accessory pathways in vivo. Accessory pathway potentials have been recorded [5] and this has allowed study of the properties of the pathway and of the effect of various interventions.

Atria1 fibrillation has long been known as a potentially serious complication of the Wolff- Parkinson-White syndrome, and within the past decade its importance and its relationship to ven- tricular fibrillation and/or sudden death have been described [6].

The role of electrophysiologic testing in pa- tients with a history of ventricular tachycardia and fibrillation has been defined [7-91, particu- larly in ischaemic heart disease. Progress has also

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been made in understanding the significance of nonsustained ventricular tachycardia [ lo,1 11.

Therapy

Application of electrophysiological techniques both to the selection of therapy and to assess- ment of its efficacy has probably been the major clinical advance in the last decade.

Drug therapy

There have been few new antiarrhythmic drugs. Amiodarone has become much more widely used [121, and with this, its side effects have been described. Class lc agents have also been more widely used [13], again with emphasis on side effects, especially arrhythmogenesis. A Class III agent, with a short onset of action, and a half life of hours, and without the side effects of amio- darone is awaited impatiently.

Although quinidine syncope has been recog- nised for many years arrhythmogenesis has been increasingly recognised [14,151 and attempts have been made to predict its occurrence [16,17].

The Cardiac Arrhythmia Suppression Trial (CAST) [18] has prompted a re-evaluation of the use of antiarrhythmic drugs and of the methods used in their assessment [19-211. This trial tested the hypothesis that suppression of ventricular ar- rhythmias after acute myocardial infarction will reduce sudden death, and was stopped after a mortality of 4.5% occurred in the patients treated with encainide or flecainide. This has emphasised the known risks of arrhythmogenesis.

Nonetheless, more information has been gained about prediction of efficacy of drugs par- ticularly in ventricular tachycardia. Programmed ventricular stimulation has been shown to dis- criminate between those with recurrences of ven- tricular tachycardia and sudden death, and those without [7-10,221.

Until recently, antiarrhythmic drug therapy in patients with malignant ventricular arrhythmias was either empiric, or at best guided by relatively brief periods of electrocardiographic monitoring. While such monitoring may be an appropriate method of assessing efficacy of treatment in the

patient with frequent and high grade ventricular ectopy many patients with malignant ventricular arrhythmias (and indeed paroxysmal supraven- tricular tachycardia) have little ectopy in between potentially life-threatening episodes. When it was shown that programmed cardiac stimulation could reliably induce arrhythmias and that administra- tion of some drugs could prevent induction of arrhythmias the concept of serial drug testing was developed. It has since been shown in patients with ventricular tachycardia that the identifica- tion and administration of a drug which prevents induction of ventricular arrhythmias is associated with freedom from arrhythmias [22]. Modification of the response (either a slower tachycardia, tachycardia made ‘harder to induce’) while asso- ciated with recurrent attacks of ventricular tachy- cardia is not associated with an increased mortal- ity [22].

Electrical ablation

The first reports of therapeutic electrical abla- tion in the treatment of arrhythmias in 1982 [23,24] followed a report in which a patient devel- oped heart block by serendipity, when a transtho- racic defibrillating shock was delivered during an electrophysiologic study, in which one of the catheters was subsequently shown to be faulty. Initially procedures were designed to destroy atri- oventricular nodal or His Purkinje function in patients with supraventricular tachycardias in- cluding atria1 fibrillation. Subsequently ablation has been used with only moderate success in the treatment of other arrhythmias. The Percuta- neous Cardiac Mapping and Ablation Registry has recorded and published data from over 50 centres 1251, and others have reported similar results [26].

Results of ablation of atrioventricular nodal function have proved less satisfactory than might have been predicted from early reports [25]. Complete heart block was achieved in 65%. A further 8% were asymptomatic with atrioventricu- lar conduction, and 12% needed additional an- tiarrhythmic therapy. The procedure was consid- ered unsuccessful in 16%. Complications are of concern: cardiac perforation or tamponade oc-

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curred in 1.9%, sepsis in 2%, procedure-related mortality was 2/552. Late sudden death occurred in 1.8%, with death from congestive cardiac fail- ure in 1.8%. Total deaths were 8%.

In order to minimise complications, modifica- tions of the original technique have been de- scribed. Low energy direct current shocks have been used with the aim of modifying rather than destroying conduction [27] and alternative power sources have been used 1281. Chemical ablation has also been described [29].

Electrical ablation techniques have also been applied to accessory pathways, but with less suc- cess. Four of 26 patients developed cardiac tam- ponade, and in the long term 33% were consid- ered failures [30].

Radiofrequency energy has however been used with impressive success to destroy accessory path- ways [31,32] and to modify but not destroy atri- oventricular nodal function by selectively destroy- ing one of two atrioventricular nodal pathways [33]. It is becoming the technique of choice.

Catheter ablation of ventricular tachycardia has been reported in 164 patients [25]. 18% are free of ventricular tachycardia, with a further 41% taking antiarrhythmic drugs. The procedure was considered unsuccessful in 41%. There were 11 procedure related deaths with a variety of other serious complications including new ar- rhythmias in 3 and complete atrioventricular block in 3. Total deaths were 40 (24%).

Antitachycardia pacing

It was first demonstrated in 1967 that critically timed extrastimuli could be used either to initiate or terminate tachycardias. Pacemakers were later implanted to allow the patient to terminate his tachycardias. These patient activated systems de- pended on the patient recognising his tachycardia and on his being able to apply a magnet. Subse- quently, a variety of automatic antitachycardia pacemakers have been developed. In the last decade, their use has become much more widespread [34]. Concerns have been expressed about automatic ventricular pacing for supraven- tricular tachycardia, and so pacing has mainly been confined to the atrium. Atria1 fibrillation is a risk, which has, perhaps, been overstated.

There have also been concerns about auto- matic ventricular pacing in ventricular tachycar- dia, because of the risks of induction of ventricu- lar fibrillation. Antitachycardia pacemakers have been used in conjunction with implantable car- dioverter defibrillators. This combination, of two independent devices is unwieldy. Now, however, there are a variety of sophisticated devices which incorporate antitachycardia pacing with car- dioversion and defibrillation [35]. Many of these are currently confined to investigational centres, but are proving successful.

Automatic defibrillation

Michel Mirowski developed the concept of the automatic implantable defibrillator, and pub- lished reports of its first implantation in 1980 1361. Since then much progress has been made. It has been shown to prevent sudden death, though the mortality rate nonetheless is about 25% at 5 years, mainly due to heart failure.

Initial reports described a total one year mor- tality of 22.9% and an arrhythmic one year mor- tality of 8.5% [373. Subsequent introduction of a device which could detect ventricular tachycardia as well as ventricular fibrillation and treat it by synchronised cardioversion, led to a reduction in total one year mortality of 16.6% and in arrhyth- mic mortality of 2%. The reported mortality from 323 patients suggested a one year arrhythmic mortality of 11.9% for the automatic implantable defibrillator and 1.9 and 1.3% for automatic im- plantable cardioverter defibrillators.

No controlled or randomised trial has been performed, and historical controls have been used, of patients mostly treated empirically with antiarrhythmic drugs, with a one year mortality of 27-66% 1371.

Surgery

Much progress has been made in surgical tech- niques for the treatment of arrhythmias in the past decade [38]. An accessory pathway was first successfully divided at operation in 1968. Since then, the technique with subsequent modifica- tions has been widely applied and other success-

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ful techniques have been developed. Surgery has now become the treatment of choice in patients with Wolff-Parkinson-White syndrome refractory to drug therapy, or with a rapidly conducting antegrade pathway.

Surgery in ventricular tachycardia is rather more controversial. It was introduced almost 20 years ago. The encircling endocardial ventriculo- tomy and subendocardial resection were intro- duced just over 10 years ago [38,39]. The latter is now a standard surgical technique for ventricular tachycardia and several large series have been reported [40,411. Most patients have chronic is- chaemic heart disease and it has been shown that these and similar techniques can be applied to patients with recent myocardial infarction [42] and indeed with pathologies other than ischaemic heart disease.

Coronary artery bypass graft surgery has also been shown to have a place in the surgical man- agement of ventricular arrhythmias and of course cardiac transplantation remains an option.

References

1 Durrer D, Schoo L, Scheuilenberg RM, Wellens HJJ. The role of premature beats in the initiation and termination of supraventricular tachycardia in the Wolff-Parkinson- White syndrome. Circulation 1967;36:644-662.

2 Scherlag BJ, Lau SH, Helfant RH, Berkowitz W, Stein E, Damato AN. Catheter technique for recording His bundle activity in man. Circulation 1969;39:12-18.

3 Simson MB. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after my- ocardial infarction. Circulation 1981;64:235-242.

4 Day CP, McComb JM, Campbell RWF. QT dispersion: an indication of arrhythmia risk in patients with long QT intervals. Br Heart J 1990,63:342-344.

5 Jackman WM, Friday KJ, Scherlag BJ, Dehning MM, Schechter E, Reynolds DW, Olsen EG, Berbari EJ, Harri- son LA, Lazzara R. Direct endocardial recording from an accessory atrioventricular pathway: localization of the site of block, effect of antiarrhythmic drugs, and attempt at nonsurgical ablation. Circulation 1983;68:906-916.

6 Klein GJ, Bashore TM, Sellers TD, Pritchett ELC, Smith WM, Gallagher JJ. Ventricular fibrillation in the Wolff- Parkinson-White syndrome. N Engl J Med 1979;301:1080- 1085.

7 Ruskin JN, DiMarco JP, Garan H. Out of hospital cardiac arrest Electrophysiologic observations and selection of long term antiarrhythmic therapy. N Engl J Med 1980;303:607- 613.

8 Swerdlow CD, Winkle RA, Mason JW. Determinants of survival in patients with ventricular tachyarrhythmias. N Engl J Med 1983;308:1436-1342.

9 Wilber DJ, Garan H, Finkelstein D, Kelly E, Newell J, McGovern B, Ruskin JN. Out of hospital cardiac arrest. Use of electrophysiologic testing in the prediction of long term outcome. N Engl J Med 1988;318:19-24.

10 Wilber DJ, Olshansky B, Moran JF, Scanlon PJ. Electro- physiologic testing and non-sustained ventricular tachycar- dia. Use and limitations in patients with coronary artery disease and impaired ventricular function. Circulation 1990;82:350-358.

11 Wellens HJ. The approach to nonsustained ventricular tachycardia after a myocardial infarction. Circulation 1990;82:633-635.

12 Mason JW. Amiodarone. N Engl J Med 1987;455-466. 13 Morganroth J, Horowitz LN. Flecainide: its proarrhythmic

effect and expected changes on the surface electrocardio- gram. Am J Cardiol 1984;53:89B-94B.

14 Velebit V, Podrid P, Lawn B, Cohen BH, Graboys TB. Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs. Circulation 1982;65:886-894.

15 Coplen SE, Antman EM, Berlin JA, Hewitt P, Chalmers TC. Efficacy and safety of quinidine therapy for mainte- nance of sinus rhythm after cardioversion. A meta-analysis of randomized control trials. Circulation 1990,82:1106- 1116.

16 Ruskin JN, McGovern B, Garan H, DiMarco JP, Kelly E. Antiarrhythmic drugs: a possible cause of out of hospital cardiac arrest. N Engl J Med 1983;309:1302-1306.

17 Slater W, Lampert S, Podrid PJ, Lown B. Clinical predic- tors of arrhythmia worsening by antiarrhythmic drugs. Am J Cardiol 1988;61:349-353.

18 Preliminary report: effect of encainide and flecainide on mortality in a randomised trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989;321:406- 412.

19 Ruskin JN. The Cardiac Arrhythmia Suppression Trial (CAST). N Engl J Med 1989;321:386-388.

20 Flecainide and CAST. Lancet 1989;481-482. 21 Gottlieb SS. The use of antiarrhythmic agents in heart

failure: implications of CAST. Am Heart J 1989;118:1074- 1077.

22 Waller TJ, Kay HR, Spielman SR, Kutalek SP, Greenspan AM, Horowitz LN. Reduction in sudden death and total mortality by antiarrhythmic therapy evaluated by electro- physiologic drug testing: criteria of efficacy in patients with sustained ventricular tachyarrhythmia. J Am Co11 Cardiol 1987;10:83-89.

23 Gallagher JJ, Svenson RH, Kasell JH, German LD, Bardy GH, Broughton A, Critelli G. Catheter technique for closed chest ablation of the atrioventricular conduction system. N Engl J Med 1982;306:194-200.

24 Scheinman MM, Morady F, Hess DS, Gonzalez R. Catheter induced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. J Am Med Assoc 1982;248:851-855.

355

25 Evans GT, Scheinman MM and the Executive Committee of the Registry. The Percutaneous Cardiac Mapping and Ablation Registry: final summary of results. PACE 1988;11:1621-1626.

26 Levy S, Bru P, Aliot E, Attuel P, Barnay C, Clementy J, Ebagosti A, Fauchier J-P, Fontaine G, Leclercq J-F. Long-term followup of atrioventricular junctional trans- catheter electrical ablation. PACE 1988;11:1149-1153.

27 McComb JM, McGovern B, Garan H, Ruskin JN. Man- agement of refractory supraventricular tachyarrhythmias using low energy transcatheter shocks. Am J Cardiol 1986;58:959-963.

28 Rowland E, Cunningham AD, Ahsan AJ, Rickards AF. Transvenous ablation of atrioventricular conduction with a low energy power source. Br Heart J 1989;62:361-366.

29 Brugada P, de Swart H, Smeets JLRM, Wellens HJJ. Trans-coronary chemical ablation of atrioventricular con- duction. Circulation 1989;79:475-482.

30 Fisher JD, Brodman R, Kim SG et al. Attempted non surgical ablation of accessory pathway via the coronary sinus in the Wolff-Parkinson-White syndrome. J Am Coll Cardiol 1984;4:685-694.

31 Jackman WM, Wang X, Friday KJ et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson- White syndrome) by radiofrequency current. N Engl J Med 1991;324:1605-1611.

32 Calkins H, Sousa J, El-Atassi R et al. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysi- ologic test. N Engl J Med 1991;324:1612-1618.

33 Langberg JJ, Chin MC, Rosenqvist M et al. Catheter ablation of the atrioventricular junction with radiofre- quency energy. Circulation 1989;80:1527-1535.

34 McComb JM, Jameson S, Bexton RS. Antitachycardia

pacing in patients with supraventricular tachycardias: ex- perience with the Intertach pacemaker. Pacing Clin Elec- trophysiol 1990;13:1948-1954.

35 Leitch JW, Gillis AM, Wyse DG et al. Reduction in defibrillator shocks with an implantable device combining antitachycardia pacing and shock therapy. J Am Coll Car- diol 1991;18:145-151.

36 Mirowski M, Reid PR, Mower MM et al. Termination of malignant ventricular arrhythmias with an implanted auto- matic defibrillator in human beings. N Engl J Med 1980;303:322-324.

37 Mirowski M. The automatic implantable cardioverter de- fibrillator: an overview. J Am Coll Cardiol 1985;6:461-466.

38 Cox JL, Ferguson TB. Cardiac arrhythmia surgery. Cur- rent problems in surgery 1989;26.

39 Guiraudon G, Fontaine G, Frank R et al. Encircling endocardial ventriculotomy: a new surgical treatment of life threatening ventricular tachycardias resistant to medi- cal treatment following myocardial infarction. Ann Thorac Surg 1978;26:438.

40 Josephson ME, Harken AH, Horowitz LN et al. Endocar- dial excision: a new surgical technique for the treatment of recurrent ventricular tachycardia. Circulation 1979;60: 1430-1439.

41 Ostermeyer J, Borggrefe M, Breithardt G et al. Direct operations for the management of life threatening is- chemic ventricular tachycardia. J Thorac Cardiovasc Surg 1987;94:848-865.

42 Bourke JP, Hilton CJ, McComb JM, Cowan JC, Tan- suphaswadikul S, Kertes PJ, Campbell RWF. Surgery for control of recurrent life-threatening ventricular tachy- arrhythmias within two months of myocardial infarction. J Am Coll Cardiol 1990;16:37-41.