BMJ  2003;327:333-336 (9 August), doi:10.1136/bmj.327.7410.333

Clinical review

ABC of interventional cardiology

Implantable devices for treating tachyarrhythmias

Castle Hill Hospital, Hull

Introduction

Pacing treatment for tachycardia control has achieved success, notably in supraventricular tachycardia. Pacing termination for ventricular tachycardia has been more challenging, but an understanding of arrhythmia mechanisms, combined with increasingly sophisticated pacemakers and the ability to deliver intracardiac pacing and shocks, have led to success with implantable cardioverter defibrillators.

Mechanisms of pacing termination

There are two methods of pace termination.

Underdrive pacing was used by early pacemakers to treat supraventricular and ventricular tachycardias. Extrastimuli are introduced at a constant interval, but at a slower rate than the tachycardia, until one arrives during a critical period, terminating the tachycardia. Because of the lack of sensing of the underlying tachycardia, there is a risk of a paced beat falling on the T wave, producing ventricular fibrillation or ventricular tachycardia, or degenerating supraventricular tachycardias to atrial fibrillation. It is also not particularly successful at terminating supraventricular tachycardia or ventricular tachycardia and is no longer used routinely.

View larger version (84K): [in this window] [in a new window]   Changes in implantable cardioverter defibrillators over 10 years (1992-2002). Apart from the marked reduction in size, the implant technique and required hardware have also dramatically improved—from the sternotomy approach with four leads and abdominal implantation to the present two-lead transvenous endocardial approach that is no more invasive than a pacemaker implant

 

Overdrive pacing is more effective for terminating both supraventricular and ventricular tachycardias. It is painless, quick, effective, and associated with low battery drain of the pacemaker. Implantation of devices for terminating supraventricular tachycardias is now rarely required because of the high success rate of radiofrequency ablative procedures (see previous article). Overdrive pacing for ventricular tachycardia is often successful but may cause acceleration or induce ventricular fibrillation. Therefore, any device capable of pace termination of ventricular tachycardia must also have defibrillatory capability.

View this table: [in this window] [in a new window]   Mechanisms of arrhythmias

 

Implantable cardioverter defibrillators

Initially, cardioverter defibrillator implantation was a major operation requiring thoracotomy and was associated with 3-5% mortality. The defibrillation electrodes were patches sewn on to the myocardium, and leads were tunnelled subcutaneously to the device, which was implanted in a subcutaneous abdominal pocket. Early devices were large and often shocked patients inappropriately, mainly because these relatively unsophisticated units could not distinguish ventricular tachycardia from supraventricular tachycardia.

View this table: [in this window] [in a new window]   Arrhythmias associated with re-entry

 

Current implantation procedures
Modern implantable cardioverter defibrillators are transvenous systems, so no thoracotomy is required and implantation mortality is about 0.5%. The device is implanted either subcutaneously, as for a pacemaker, in the left or right deltopectoral area, or subpectorally in thin patients to prevent the device eroding the skin.

The ventricular lead tip is positioned in the right ventricular apex, and a second lead can be positioned in the right atrial appendage to allow dual chamber pacing if required and discrimination between atrial and ventricular tachycardias. The ventricular defibrillator lead has either one or two shocking coils. For two-coil leads, one is proximal (usually within the superior vena cava), and one is distal (right ventricular apex). During implantation the unit is tested under conscious sedation. Satisfactory sensing during sinus rhythm, ventricular tachycardia, and ventricular fibrillation is established, as well as pacing and defibrillatory thresholds. Defibrillatory thresholds should be at least 10 joules less then the maximum output of the defibrillator (about 30 joules).

New developments
An important development is the implantable cardioverter defibrillator's ability to record intracardiac electrograms. This allows monitoring of each episode of anti-tachycardia pacing or defibrillation. If treatment has been inappropriate, then programming changes can be made with a programming unit placed over the defibrillator site.

Current devices use anti-tachycardia pacing, with low and high energy shocks also available—known as tiered therapy. Anti-tachycardia pacing can take the form of adaptive burst pacing, with cycle length usually about 80-90% of that of the ventricular tachycardia. Pacing bursts can be fixed (constant cycle length) or autodecremental, when the pacing burst accelerates (each cycle length becomes shorter as the pacing train progresses). Should anti-tachycardia pacing fail, low energy shocks are given first to try to terminate ventricular tachycardia with the minimum of pain (as some patients remain conscious despite rapid ventricular tachycardia) and reduce battery drain, thereby increasing device longevity.

With the advent of dual chamber systems and improved diagnostic algorithms, shocking is mostly avoided during supraventricular tachycardia. Even in single lead systems the algorithms are now sufficiently sophisticated to differentiate between supraventricular tachycardia and ventricular tachycardia. There is a rate stability function, which assesses cycle length variability and helps to exclude atrial fibrillation.

Device recognition of tachyarrhythmias is based mainly on the tachycardia cycle length, which can initiate anti-tachycardia pacing or low energy or high energy shocks. With rapid tachycardias, the device can be programmed to give a high energy shock as first line treatment.

Complications
These include infection; perforation, displacement, fracture, or insulation breakdown of the leads; oversensing or undersensing of the arrhythmia; and inappropriate shocks for sinus tachycardia or supraventricular tachycardia. Psychological problems are common, and counselling plays an important role. Regular follow up is required. If antiarrhythmic drugs are taken the potential use of an implantable cardioverter defibrillator is reduced.

Driving and implantable cardioverter defibrillators
The UK Driver and Vehicle Licensing Agency recommends that group 1 (private motor car) licence holders are prohibited from driving for six months after implantation of a defibrillator when there have been preceding symptoms of an arrhythmia. If a shock is delivered within this period, driving is withheld for a further six months.

Any change in device programming or antiarrhythmic drugs means a month of abstinence from driving, and all patients must remain under regular review. There is a five year prohibition on driving if treatment or the arrhythmia is associated with incapacity.

View larger version (42K): [in this window] [in a new window]   Intracardiac electrograms from an implantable cardioverter defibrillator. Upper recording is intra-atrial electrogram, which shows atrial fibrillation. Middle and lower tracings are intracardiac electrograms from ventricle

 

Drivers holding a group 2 licence (lorries or buses) are permanently disqualified from driving.

View larger version (71K): [in this window] [in a new window]   Intracardiac electrograms from implantable cardioverter defibrillators. Top: Ventricular tachycardia terminated with a single high energy shock. Second down: Ventricular tachycardia acceleration after unsuccessful ramp pacing, which was then terminated with a shock. Third down: Unsuccessful fixed burst pacing. Bottom: Successful ramp pacing termination of ventricular tachycardia

 

Indications for defibrillator use

Primary prevention
Primary prevention is considered in those who have had a myocardial infarction, depressed left ventricular systolic function, non-sustained ventricular tachycardia, and inducible sustained ventricular tachycardia at electrophysiological studies.

The major primary prevention trials, MADIT and MUSTT, showed that patients with implanted defibrillators had > 50% improvement in survival compared with control patients, despite 75% of MADIT control patients being treated with the antiarrhythmic drug amiodarone. A recent trial (MADIT-II) randomised 1232 patients with any history of myocardial infarction and left ventricular dysfunction (ejection fraction < 30%) to receive a defibrillator or to continue medical treatment and showed that patients with the device had a 31% reduction in risk of death. Although these results are good news clinically, they raise difficult questions about the potentially crippling economic impact of this added healthcare cost.

Implantation is also appropriate for cardiac conditions with a high risk of sudden death—long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, arrhythmogenic right ventricular dysplasia, and after repair of tetralogy of Fallot.

Secondary prevention
Secondary prevention is suitable for patients who have survived cardiac arrest outside hospital or who have symptomatic, sustained ventricular tachycardia. A meta-analysis of studies of implanted defibrillators for secondary prevention showed that they reduced the relative risk of death by 28%, almost entirely due to a 50% reduction in risk of sudden death.

View this table: [in this window] [in a new window]   Guidelines for implanting cardioverter defibrillators

 

When left ventricular function is impaired and heart failure is highly symptomatic, addition of a third pacing lead in the coronary sinus allows left ventricular pacing and resynchronisation of ventricular contraction. Indications for these new "biventricular" pacemakers include a broad QRS complex (> 115-130 ms), left ventricular dilatation, and severe dyspnoea (New York Heart Association class 3). Biventricular pacing improves symptoms and, when combined with an implantable cardioverter defibrillator, confers a significant (40%) mortality benefit (COMPANION study).

View this table: [in this window] [in a new window]   Names of trials

 

Atrial flutter and fibrillation
Pacing to prevent atrial tachycardias, including atrial fibrillation, is presently under intense scrutiny as early results have been favourable. Atrial fibrillation is often initiated by atrial extrasystoles, and attention has focused on pacing to suppress atrial extrasystole, thereby preventing paroxysmal and sustained atrial fibrillation.

Atrial flutter
Termination of atrial flutter is most reliable with burst pacing from the coronary sinus or right atrium and usually requires longer periods of pacing (5-30 s). The shorter the paced cycle length, the sooner the rhythm converts to sinus. Direct conversion to sinus rhythm is achievable with sustained overdrive pacing. However, the success of radiofrequency ablation means these techniques are rarely used.

View larger version (45K): [in this window] [in a new window]   Continuous electrocardiogram showing sinus rhythm with frequent atrial extrasystoles (top) arising from the pulmonary veins degenerating into atrial fibrillation (bottom)

 

Atrial fibrillation
Prevention with pacing—Retrospective studies have shown that atrial based pacing results in a reduced burden of atrial fibrillation compared with ventricular based pacing. Pacing the atria at high rates may prevent the conditions required for re-entry and thus prevent atrial fibrillation. Current research is based on triggered atrial pacing, and specific preventive and anti-tachycardia pacing systems are now available for patients with symptomatic paroxysmal atrial tachycardias that are not controlled by drugs. Such devices continually scan the sinus rate and monitor atrial extrasystoles. Right atrial overdrive pacing at 10-29 beats per minute faster than the sinus rate suppresses the frequency of extrasystoles. The pacing rate then slows to allow sinus activity to take over, provided no further extrasystoles are sensed. In some patients atrial fibrillation is initiated during sleep, when the sinus rate is vagally slowed. Resynchronisation (simultaneous pacing at two different atrial sites) in patients with intra-atrial conduction delay may be beneficial. Clinical trials will help answer the question of which form of pacing best prevents atrial fibrillation.

Cardioversion with implantable atrial defibrillators—These are useful in some patients with paroxysmal atrial fibrillation. It is known that rapid restoration of sinus rhythm reduces the risk of protracted or permanent atrial fibrillation. Cardioversion is synchronised to the R wave, and shocks are given between the coronary sinus and right ventricular leads. The problem is that shocks of > 1 joule are uncomfortable, and the mean defibrillation threshold is 3 joules. Thus, sedation is required before each shock.

Future developments
With the development of anti-atrial fibrillation pacing, focal ablation to the pulmonary veins, and flutter ablation, implantable cardioverter defibrillators will be used less often in years to come. The future of device therapy for atrial fibrillation and atrial flutter probably lies in the perfection of radiofrequency ablation and atrial pacing, although there will still be a place for atrioventricular nodal ablation and permanent ventricular pacing in selected patients.

Further reading • O'Keefe DB. Implantable electrical devices for the treatment of tachyarrhythmias. In: Camm AJ, Ward DE, eds. Clinical aspects of cardiac arrhythmias. London: Kluwer Academic Publishers, 1988: 337-57 • Cooper RAS, Ideker RE. The electrophysiological basis for the prevention of tachyarrhythmias. In: Daubert JC, Prystowsky EN, Ripart A, eds. Prevention of tachyarrhythmias with cardiac pacing. Armonk, NY: Futura Publishing, 1997: 3-24 • Josephson ME. Supraventricular tachycardias. In: Bussy K, ed. Clinical cardiac electrophysiology. Philadelphia: Lea and Febiger, 1993: 181-274 • Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH, Zipes DP, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. Eur Heart J 2000;21: 2071-8[Abstract/Free Full Text] • Mirowski M, Mower MM, Staewen WS, Denniston RH, Mendeloff AI. The development of the transvenous automatic defibrillator. Ann Intern Med 1973;129: 773-9

 

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Competing interests: TH has been reimbursed by Guidant for attending a conference in 2001.

The figure of implantable cardioverter defibrillators from 1992 and 2002 is supplied by C M Finlay, CRT coordinator, Guidant Canada Corporation, Toronto.

The ABC of interventional cardiology is edited by Ever D Grech and will be published as a book in autumn 2003. Ever D Grech is consultant cardiologist at the Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada, and assistant professor at the University of Manitoba, Winnipeg.

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Clinical Review ABC Interventional Cardiology

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