Implantable devices for treating tachyarrhythmias

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.

Figure 1.

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.

Table 1.

Mechanisms of arrhythmias

Unicellular	Multicellular
• Enhanced automaticity	• Re-entry
• Triggered activity—early or delayed after depolarisations	• Electrotonic interaction
	• Mechanico-electrical coupling

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.

Table 2.

Arrhythmias associated with re-entry

• Atrial flutter

• Sinus node re-entry tachycardia

• Junctional re-entry tachycardia

• Atrioventricular reciprocating tachycardias (such as Wolff-Parkinson-White syndrome)

• Ventricular tachycardia

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.

Figure 2.

Chest radiograph of a dual chamber implantable cardioverter defibrillator with a dual coil ventricular lead (black arrow) and right atrial lead (white arrow)

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.

Figure 3.

Posteroanterior and lateral chest radiographs of transvenous implantable cardioverter defibrillator showing the proximal and distal lead coils (arrows)

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.

Figure 5.

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.

Figure 6.

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.

Table 3.

Guidelines for implanting cardioverter defibrillators

For “primary prevention”

• Non-sustained ventricular tachycardia on Holter monitoring (24 hour electrocardiography)

• Inducible ventricular tachycardia on electrophysiological testing

• Left ventricular dysfunction with an ejection fraction <35% and no worse than class 3 of the NYHA functional classification of heart failure

For “secondary prevention”

• Cardiac arrest due to ventricular tachycardia or ventricular fibrillation

• Spontaneous sustained ventricular tachycardia causing syncope or substantial haemodynamic compromise

• Sustained ventricular tachycardia without syncope or cardiac arrest in patients who have an associated reduction in ejection fraction (<35%) but are no worse than class 3 of NYHA functional classification of heart failure

NYHA=New York Heart Association

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).

Table 4.

Names of trials

• MADIT—Multicenter automatic defibrillator implantation trial

• MUSTT—Multicenter unsustained tachycardia trial

• COMPANION—Comparison of medical therapy, pacing, and defibrillation in chronic heart failure

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.

Figure 7.

Chest radiograph showing biventricular pacemaker with leads in the right ventricle, right atrium, and coronary sinus (arrows)

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.

Figure 8.

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.