By: Steven J. Compton, MD, FACC, FACP
Alaska Heart Institute, Anchorage
The field of interventional cardiac electrophysiology has exploded in the past decade, due to new arrhythmia cures and device-based options for bradycardia, sudden death, and congestive heart failure. This article will summarize some of the current strategies employed in a relatively new field of medicine.
Although modern electrophysiology really began in 1903 with Einthoven's first electrocardiogram recordings, the next several decades were spent trying to sort out the meaning of the P, QRS, and T wave complexes on the electrocardiogram. After 100 years of investigation, however, the reader may be surprised to hear that the U wave still eludes definitive explanation and remains a source of much controversy in the field.
The advent of nuclear cardiology and echocardiography, along with Holter monitoring, allowed characterization of the natural history of heart diseases and arrhythmias by the 1960s and 1970s. By the early 1980s it was very clear that the risk of sudden cardiac death could be accurately predicted based upon left ventricular function measurements. Meanwhile, invasive electrocardiography began in the early 1970s with the first successful endocardial recording of the His bundle potential. Invasive diagnostic electrophysiology allowed definitive descriptions of arrhythmia mechanisms to be described for the first time in humans. In 1985, surgical ablation of arrhythmia was begun with the successful surgical transection of an accessory atrial ventricular conduction pathway in a patient with Wolff -Parkinson-White syndrome. The necessity for a thoracotomy limited widespread use of surgery for arrhythmia but proved that reentrant arrhythmias could be cured clinically by simply interrupting reentrant pathways.
A revolution in arrhythmia management occurred in the early 1990s when transvenous catheters allowed delivery of radiofrequency energy to tissue within the heart. These movable electrode catheters can be placed fluoroscopically, and pacing maneuvers performed to sort out the arrhythmia mechanism. Several dozen different flavors of SVT have been identified, and all of them are potentially curable with catheter ablation. The first catheters allowed destruction of arrhythmogenic tissue using a modified cautery current to simply cook the offending muscle. More recently catheters have been developed to allow endocardial cooling and freezing to achieve the same effect, often with better safety.
 The first arrhythmias tackled in the early 1990s were also, for obvious reasons, the simplest. Wolff -Parkinson-White syndrome is typically caused by a single abnormal muscular pathway transmitting electrical impulses across the tricuspid or mitral valves. This allows reciprocating reentry circuits to develop between the atrium and ventricle and may also cause sudden death due to rapidly conducted atrial fibrillation. Techniques were rapidly developed for mapping these pathways and destroying them from the inside of the heart, creating discrete 4-5mm scar lesions (Figure 1).
By around 1995 it became apparent that atrial flutter could also be targeted with a similar approach, though in this case interruption of the circuit requires a linear lesion to be placed across a wider band of tissue. We now know that the typical atrial flutter circuit involves a counterclockwise reentrant activation around the atrial side of the tricuspid valve. This circuit is easily interrupted by creating a line of scar tissue between the tricuspid valve and the inferior vena cava. Success rates for SVT and fl utter are now typically greater than 98% in experienced laboratories.
Between 1990 and 2000, a number of less common arrhythmias were also described, and curative ablative techniques developed. These rhythms included ectopic atrial tachycardias, atypical atrial flutters frequently involving prior surgical scar and ventricular tachycardias in both normal and diseased hearts.
 Some of the more colorful tools for ablation include threedimensional electrical anatomical mapping tools that allow the physician to map the three-dimensional geometry and electrical activation of the heart chamber(s) of interest. Electrical voltage or electrical activation maps can be displayed over a threedimensional layout of the chamber being mapped, allowing more precise localization of an arrhythmia focus or reentry circuit. (Figure 2.)
Atrial fibrillation has remained the Holy Grail of catheter ablation and has only been seriously addressed with catheters in the past six years. In 1999, groups from Bordeaux and Taipei independently reported that the pulmonary veins are involved in the genesis of atrial fibrillation. This caught the cardiology community by surprise, as the very name of the arrhythmia had always suggested an atrial origin. We now know that a majority of patients with paroxysmal atrial fibrillation actually develop arrhythmias arising from muscular extensions in the lining of the pulmonary veins. Since the pulmonary veins are electrically contiguous with the left atrium, this results in rapid activation of left atrial arrhythmias and fibrillatory activity. Early attempts at curative ablation for paroxysmal atrial fibrillation carried a long-term success rate of around 40% when focal arrhythmogenic areas were targeted for ablation within the pulmonary veins. The most commonly used approach in 2005 involves mapping and electrical isolation of each of the pulmonary veins from the left atrium so that rapid pulmonary vein arrhythmias will no longer enter the heart. With current techniques, long-term success rates have been reported in the
range of 70-80%.
 In 2005, the FDA approved the use of new software to allow the use of gated cardiac CT scans. With this approach, the patient receives a chest CT prior to the procedure. A three-dimensional reconstruction of the left atrium and pulmonary veins can be developed from this data. This anatomic reconstruction can be downloaded onto the mapping system used for navigation and catheter ablation. Figure 3 demonstrates the left atrial geometry of the first Alaskan patient to undergo such a procedure. It is noteworthy that human pulmonary venous anatomy is highly variable and this particular atrium actually shows five pulmonary veins rather than the standard issue of four. A clear delineation of the patient's anatomy is obviously instrumental in executing a successful procedure.
Historically, atrial fibrillation and atrial fl utter have been treated with the same antiarrhythmic drugs, rate control agents, and anticoagulants. Since the advent of curative ablative procedures, the distinction between fl utter and fibrillation has become far more important. A common right atrial fl utter ablation can typically be performed in the right atrium in well under two hours with procedural risks comparable to those of placing a Swan-Ganz catheter. Since the ablative procedure is clearly safer than antiarrhythmic medications, catheter ablation has become the standard of care for viable patients with recurrent fl utter. On the other hand, curative atrial fibrillation ablation is still evolving, requires transseptal puncture, and may be associated with risk of embolic stroke or other injuries. Curative a- fib ablation is still reserved for patients with symptomatic drug-refractory atrial fibrillation. A recent observational study demonstrated lower stroke rates and better survival in patients who opted for catheter ablation. Randomized trials are currently underway comparing ablation vs. drug therapy.
Finally, the ablation strategies developed with catheter techniques have also been generalized to the operating room where patients can undergo endocardial or epicardial atrial fibrillation ablation at the time of concomitant valve or coronary bypass procedures. The e surgical success rates are similar to those achieved with catheters.
DEVICE THERAPY
Although human bradycardia pacing has been around since the late 1950s, there have been steady improvements in pacemaker design, size, features, and pacing lead survival. Pacemakers have dropped in size from that of a hockey puck to devices as small as three stacked quarters. Rate responsive pacemakers have been developed to deal more effectively with sinus node dysfunction by increasing the patient's heart rate in a physiologic manner during exercise using a number of different activity sensors. The two biggest developments in the past decade have been related to defibrillator therapy and biventricular (resynchronization) pacing.
The first human defibrillator was implanted in 1983. This primitive epicardial device was released by the FDA in 1985. The initial implantable defibrillators were too small to be implanted anywhere but the abdomen and typically had a battery life of around 18 months. Success of these devices in sudden death prevention led to further technology breakthroughs with reductions in device size and improvements in lead function. By 1992, transvenous defibrillators and leads were developed, allowing pectoral transvenous device placement with a marked reduction in operative risk. This technology development prompted clinical trials evaluating the efficacy of ICD therapy in patient groups known to be at high risk for sudden death. Before long, trial data had accumulated showing survival benefit in patients with prior cardiac arrest, hemodynamically significant ventricular tachycardia, and patients with syncope and left ventricular dysfunction who proved to have inducible ventricular tachycardia at electrophysiology study.
The first round of ICD trials targeted patients with known ventricular arrhythmias and resuscitated cardiac arrest. A limitation to this approach lay in the fact that more than 95% of cardiac arrest patients don't survive their first episode. A meaningful application of ICD technology would require better identification of high-risk patients prior to their first cardiac arrest.
A number of trials have now examined the utility of primary ICD therapy in patients known to be at high risk for ventricular arrhythmia and sudden death. For example, MADIT II simply included patients with a history of prior myocardial infarction and left ventricular ejection fraction of 30% or less. ICD therapy resulted in a 31% mortality reduction within 20 months of randomization. More recently, the SCD-HeFT trial demonstrated a similar mortality reduction when ICDs were applied to patients with class II or III heart failure and left ventricular ejection fractions less than or equal to 35%. Since ventricular arrhythmia is the single most common cause of death in these high-risk subgroups, addition of ICD therapy to medical management has become the standard of care in otherwise viable patients.
CONGESTIVE HEART FAILURE PACING
The presence of left bundle branch block activation is associated with abnormal left ventricular motion due to a time lag between the septal and left ventricular free wall contraction. This results in characteristic echocardiographic findings that were first reported several decades ago. A consistent finding in studies with patients with congestive heart failure has been that mortality correlates strongly with the duration of the QRS (i.e. the time required to electrically activate the ventricles). This finding generated the hypothesis that synchronous pacing of these two walls would improve mechanical function and cardiac output. In patients with class III-IV heart failure, biventricular device placement has now been shown to improve exercise capacity, quality of life, left ventricular ejection fraction, hospital use, and overall survival.
 The challenge of this technique is that left ventricular pacing requires a transvenous lead to be threaded into the right atrium, backwards through the coronary sinus, and upstream into a lateral epicardial vein overlying the left ventricular free wall (Figure 4). Since venous anatomy is highly variable, the use of this procedure varies considerably from patient to patient. Occasionally limitations from venous access require placement of epicardial pacing leads with the older thoracotomy approach. Since patients receiving biventricular-pacing devices are also at risk for ventricular arrhythmia due to left ventricular dysfunction, they are typically offered a combination biventricular pacer/defibrillator.
GENETIC ELABORATION OF ARRHYTHMIA MECHANISMS
Finally, the past decade has seen tremendous advances in our understanding of the structure and function of cardiac ion channels. A lot of the progress in this field has been related to identification of genetic mutations in familial arrhythmia syndromes such as the long Q-T syndrome (LQTS). In LQTS the common finding is that a gene mutation results in delayed ventricular repolarization, increasing the risk of triggered ventricular tachyarrhythmias and sudden death. Most of the LQTS genes are related to reduction in cardiac potassium channel function, delaying electrical recovery. It is interesting to note that "opposite" mutations cause gain of function in the same channels, and can predispose patients to familial atrial fibrillation. Advances in our knowledge of cardiac ion channels have already led to early development of chamber-specific antiarrhythmic drugs which are expected to be considerably safer than the currently approved medications. A number of potentially harmful medications (e.g., Seldane) have been removed from the market due to our understanding of ion channel blockade and sudden death risk.
SUMMARY
The past decade has seen remarkable strides in the treatment and cure of reentrant and automatic tachyarrhythmias in both atrium and ventricle, as well as the development of effective device therapy for sudden death prevention and congestive heart failure management. Advances in basic science characterizing ion channel function are improving clinical understanding of arrhythmia and are likely to lead to the development of safer cardiac and noncardiac drugs.
Alaska Heart Institute
Steven J. Compton, M.D., FACC, FACP
(907) 561-3211 (888) 561-3211
3220 Providence Drive, Suite E3-106
Anchorage, AK 99508
Published November 2005, Physicians Practice
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