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Epicardial Radiofrequency Catheter Ablation for Ventricular Arrhythmias

Since the release of enhanced indications (earlier in the past decade) for implantable cardioverter-defibrillator (ICD) placement, patients at risk of ventricular arrhythmias have received life-extending device therapies. Thus, tertiary electrophysiology centers across the country are faced with an increasing number of patients who have ICD/drug-refractory reentrant ventricular arrhythmias and electrical storm (ES).

From prior studies, it is believed that more than 10% of ICD patients experience ES within 2 years of implantation. Further, with the introduction in the past 15 years of nontransplant strategies such as left ventricular assist devices and cardiac resynchronization therapy (CRT) for management of drug-refractory congestive heart failure (CHF), additional patients who would otherwise have died from CHF are experiencing ES, requiring medical attention.

For patients with ES, Class I–indicated treatments (according to the ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) include coronary artery bypass grafting, percutaneous coronary intervention, intravenous β-blockers, and intravenous amiodarone.

The major Class II treatment is radiofrequency ablation (RFA), used as a required modality in at least 10% of ES patients presenting to large tertiary centers.

Two important trials of ventricular tachycardia (VT) ablation for secondary prevention of ES in patients with structural heart disease have appeared recently in the literature. These studies used saline-irrigated, cooled-tip RFA devices to create deeper endocardial lesions. Nonetheless, only 60% of patients in each trial were free of shocks at 6 months of follow-up.

Multiple VT circuits, CHF, age, and lack of an incessant, hemodynamically well-tolerated VT to map were predictive of recurrence. Many left ventricular (LV) walls have a muscle thickness of more than 1 cm, beyond the lesion field depth of current catheter technologies. Furthermore, patients with dilated cardiomyopathy may have a higher scar density appropriate for anchoring linear RFA lesions on the outside of the heart, rather than the endocardial surfaces.

Image of electrocardiogram from a 57-year-old man with prior inferior myocardial infarction

Figure 1. Electrocardiogram from a 57-year-old man with prior inferior myocardial infarction

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Image of right anterior oblique fluoroscopic projection for 57-year-old man with prior inferior myocardial infarction

Figure 1. Right anterior oblique fluoroscopic projection for 57-year-old man with prior inferior myocardial infarction

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Image of electrocardiogram for 48-year-old man

Figure 2. Electrocardiogram for 48-year-old man

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Image of simultaneous epicardial and endocardial activation maps for 48-year-old man

Figure 2. Simultaneous epicardial and endocardial activation maps for 48-year-old man

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Image of voltage maps of endocardial surfaces illustrating catheter positions in a 48-year-old man

Figure 3. Voltage maps of endocardial surfaces illustrating catheter positions in a 48-year-old man

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Image of voltage maps of epicardial surfaces illustrating catheter positions in a 48-year-old man

Figure 3. Voltage maps of epicardial surfaces illustrating catheter positions in a 48-year-old man

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Image of left anterior oblique fluoroscopic views of the endocardial and epicardial ablation catheters in a 48-year-old man

Figure 4. Left anterior oblique fluoroscopic views of the endocardial and epicardial ablation catheters in a 48-year-old man

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Image of right anterior oblique fluoroscopic views of the endocardial and epicardial ablation catheters in a 48-year-old man

Figure 4. Right anterior oblique fluoroscopic views of the endocardial and epicardial ablation catheters in a 48-year-old man

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Epicardial mapping and ablation

Such is the case with a disease of the Amazon jungle, Chagas disease, caused by the parasitic protozoan Trypanosoma cruzi and transmitted by the blood-sucking assassin bug (kissing bug). Chagas disease causes heart failure, conduction system disease, and ventricular arrhythmias.

South American medical colleagues were quick to discover that the scars that produced the VT in these patients were chiefly epicardial, not endocardial, and could be more readily mapped and ablated from outside the heart rather than from the inside. While mapping and ablation could be accomplished surgically, a less invasive percutaneous approach was needed.

The initial experiences with epicardial mapping and ablation using a percutaneous approach were developed by Eduardo Sosa, M.D. and colleagues at the Heart Institute (InCor), University of São Paulo Medical School in Brazil. They reported a percutaneous epicardial approach for placement of electrophysiologic hardware in 1999. This technique involves the subxiphoid placement of sheaths into an intact, closed pericardial space.

The pericardium typically contains 30 to 50 mL of straw-colored fluid and as such is a virtual space. By accessing the pericardial space, electrophysiologists can map and ablate simultaneously from the endocardial and epicardial surfaces, thus facilitating full-thickness lesion generation in the left ventricle.

Additional care must be taken in the epicardial space to avoid adjacent structures that are normally protected from thermal trauma on the inside of the heart (coronary arteries, phrenic nerve, pulmonary tissues). Several groups in Europe, Asia, and North America have visited São Paulo to gain experience with this important technique.

The percutaneous epicardial ablation program at Mayo Clinic began in 2004. Multiple patients have undergone endocardial mapping and ablation with no obvious scar even being noted; subsequent epicardial mapping demonstrated a definite epicardial scar substrate to which ablation could be applied, alleviating the patient's ventricular arrhythmia.

While the typical patient has underlying structural heart disease, many patients with normal hearts and highly symptomatic premature ventricular contraction (PVC) or VT foci in the left ventricle (which cannot be accessed from traditional approaches using the LV outflow tract or the aortic cusp) are presenting for epicardial treatment.

Both fluoroscopic and echocardiographic imaging with contrast dye is used to facilitate access to the pericardial space. Most patients have the pericardial sheath removed either the evening of the procedure or within 48 hours after placement. The images shown in Figure 1 are from a 57-year-old man with prior inferior myocardial infarction, ICD placement for recurrent VT, shocks despite amiodarone, and 2 prior endocardial mitral isthmus ablations.

Another example is a 48-year-old man whose VT is shown in Figure 2. He had dilated cardiomyopathy, LV ejection fraction of 25%, an ICD enabled with CRT with multiple ICD shocks, and 2 prior unsuccessful ablation attempts.

Figure 3 shows voltage maps of the endocardial and epicardial surfaces, illustrating catheter positions in the same patient shown in Figure 2.

Figure 4 shows fluoroscopic views of the endocardial and epicardial ablation catheters across from each other at anterolateral LV sites in the same patient.

In these examples, epicardial activation, voltage mapping, and epicardial RFA were critical and necessary to achieve the desired clinical effects. Both ventricular rhythms terminated with epicardial energy delivery.

As experience with ablation of patients with structural heart disease and reentrant VT (as well as younger patients with focal epicardial VT or PVC foci and associated tachycardia-induced cardiomyopathy) has widened, electrophysiologists and cardiologists are exploring other areas that could prove fruitful if assisted by this valuable percutaneous epicardial access technique.

In the future this approach will include devices for left atrial appendage occlusion, reservoirs for drug delivery, epicardial pacing, and genotherapies.

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