Clinical Considerations

VT originating from the subepicardium is an important cause of failure of endocardial ablation approaches. Mapping arrhythmia foci or circuits that are deep within the myocardium or in the epicardium can be attempted via the coronary sinus (CS) or pericardial space. The CS approach, however, has important limitations. Catheter manipulation is limited by the anatomical distribution of the cardiac veins, and epicardial circuits may be identified only when the vessel cannulated happens to be in the region of the circuit. An alternative epicardial approach involves inserting an introducer sheath percutaneously into the pericardial space in the manner used for pericardiocentesis. The subxiphoid approach to the epicardial space allows extensive and unrestricted mapping of the epicardial surface of both ventricles, and has been used most commonly for VT mapping and ablation (far less so for supraventricular arrhythmias). Nonetheless, mapping of the CS and accessible coronary venous branches can be performed prior to the percutaneous epicardial approach to look for clues of an epicardial origin of the VT circuit, and has been particularly useful in idiopathic outflow tract VTs.^4,9

Catheter ablation from the epicardium is often required for elimination of VTs due to nonischemic CMP and is occasionally useful for VTs in a variety of other diseases, as well as some idiopathic VTs. Nonetheless, despite the increasing recognition that ventricular arrhythmias may originate from epicardial foci, epicardial VT ablation remains a specialized procedure and is performed at relatively few centers. In the majority of reported cases, percutaneous epicardial VT ablation has been performed only after failure of a thorough endocardial mapping and ablation session, at a separate setting or during the same setting after exhausting endocardial mapping efforts. Simultaneous endocardial and epicardial mapping can have several advantages (Fig. 27-1), such as a better chance to map and ablate all inducible VTs, reduce the number of procedures required for patients with suspected epicardial VTs, and an opportunity to acquire more expertise with the technique.⁴ Also, epicardial mapping and ablation may be useful as a first procedure when endocardial mapping is not an option because of intraventricular thrombi or in patients with metallic prostheses in the aortic and mitral valves.⁴

FIGURE 27-1 Combined endocardial and epicardial mapping of ventricular tachycardia (VT) in dilated nonischemic cardiomyopathy. Shown are fluoroscopic views of endocardial and epicardial ablation catheter positions. VT was eventually eliminated with endocardial ablation at the site shown (basal left ventricle). ICD = implantable cardioverter-defibrillator.

There are several conditions that can significantly limit the feasibility of percutaneous epicardial mapping and ablation. Previous cardiac surgery usually results in significant pericardial fibrosis, and the pericardial space is often, but not always, virtually replaced by fibrotic adhesions. In this setting, percutaneous cannulation of the pericardial sac is very difficult; even when percutaneous cannulation is successful, manipulation of the instruments is extremely limited and difficult. Additionally, pericardial venous varices have been reported in patients with SVC and azygous venous occlusion. Thus, catheter manipulation and ablation inside the pericardial space of a patient with pericardial varices can result in severe bleeding complications. When pericardial varices are suspected, the diagnosis can be made by three-dimensional (3-D) computed tomography (CT) angiography. Also, the presence of a large hiatal hernia can predispose to inadvertent perforation (and subsequent mediastinal infections) during cannulation attempts. Congenital absence of the pericardium is a rare congenital anomaly (approximately 1 in every 10,000 autopsies) that is most often asymptomatic and can be an incidental finding after the patient is referred for a pericardial procedure. In the preprocedural evaluation, this rare anomaly may be suspected by an abnormal cardiac rotation or silhouette on the chest x-ray film. Definitive diagnosis can be made by CT or magnetic resonance (MR) imaging.¹⁰

Preablation Evaluation

Epicardial access should be obtained only when an epicardial origin of the VT circuit is strongly suspected based on a thorough preprocedural assessment. In a recent study employing simultaneous endocardial and epicardial mapping, the endocardium was ultimately thought to be a better target than the epicardium in up to 21% of patients. This highlights the importance of preoperative evaluations and procedure planning.

Careful analysis of the ECG during VT or premature ventricle complexes (PVCs) is essential. As noted, different ECG criteria for recognizing an epicardial origin of arrhythmia have been proposed. Additionally, MR imaging can help identify epicardial substrate in cardiomyopathies.³ Furthermore, evaluation should include comprehensive clinical assessment and imaging studies to recognize any preexisting contraindications, and to minimize complications. Chest radiograph, echocardiography, and cardiac CT or MR imaging have proven to be useful for screening these patients.

Contrast-Enhanced Magnetic Resonance Imaging

Delayed contrast-enhanced MR imaging delineates regions of scar tissue potentially forming part of the arrhythmia substrate in patients with ischemic and nonischemic CMP, and enables the depiction of transmural and nontransmural scars with high spatial resolution, allowing determination of whether the scar is endocardial, intramyocardial, or epicardial (Fig. 27-2).

FIGURE 27-2 Epicardial fat and scar. A, Extracted epicardial fat (yellow) together with the epicardium (dark red) in a patient with nonischemic cardiomyopathy. B, Short-axis magnetic resonance imaging indicates an epicardial scar in the inferolateral left ventricular area (white arrows). C, Voltage map in the same patient, indicating an area of low voltage extending from the basolateral free wall of the left ventricle to the left ventricular apex. The epicardial fat (yellow) is merged with the electroanatomical voltage map. The low-voltage area projects on the left ventricular epicardium that is devoid of fat.

(From Desjardins B, Morady F, Bogun F: Effect of epicardial fat on electroanatomical mapping and epicardial catheter ablation, J Am Coll Cardiol 56:1320-1327, 2010.)

The suspicion of an epicardial VT substrate can facilitate planning of VT ablations, such as for a combined endocardial and epicardial approach, especially given the fact that visualization of epicardial or intramyocardial scar on preprocedure delayed enhancement MR imaging was found to be predictive of failure of the endocardial approach and of the need for the epicardial approach for VT ablation.¹¹

Cardiac MR imaging can also help determine the underlying etiology of nonischemic CMP in some patients, such as myocarditis, sarcoidosis, and ARVD, which can be associated with a higher susceptibility for VT. Furthermore, in patients undergoing epicardial mapping and ablation procedures, registration of preacquired MR images with real-time electroanatomical mapping allows visualization of ventricular anatomy and obstacles to procedural success, such as epicardial fat, which can be helpful during the mapping procedure in differentiating the cause of low epicardial voltages (fat versus scar).¹¹

One potential disadvantage concerns the safety of MR imaging in patients with implantable cardioverter-defibrillators (ICDs). In these patients, cardiac CT may be used for scar and fat imaging.

Anatomical Considerations

The pericardium is a double-walled, flask-shaped sac that contains the heart and the roots of the great vessels, superior vena cava (SVC), and pulmonary veins (PVs). By separating the heart from its surroundings—the descending aorta, lungs, diaphragm, esophagus, trachea, and tracheobronchial lymph nodes—the pericardial space allows complete freedom of cardiac motion within this sac.¹⁰

The pericardium consists of two sacs intimately connected with one another: an outer fibrous envelope (the fibrous pericardium) and an inner serous sac (the serous pericardium). The fibrous pericardium consists of fibrous tissue and forms a flask-shaped bag, the neck of which is closed by its fusion with the external coats of the great vessels, while its base is attached by loose fibroareolar tissue to the central tendon and to the muscular fibers of the left side of the diaphragm. The fibrous pericardium is also attached to the posterior sternal surface by superior and inferior sternopericardial ligaments.¹⁰ These attachments are essential to maintain the normal cardiac position in relation to the surrounding structures, to restrict the volume of the thin-walled cardiac chambers (right atrium and ventricle), and also to serve as direct protection against injuries.

The vessels receiving fibrous prolongations from the fibrous pericardium are the aorta, the SVC, the right and left pulmonary arteries, and the four PVs. The inferior vena cava (IVC) enters the pericardium through the central tendon of the diaphragm, and receives no covering from the fibrous layer.

The serous pericardium is a delicate membrane that lies within the fibrous pericardium and lines its walls; it is composed of two layers: the parietal pericardium and the visceral pericardium. The parietal pericardium is fused to and inseparable from the fibrous pericardium. On the other hand, the visceral pericardium, which is composed of a single layer of mesothelial cells, is part of the epicardium (i.e., the layer immediately outside of the myocardium) and covers the heart and the great vessels except for a small area on the posterior wall of the atria. The visceral layer extends to the beginning of the great vessels, and is reflected from the heart onto the parietal layer of the serous pericardium along the great vessels in tubelike extensions. This happens at two areas: where the aorta and pulmonary trunk leave the heart and where the SVC, IVC, and PVs enter the heart.¹⁰ The serous pericardium is also metabolically active.

At the pericardial reflections and at the posterior wall between the great vessels, the pericardial space is divided up into a contiguous network of recesses and sinuses. There are three sinuses in the pericardial space: the superior sinus, the transverse sinus, and the oblique sinus. The superior sinus (superior aortic recess) lies anterior to the upper ascending aorta and main pulmonary artery. The transverse sinus is limited by a pericardial reflection between the superior PVs and contains the right pulmonary artery. The oblique sinus is confined by the pericardial reflections around the PVs and the IVC. The postcaval recess lies behind the SVC, the right pulmonary artery, and the right superior PV. The right and left PV recesses extend between their respective superior and inferior PVs.¹⁰

The pericardial cavity or sac is a continuous virtual space that lies between the parietal and visceral layers of serous pericardium. The heart invaginates the wall of the serous sac from above and behind, and practically obliterates its cavity, the space being merely a potential one. The sac normally contains 20 to 40 mL of clear fluid that occupies the virtual space between the two layers. Because all pericardial reflections are located basally in relation to the great vessels, the entire epicardial surface is accessible from the pericardial space, except for the atrial and ventricular septa, which are not in direct contact with the pericardium. Unlike the endovascular approach, the pericardial space is notable for the absence of obstacles and the relative ease with which catheter manipulation can be performed.¹⁰ By the same token, achieving firm, stable contact with the catheter tip at the target site may be difficult.

Technical Considerations

Although the procedure is usually performed in the electrophysiological (EP) laboratory, it is more ideal to perform percutaneous pericardial procedures in a hybrid laboratory where cardiac surgery can be performed promptly.

The subxiphoid approach procedure may be performed under conscious sedation, deep sedation with the support of an anesthesiologist, or general anesthesia. Deep sedation or general anesthesia allows better control of respiratory motion, which can potentially reduce the chance of unintentional RV puncture, as well as better pain control, given the fact that epicardial radiofrequency (RF) ablation is usually associated with significant pain and patient discomfort. On the other hand, if patients are paralyzed under general anesthesia, diaphragmatic motion with phrenic nerve stimulation during pacing may not occur to warn of proximity of RF applications.⁴ Intravenous antibiotics should be routinely administered within an hour prior to the procedure. Previous heparin administration should be reversed before pericardial access; this is accomplished by protamine infusion to decrease the activated clotting time to less than 150 seconds.

Initially, catheters are positioned in the CS and RV apex through the femoral approach. The pericardial space is accessed using a 17- or 19-gauge Tuohy needle (Codman Inc., Raynham, Mass.), which is also used to enter the epidural space when administering epidural anesthesia (typically approximately 100 mm in overall length and a 1.5-mm outer diameter). The puncture is performed at the angle between the left border of the subxiphoid process and the lower left rib, with the needle pointing to the left shoulder. The puncture needle approaches the site with a shallow angle in order to penetrate the skin and slide under the rib cage. After crossing the subcutaneous tissue, the stylet is removed, and a 10-mL syringe containing 1% lidocaine or a nonionic contrast agent is attached to the proximal port of the needle. The needle is then advanced under fluoroscopic guidance (40-degree left anterior oblique [LAO] view or, preferably, biplane right anterior oblique [RAO] and LAO projections) until close to the cardiac silhouette. The needle angle is adjusted according to the region that the operator wishes to access. Directing the needle superiorly at a relatively shallow angle, aiming for the RV apex in the RAO projection, generally allows entry into the pericardial space anteriorly over the RV and facilitates access to the anterior aspect of the RV and LV. Directing the needle more posteriorly and toward the left shoulder allows it to enter the pericardium over the diaphragmatic portion of the heart, such that the sheath typically tracks along the posterior aspect of the LV, as observed in the LAO projection. The medial third of the RV is the preferred entry region because of the absence of major coronary vessels in this region.^9,14

In the 40-degree LAO view, injection of a small amount of contrast (approximately 1 mL) can help assess the relation of the needle to the parietal pericardium (Video 21 ). If the diaphragm has not been reached, the contrast will be seen in the subdiaphragmatic area. Once tenting of the pericardium is seen, a slight advance achieves entry into the space, and often one can feel the “pop” as the needle penetrates the fibrotic parietal pericardial wall. Contact of needle with the myocardium can be suggested by tactile feedback, occurrence of ventricular ectopy, or observation of a current of injury from a crocodile clip attached to the shaft of the needle. In this setting, further advancement of the needle can result in ventricular puncture and should be avoided.¹⁵

When the needle reaches the pericardial sac, aspiration without blood indicates that the needle has not entered the RV, and injected contrast will spread around the heart, restricted to its silhouette. In some cases, the needle will get close enough to the heart, but the contrast will not be clearly identified in the pericardial sac. In this situation, despite the needle being out of the pericardial sac, it is likely that a defect has been created in the membrane, through which it is possible to advance a soft-tipped guidewire and enter the pericardial sac. If the needle is not close enough to the pericardial membrane, the guidewire will move toward the subdiaphragmatic area. In these cases, the wire must be pulled back and small movements with the needle and the wire must be performed until the pericardial space is reached.⁹

Confirmation that the wire is intrapericardial and has not been inadvertently inserted into a cardiac chamber is obtained by observing the course of the wire in multiple fluoroscopic projections confirming that it crosses multiple cardiac chambers, hugging the edge of the cardiac silhouette in the 40-degree LAO view, circumferential to both the right and left heart, and without induction of PVCs. Observation in the RAO or anterior-posterior projection alone can be misleading, as a wire that enters the RV and passes into the right atrium (RA) or pulmonary artery can be misinterpreted as intrapericardial.^9,15

Inadvertent RV puncture is not rare, but is usually benign if only the needle or wire has entered the chamber in a patient who is not anticoagulated. When the RV is inadvertently entered with the needle (indicated by aspiration of blood or contrast injection passing to the pulmonary artery), the needle can be withdrawn slightly (reentering the pericardial space after exiting the ventricle); contrast injection can then show silhouetting of the heart, and at that point the guidewire is advanced into the pericardial space. The small hole in the RV generally seals without incident. If the dilator and sheath have been passed into the RV, the larger hole may require surgical repair.⁴

Attempted epicardial access fails in approximately 10% of patients. The percutaneous approach to the pericardial space can be difficult in patients with pericardial adhesions (e.g., following cardiac surgery or pericarditis). In postsurgical patients, the adhesions are mostly concentrated in the anterior portion of the heart; therefore, the puncture must be directed toward the diaphragmatic area. In contrast, adhesion can be more diffuse in postpericarditis patients. Surgical creation of a subxiphoid pericardial window and manual dissection and lysis of the lesions to allow catheter mapping and ablation in the EP laboratory have been shown to be feasible in a small series.⁴

After reaching the pericardial space, a long soft “J” tip guidewire is advanced far enough to silhouette the pericardial space. The puncture needle is then withdrawn and an 8 Fr dilator is advanced over the guidewire under fluoroscopic guidance for predilation, followed by insertion of a standard 8 Fr sheath (see Video 21 ). If it is necessary to insert another catheter, a second guidewire can be advanced through the sheath, which should be removed, leaving two wires inside the pericardial space. Subsequently, a separate sheath is introduced over each of the guidewires. Alternatively, a second puncture of the pericardial sac may be performed, using the same steps described for the first puncture. Before removing the dilator out of the sheath, the sheath must be pushed against the chest to ensure that the tip of the sheath is placed inside the pericardial sac. Although using a standard 15 cm, 8 Fr sheath may suffice for inferior wall VT circuits, the use of longer sheaths (e.g., Agilis; St. Jude Medical, St. Paul, Minn.) should be considered, especially in patients with a larger thoracic anteroposterior dimension.

There is concern that abrasion or laceration of pericardial structures can occur by the edges of a stiff sheath if the sheath is left in the pericardium without a catheter protruding from the lumen. Therefore, it is recommended not to leave a large sheath in the pericardial space without a catheter in place. Also, it is important to lead with a wire or ablation catheter before advancing or moving the curl of the sheath to avoid damaging epicardial structures.⁹

Before introducing the mapping-ablation catheter, the sheath must be aspirated to check for bleeding. Approximately 10% to 20% of patients experience pericardial bleeding, particularly if inadvertent RV puncture has occurred. Bleeding is managed by frequent aspiration from the pericardial access sheath. It is not uncommon to aspirate 10 to 30 mL of bloody drainage from the pericardial sheath early in the procedure. At this point, anticoagulation should not have been administered; therefore, any bleeding should be self-limited and is generally considered a minor complication because it is not necessary to interrupt the procedure. Major bleeding is rare, and it can be related to the learning curve. Systemic anticoagulation with intravenous heparin is started when subsequent LV endocardial mapping, coronary angiography, or both are desired only after verifying the absence of continued pericardial bleeding.⁹

When bleeding is under control, the mapping-ablation catheter can be introduced. Once it is inside the pericardial sac, the catheter can be easily moved, allowing exploration of the entire epicardial surface. In patients with pericardial adhesions, the catheter can be used to perform blunt dissection of the adhesions; however, care must be taken to avoid cardiac perforation with the catheter tip in these cases. If the area of interest is too close to the tip of the sheath, a simple pull-back in the catheter can lead to the loss of pericardial access. Therefore, it is preferable to advance the catheter inside the pericardial space and return to the point of interest by deflecting the tip of the catheter back toward it.

Percutaneous Epicardial Mapping

Once an introducer sheath and catheter are in place, the catheter can be moved freely in the pericardial sac, constrained only by the reflections of the pericardial membrane located around the PVs and great vessels. Catheter mapping of the epicardium can be performed using fluoroscopy, an electroanatomical mapping system, or both. Atrial surface mapping can be limited by the normal pericardial reflections and by the atrial irregular anatomy (right and left atrial appendages). Ventricular surface mapping, however, can be performed more easily. During manipulation of the sheath, small amounts of air can reach the pericardial space, which can easily be detected by fluoroscopy. The presence of air can induce instability to the catheter secondary to the lack of contact between the parietal and visceral membranes of the pericardial sac. Aspiration of air will restore contact characteristic of the pericardial space.

The approach to epicardial mapping is essentially the same as for endocardial ablation, including activation mapping, entrainment mapping, substrate mapping, and pace mapping, discussed in detail in Chapter 22. The following discussion highlights certain peculiarities pertaining to the percutaneous epicardial approach to mapping.

Electroanatomical Substrate Mapping

Substrate and VT mapping approaches are similar to those described for the endocardium. Areas of infarction or scar have low-amplitude electrograms similar to findings during endocardial mapping. However, epicardial fat, which is concentrated along the coronary sulcus and the interventricular grooves, can cause low-amplitude electrograms, falsely suggesting scar in voltage maps. Normal epicardial electrograms demonstrate bipolar signal amplitude typically above 0.94 to 1.5 mV; whereas signal amplitude associated with fat, large vessel coronary anatomy, or both might demonstrate significantly lower amplitude.^4,9,13,16

As noted, epicardial fat less than 0.8 to 5 mm in thickness interposed between the ablating catheter and the epicardium usually does not modify the amplitude or duration of the bipolar epicardial electrogram. However, in areas with a layer of epicardial fat greater than 5 mm in thickness the amplitude of the bipolar epicardial electrogram can decrease, resulting in ventricular noncapture, which may confound the ability to discriminate between fat and scar. Importantly, despite the lower electrogram amplitude, epicardial fat will not produce “abnormal” (fractionated and split) electrograms. Therefore, to avoid a misclassification of low-voltage areas due to epicardial fat or major coronary vasculature as abnormal, it is important to analyze the location and extent of the confluent voltage abnormality as well as the electrogram signal characteristics. The presence of abnormal electrograms (fractionated, split, or late potentials) is usually a more reliable indicator of scar.^1,13,14

Registration of preacquired CT or MR images detailing the LV substrate with the real-time 3-D electroanatomical voltage map allows visualization of regions of scar tissue and can potentially facilitate mapping and ablation (see Fig. 27-2). CT and MR imaging can also be used to characterize the extent of fat tissue by extracting and integrating epicardial fat information into the electroanatomical voltage maps, thereby helping to distinguish epicardial fat from scar tissue and identify areas that are difficult to penetrate because of extensive epicardial fat (Fig. 27-3).¹³

FIGURE 27-3 Distribution of epicardial fat and electroanatomical mapping. A, Epicardial voltage map of a patient with nonischemic cardiomyopathy. The voltage map shows surface reconstruction of the anterior surface of the heart. There is a low-voltage area (red) extending from the right ventricular outflow tract to the apex and following the lateral inferior margin to the base of the right ventricle. B, Gross pathology of the same heart after cardiac transplantation illustrating that the area of low voltage on the left largely corresponds to an area of epicardial fat. C, The extracted epicardial fat from the computed tomography data in this patient is shown in yellow. The remaining epicardial surface (dark red) is devoid of fat. The three-dimensional epicardial fat map was integrated with the voltage map. Low-voltage points are bright red and normal voltage points are purple.

(From Desjardins B, Morady F, Bogun F: Effect of epicardial fat on electroanatomical mapping and epicardial catheter ablation, J Am Coll Cardiol 56:1320-1327, 2010.)

Percutaneous Epicardial Ablation

Outcome

Percutaneous epicardial catheter techniques have expanded the options for investigating and treating arrhythmias. Percutaneous pericardial access can be obtained in more than 90% of patients who have not had prior cardiac surgery or clinical pericarditis, even in those who required repeated epicardial procedures. However, pericardial adhesions after cardiac surgery often prevent percutaneous access, although limited access is possible in some patients. A direct surgical approach to the pericardial space via a subxiphoid pericardial window or thoracotomy can achieve access in most patients.^9,21

Percutaneous access to the pericardial space has improved the outcome of catheter ablation in patients with scar-related VT. In several reports, arrhythmia control with epicardial ablation was achieved in 63% to 78% of patients.^3,9 However, it is important to note that these findings reflect practices at centers that specialize in arrhythmia management and may not be applicable to less experienced operators or centers. Careful patient selection is important, and the procedure should be performed by experienced operators with surgical backup.³

The transthoracic epicardial mapping and ablation technique is a relatively safe procedure. Severe complications have been relatively infrequent (approximately 5%), but several potential risks require attention. RV perforation and hemopericardium can be observed in up to 30% of cases. The amount of blood drained from the pericardial space usually ranges from 20 to 300 mL. Thus, most of the time, the occurrence of hemopericardium does not preclude the continuation of the procedure, although repeated aspiration of the pericardial space may be required throughout the procedure. However, major pericardial bleeding remains the most common complication (4.5%), occasionally requiring surgical intervention. Therefore, precautions must be in place for managing severe bleeding, including availability of appropriate surgical expertise.³

Several precautions are important to avoid injury to adjacent structures. RF injury to coronary arteries can cause acute thrombosis or damage to the arterial wall. Coronary angiography must be performed immediately before ablation to select a safe area for RF applications.⁴

Left phrenic nerve injury and diaphragmatic paralysis can result from RF ablation over the lateral LV wall. As noted, different strategies have been proposed with the aim of localizing the nerve, defining the nerve course, and then increasing the distance between the ablation site and the nerve itself.²⁰

Infrequently, hemoperitoneum can result after injuring a subdiaphragmatic vessel during the puncture, and these patients may require surgery to control the intraabdominal bleeding. Hepatic laceration and bleeding are also potential risks.^4,14

Symptomatic pericarditis is common after the procedure, occurring in approximately 30% of patients. In the majority of cases, pericardial inflammation is mild and resolves within a few days with nonsteroidal antiinflammatory medications. Administration of methylprednisolone at 0.5 to 1 mg/kg into the epicardial space at the end of the procedure can potentially help reduce the pericardial inflammatory reaction. It is important to note that inflammatory pericarditis can render the epicardial space percutaneously inaccessible for repeat procedures because of the development of adhesions.^4,9,14

Clinical Considerations

Coronary veins provide endovascular access to the epicardial regions of the ventricles, and have been used for mapping and ablation of arrhythmia foci or circuits that are deep within the myocardium or in the epicardium without having to access the epicardium percutaneously. Access through the great cardiac and anterior interventricular veins allows mapping over a wide area of the anterolateral LV wall, whereas access through the middle cardiac vein allows mapping over the inferior wall of the ventricles and posterior aspect of the interventricular septum.

Up to 14% of patients with idiopathic PVCs can have an epicardial site of origin identified within the coronary venous system, most often in the great cardiac vein. Successful long-term ablation of these arrhythmias was achieved from within the coronary venous system in approximately 70% of patients.⁸

However, epicardial mapping and ablation via the coronary venous system has important limitations. Epicardial circuits may be identified only when the cannulated vessel happens to be in the region of the circuit. Additionally, catheter manipulation is limited by the anatomical distribution and size of these vessels. Currently available ablation catheters often are difficult to advance beyond the distal great cardiac vein or the proximal portions of the middle cardiac vein because of the tortuosity, sharp angulation, and small caliber of the distal veins. Furthermore, a conventional ablation catheter may completely occlude a branch of the CS, preventing cooling of the ablation electrode and resulting in high impedance when RF energy is delivered. This markedly reduces the amount of power that can be delivered and may result in adherence of the ablation electrode to the wall of the vein. In fact, delivery of more than 10 to 15 W seldom is possible. An external saline-cooled ablation catheter allows more consistent delivery of RF energy, with less heating at the electrode-tissue interface.⁷

Anatomical Considerations

The myocardium drains mainly by three groups of veins: (1) the CS and its tributaries, which return blood from almost the whole heart; (2) the anterior cardiac veins, which primarily drain the anterior regions of the RV and the right cardiac border, ending principally in the RA; and (3) the Thebesian venous network (venae cordis minimae), which is the smaller cardiac venous system and is composed of small venous branches made primarily of endothelial cells, which are continuous with the lining of the cardiac chambers, and drains the subendocardium. The Thebesian veins open directly into any of the four chambers but are more prominent on the right and, to a lesser extent, the LA and sometimes the LV.^22–24

Normally, the CS has five first-order tributaries: the great cardiac vein, the middle cardiac vein, the small cardiac vein, the posterior cardiac vein of the LV, and the oblique vein of the LA (oblique vein of Marshall). These tributaries then branch into second- and third-order tributaries. The CS returns the blood to the RA from the whole heart (including its septa) except the anterior region of the RV and small, variable parts of both atria and the LV.

The CS begins as a continuation of the great cardiac vein, extending from the valve of Vieussens (which often marks the junction of the CS with the great cardiac vein) to the ostium of the CS as it terminates in the RA. The length of the CS varies from 30 to 55 mm and its diameter varies from 6 to 16 mm in its middle portion (depending on the loading conditions and the presence of underlying cardiac disease or prior cardiac surgery).^22,23

The CS invariably lies in the posterior aspect of the atrioventricular (AV) groove in the sulcus between the LA and LV and opens into the RA. The CS ostium (CS os) is 5 to 15 mm in diameter and is located on the posterior interatrial septum anterior to the Eustachian ridge and valve and posterior to the tricuspid annulus. The CS os is guarded by the highly variable, crescent-shaped Thebesian valve. This valve usually covers the superior and posterior surfaces of the CS os, but may nearly completely cover the os with formation of fenestrations and can hinder cannulation of the CS.^22–24

The anterior interventricular vein is the largest and most consistent of the cardiac veins. It drains a significant portion of the LV anterior wall and the interventricular septum, begins at the cardiac apex, and ascends toward the base of the heart in the anterior interventricular sulcus, parallel to the left anterior descending coronary artery. The phrenic nerve may lie close to lateral branches of this vein. The anterior interventricular vein is the most anterior vein seen in the RAO projection. At the base of the heart, near the bifurcation of the left coronary artery, the anterior interventricular vein turns laterally and becomes the “great cardiac vein,” which courses along the left AV groove (parallel to the left circumflex coronary artery) and wraps around the left side of the heart.^22–24

The great cardiac vein is joined by the LA oblique vein of Marshall and the posterolateral vein of the LV to form the CS. In addition to several smaller tributaries from the LA and ventricles, the great cardiac vein receives two main branches, namely, the large left marginal vein (along the lateral border of the heart) and the posterior cardiac vein of the LV (also known as the posterolateral vein).^22–24

The middle (or “posterior interventricular”) cardiac vein is the largest proximal tributary of the CS and is present in nearly all hearts. This vein drains the inferior walls of both ventricles and interventricular septum and courses with the posterior descending coronary artery in the posterior interventricular groove, joining the CS close to the RA orifice or, rarely, entering the RA directly.

The small cardiac vein is an inconstant vessel that receives blood from the back of the RA and RV, runs in the coronary sulcus between the RA and RV parallel to the right coronary artery, and empties into either the CS, the middle cardiac vein, or the RA.

Of all of the branches of the coronary venous system, the great cardiac and middle cardiac veins are the two most consistently present branches. Unlike the middle cardiac vein, the great cardiac vein varies considerably in its course. Lateral and posterior venous branches together are seen in approximately 50% of human hearts, unlike the anterior interventricular and middle cardiac veins, which are seen in more than 90%.

The venous valves can hinder catheter access within the coronary venous system, especially the Thebesian valve, which may completely cover the CS os in a variety of forms or be imperforate. Other venous valves, like the valve of Vieussens, are often present at the entrances of the ventricular veins into the great cardiac vein, or at the entrance of a smaller vein into a larger vein. These tend to be flimsy endothelial ridges but can present some resistance on probing or when trying to pass a catheter.^22–24

Technical Considerations

CS venography is typically required to help delineate its anatomy and guide ablation. The great cardiac and the anterior interventricular veins allow epicardial access to the anterior basal ventricular surface. The middle cardiac vein allows epicardial access to the inferior ventricular surface.

Small electrode catheters (e.g., the 2.5 Fr multipolar catheter Pathfinder; Cardima, Inc., Fremont, Calif.) can be introduced into the CS and advanced out into the cardiac veins. The catheter can be positioned in different coronary venous branches to map different regions of the epicardial surface of the ventricles.⁸

Once the ablation catheter is positioned at the target site, and before energy delivery, coronary angiography should be performed to assess the distance of the catheter tip to a major epicardial coronary artery (see Fig. 23-19). If this distance is less than 4 mm ablation should not be attempted. In this situation, cryoablation can be performed with little or no risk of coronary artery injury. Additionally, pacing from the distal ablation electrode should be performed at an output of 20 mA. If diaphragmatic capture can be demonstrated, then ablation should not be attempted to avoid phrenic nerve injury.

RF ablation within the coronary venous system is usually performed with a 3.5-mm open-irrigated-tip catheter at a power output of 15 to 25 W for up to 60 seconds (Fig. 27-4). If this catheter cannot be maneuvered to the ablation target site, a 5 Fr, 6 Fr, or 7 Fr ablation catheter may be used. For nonirrigated-tip catheters, the target temperature is usually set to 55°C to 60°C with a power output of 15 to 30 W. Impedance should be monitored during RF applications, and RF energy delivery should be stopped if impedance rises significantly. If RF energy delivery is limited, cryoablation using a 6-mm CryoAblation catheter (Medtronic, Minneapolis, Minn.) may be considered, although this catheter is less maneuverable than an RF catheter.⁸

FIGURE 27-4 Idiopathic epicardial ventricular tachycardia (VT). A, Surface ECG of a slow VT that was ablated from the coronary sinus (CS) after both endocardial and epicardial mapping failed to eliminate the VT. B, Right anterior oblique (RAO) and left anterior oblique (LAO) fluoroscopic views of catheter location for VT ablation from the CS.

Outcome

The outcome of the ablation procedure is a function of the proximity of the ideal target site to accessible portions of the coronary venous system as well as the ability to deliver an effective amount of ablative energy to the target site. Despite the anatomical constraints, ablation via the coronary venous system has yielded success rates of approximately 70%. Using the coronary venous system for mapping and ablation can potentially result in a lower complication rate than the percutaneous pericardial approach because damage to the RV or extracardiac structures is less likely to occur.⁷

Coronary artery injury is an ever-present risk, especially near the proximal part of the anterior interventricular vein. Arterial injury, including thrombosis, medial necrosis, and hyperplasia, is inversely proportional to vessel diameter; there is little evidence of injury when vessel diameter exceeds 0.5 to 1.0 mm. Similar findings were reported for cryoablation. As noted, coronary angiography should be performed before delivering RF energy near or within a branch of the CS to determine whether there are any branches of the right or left coronary artery in proximity to the ablation site.⁷