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Percutaneous access to the pericardial space has improved our ability to characterize and modify arrhythmogenic epicardial scar substrates.
Knowledge of pericardial anatomy and relevant surrounding structures is important for reducing and recognizing complications.
Although implementation of epicardial mapping and ablation is variable, substrates with a high likelihood of epicardial scar and prior failed endocardial ablation are most likely to derive benefit from this adjunctive approach.
Understanding fluoroscopic views for both anterior and inferior approaches optimizes the safety and efficacy of the percutaneous puncture.
Surgical access can safely be performed in a sterile electrophysiology laboratory to enable catheter ablation in patients with prior cardiac surgery or adhesions via subxiphoid window for inferior wall substrates and by limited anterior thoracotomy for anterior, apical, and lateral substrates.
Intrapericardial steroids may reduce pericarditis, although repeat access to the pericardial space is possible in the majority of patients.
Careful attention to the anatomic course of the phrenic nerve and coronary arteries is important before radiofrequency delivery to minimize complications.
The presence of epicardial fat can confound the diagnosis of scar in low-voltage regions and impair the penetration of radiofrequency energy delivery into the myocardium.
The most common complication related to epicardial access is pericardial bleeding, which can result from right ventricular puncture, or trauma from mechanical sheath or catheter manipulation and ablation.
A combined epicardial-endocardial ablation strategy provides more comprehensive 2-dimensional modification of 3-dimensional complex scar substrates. Observational cohort studies have demonstrated increased freedom from ventricular tachycardia recurrence with a combined strategy when compared with endocardial ablation alone.
The pericardial space has been historically viewed as a region accessed only in the clinical event of a hemodynamically significant effusion to therapeutically alleviate tamponade or sample fluid for diagnosis. In 1996, Sosa et al. described a percutaneous method similar to a pericardiocentesis to access a “dry” pericardial space. This innovative, yet seemingly high-risk approach opened up a new frontier in complex ablation of arrhythmias, whereby the epicardial surface of the heart could be mapped and ablated by catheters without the need for sternotomy.
The presence of epicardial reentrant circuits may be an important reason for the relatively low historical success rates (50%) of endocardial ablation for scar-mediated ventricular tachycardia (VT). As scar is often transmural and spatially complex, epicardial ablation allows for more comprehensive modification of arrhythmogenic substrates. Since the advent of this percutaneous approach, electroanatomic mapping in the pericardial space has improved our understanding and characterization of the transmural extent and anatomic propensity of scars across a diverse range of substrates. As the complications associated with this approach are related to collateral injury during access and ablation, knowledge of the relevant anatomy is critical to maximize the safety and efficacy of the procedure.
The pericardium is a continuous self-enclosed sac that consists of three layers—a serous visceral pericardium, serous parietal pericardium, and fibrous layer. Embryologically, the serous pericardium consists of a visceral layer (epicardium) and a parietal layer that is reflected onto the outer fibrous layer (epipericardium). A physiologic amount of serous fluid (20–60cc) between the visceral and parietal layer is contained in the pericardial space to lubricate the movement of the epicardium on the parietal pericardium. The normal range of pericardial thickness is 1 to 3.5 mm.
The pericardium serves to protect the heart from trauma, adhesions, and infection. Importantly, it suspends and anchors the heart in a fixed position in the thorax. Superiorly, the pericardium is fixed to the great arteries, surrounding the aorta and pulmonary artery several centimeters above the heart. Inferiorly, the parietal pericardium is attached and anchored to the central tendinous aponeurosis of the diaphragm. Anteriorly, pericardiosternal ligaments attach the fibrous pericardial layer to the manubrium and xiphoid process ( Fig. 34.1 ).
The two major sinuses relevant to electrophysiologic procedures are the transverse and oblique sinuses. The transverse sinus lies superior to the left atrium and posterior to the ascending aorta ( Fig. 34.2 ). The roof of the transverse sinus is marked by the right pulmonary artery as it courses through the aortic arch ( Fig. 34.3 ). It is through the transverse sinus that crossing between the left and right side of heart can be achieved. More commonly, access from the left to the right side of the heart during percutaneous access procedures occurs anterior to the great vessels.
The oblique sinus lies directly posterior to the left atrium and anterior to the esophagus and descending aorta. It is bounded by the venous reflections of the inferior vena cava and four pulmonary veins ( Fig. 34.3 ). As a result, manipulation in the oblique sinus is difficult because of the numerous reflections but anatomically is not required for ablation of VT.
Nerve fibers from the parietal layer of the pericardium transmitted by the phrenic nerve are sensitive to pain. Inflammation of this layer is responsible for the pleuritic pain of pericarditis. The phrenic nerves course along the anterior and lateral pericardial surface outside of the fibrous pericardium.
Access to the pericardial space for epicardial mapping is clinically indicated when a high suspicion for epicardial scar and/or site of origin is present. Currently, the indications for epicardial mapping and ablation are dependent upon the scar substrate, prior ablation history, and electrocardiographic characteristics of the targeted VT. A European Heart Rhythm Association/Heart Rhythm Society consensus statement reported that epicardial access was performed in 17% of VT ablation cases, based on a survey amongst tertiary referral centers although with significant variation in practice patterns. With increased cumulative experience that reinforces procedural safety and efficacy, a trend toward wider implementation is likely.
The characterization of various substrates, including nonischemic cardiomyopathy (NICM), arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM), and Chagasic cardiomyopathy with magnetic resonance imaging (MRI) and electroanatomic mapping, has demonstrated the presence of significant epicardial scarring that is often more extensive than scar seen on the endocardial surface ( Fig. 34.4 A and B ). In contrast, the scar of ischemic cardiomyopathy (ICM) has been reported to be wedge-shaped with primary subendocardial necrosis and variable epicardial sparing depending on the duration of coronary occlusion. This is in concert with the wave front of necrosis theory proposed by Reimer and Jennings. Earlier surgical studies that demonstrated a relative paucity of late potentials in postinfarct scars were performed predominantly on anterior infarcts with aneurysms. In comparison with nonreperfused infarcts, reperfused infarcts have been shown to have different structural and functional scar characteristics with a patchy pattern and variable epicardial sparing. In our experience, epicardial scar is frequently more extensive than endocardial scar in ICM patients without aneurysms and VT termination from the epicardium is seen in 24% of cases ( Fig. 34.5 ).
The implementation of epicardial mapping and ablation is highly variable and is more commonly performed at highly experienced centers. Wider adoption of epicardial ablation is justifiable at centers with sufficiently low risk of complications. Various practice patterns range from using epicardial ablation only in the event of a previously failed endocardial ablation to using it as part of a combined comprehensive initial strategy. However, randomized prospective data are lacking. A proposed strategy for clinical decision making to assess a patient for epicardial access is shown ( Fig. 34.6 ).
Electrocardiographic criteria have been proposed to be suggestive of an epicardial exit site. Delayed myocardial conduction from an epicardial exit is initially slow before accessing the subendocardial conduction system, with an “outside-to-in” activation pattern. Berruezo et al. demonstrated several morphologic criteria that favored an epicardial exit site: (1) a “pseudo-delta” wave duration greater than 34 ms; (2) QRS complex duration greater than 200 ms; (3) delayed intrinsicoid deflection of greater than 85 ms; and (4) RS complex duration greater than 121 ms. In NICM, a QS pattern in lead I or the inferior leads can signify the absence of “inside-to-outside” activation of the heart from the lateral and inferior walls. However, these criteria have significant limitations where the severity of cardiomyopathy, scar burden, and conduction delay associated with antiarrhythmic drugs decrease their diagnostic specificity. In the setting of structural heart disease, these electrocardiographic criteria have been shown to lack any predictive or discriminatory value by Martinek et al. in ICM and Piers et al. in NICM.
Several findings on endocardial mapping can be suggestive of an epicardial site of origin. The absence of early activation sites (diastolic or presystolic) or a diffuse, broad region of activation on electroanatomic mapping suggests that the site of origin or circuit is not limited to the endocardium. In addition, poorly matched pace map sites endocardially and the inability to terminate a mappable VT with endocardial ablation is also suggestive of an intramural or epicardial VT. A unipolar display (<5.5 mV right ventricle, <8.27 mV left ventricle) in patients with limited endocardial abnormalities identified by electroanatomic mapping has been proposed to identify scar at a greater depth using a “wider field of view” in patients with NICM and ARVC.
Percutaneous puncture via subxiphoid access first described by Sosa et al. uses the same approach as a pericardiocentesis. However, because of the risk of cardiac puncture in the absence of an effusion, additional modifications and cautionary steps are used. Importantly, fluoroscopy with contrast imaging and use of a curved tip needle for entering the pericardial space increase the safety and success of obtaining epicardial access.
Surgical backup is important for ablation centers attempting epicardial interventions in the event of complications and a typed blood sample should be obtained. Before attempting access, anticoagulant, antithrombotic, and antiplatelet agents should be discontinued to minimize the risk of bleeding. In our experience, thienopyridines have been associated with the highest incidence of bleeding. To optimize safety, epicardial access is obtained before systemic heparinization, which is necessary during endocardial mapping and ablation. In addition, we often perform epicardial mapping once access is obtained before endocardial mapping to minimize the total duration of systemic anticoagulation during the procedure.
The choice of sedation and anesthesia is an important consideration during preprocedural planning, as general anesthesia minimizes patient movement and regulates respiration. It is our opinion that epicardial access performed under general anesthesia optimizes patient safety, comfort, and overall success. However, general anesthesia may diminish the ease of VT inducibility and prolong procedural duration. This concern is more relevant when the mechanism of ventricular arrhythmia is thought to be automatic or triggered. If conscious sedation is chosen, the sedation may be deepened for the puncture and lightened after successful access is obtained.
The procedure is commenced with sterile preparation of the subxiphoid region, which is then anesthetized with topical 1% lidocaine. Antibiotics are administered at our institution to minimize any risk of bacterial pericarditis. The location of the subxiphoid process by palpation should be carefully confirmed as an anatomic miscalculation may increase the risk of the procedure. A 17-gauge curved-tipped needle, originally designed for epidural access to minimize trauma to the spinal cord, is preferred as it allows an angled guidewire course away from the myocardium when the parietal pericardium is punctured. Two lengths of Tuohy epidural needles are available at our institution: 17-gauge × 3.5 inches (90 mm, BD Medical, Franklin Lakes, NJ) and 17-gauge × 6 inches (152 mm, Hakko, Cincinnati, OH) and should be selected based on body habitus ( Fig. 34.7 ).
At our center, the puncture site is performed one fingerbreadth left of the subxiphoid process, allowing for access through Larrey’s space (trigonum sternocostale), which has been reported to be avascular. A shallow entry initially directed to the left shoulder is preferred to minimize puncture of the liver with an increase toward 45 degrees after several centimeters. Manual pressure over the right upper quadrant may be applied to minimize hepatic puncture.
Biplane fluoroscopy is useful to assess the approach of the needle for the two approaches: anterior and posterior (inferior). A helpful rule of epicardial access is to puncture at the site farther away from the desired region of mapping as acute “U turns” required of the catheter course to map the region around the puncture site are technically challenging. If an anterior puncture is desired, the needle track is continued along a shallow course (<30 degrees), and a steep lateral projection is helpful at assessing the needle track just posterior to the sternum as it approaches the anterior right ventricle ( Fig. 34.8 ). A posterior approach requires steepening of the needle (>45 degrees) course to aim for the basal portion of the heart, which is fluoroscopically marked by the coronary sinus catheter. The right anterior oblique (RAO) projection is useful for determining a basal versus apical approach angle. The left anterior oblique (LAO) projection is helpful to identify the right ventricular (RV) free wall, which forms the right heart border. It is our preference to approach with an angle that is more tangential to the inferior heart border visualized on LAO to minimize RV puncture. However, a puncture directed too septally increases the risk of posterior descending artery injury ( Fig. 34.9 ). The incidence of diaphragmatic and liver puncture with a posterior approach, but in our experience, no adverse clinical events have resulted to date. However, the anterior approach increases the probability of puncture of the superior epigastric artery, which is the more superficial and caudal continuation of the left interior mammary artery. Frequently, the diaphragmatic attachments must be punctured before accessing the pericardial space and can be misinterpreted as the parietal pericardium.
Once the needle is advanced to the inferior heart border, cardiac pulsations, an injury current detected with alligator clips, or ventricular ectopy can all signify contact and indentation of the parietal pericardium onto the epicardium. For this reason, a skin incision is often made before needle insertion to maximize tactile sensitivity. The most sensitive period for cardiac pulsations occurs during inspiration with inferior displacement of the heart increasing the contact with the needle. A pressure sensor may be useful to improve safety for access. In an awake patient, pain signals needle contact with the parietal pericardium through the fibrous layers. A minimal amount of contrast is injected to visualize “tenting” or indentation of the fibrous pericardium as large quantities of contrast injected obscure the fluoroscopic field of view ( Fig. 34.10 ). Once the pericardium is in contact with the needle, either constant pressure or a swift calculated puncture can be executed until the puncture is felt with a “pop” or more commonly, visualized with release of the contrast-stained pericardial outer surface. A slight withdrawal of the needle once puncture is sensed, as the pericardium releases, reduces the risk of RV perforation as the advanced needle frequently violates the anatomic plane of the right ventricle ( , ). Contrast is quickly injected to confirm layering within the pericardial space, and then a guidewire is advanced along the lateral heart border in the LAO projection. New tools are being tested currently that may improve safety and efficacy of approach including different needle designs and a pressure-sensing tip. A “needle-in-needle” approach with initial micropuncture entry has also been shown to be feasible and may improve safety.
Before sheath cannulation, the guidewire must be confirmed to reach the left heart border in the LAO view to exclude the possibility of RV puncture with guidewire insertion into the RV outflow tract ( Fig. 34.11 ). The optimal guidewire course for confirmation traverses several chambers and reaches the most outer portion of the fluoroscopic cardiac silhouette ( Fig. 34.12 ). Following this, we use a smaller soft tip dilator (5 F) over the wire for further confirmation. The first aspirate of pericardial fluid is obtained via this small dilator to assess for a blood and 10 to 20 mL of contrast are injected.
Contrast pericardiography is helpful to confirm the pericardial puncture and to assess for adhesions, which may limit the ability to navigate the catheter and increase the probability of pericardial bleeding as these are released and dissected with the sheath and catheter during mapping and ablation ( Fig. 34.13 ). Once this is performed, a long wire is placed across the transverse sinus or anterior to the great vessels and a long sheath is advanced under LAO projection.
We have chosen a long sheath at our center to increase the distance of the operator from the fluoroscopy tube and to minimize the risk of losing access. A steerable sheath can be used if small adhesions are encountered or to assist in mapping regions that are not easily accessible with a fixed sheath. In addition, we use a “double wire” technique and retain one wire to always maintain pericardial access in the case of inadvertent sheath withdrawal during mapping. It is important to minimize the amount of time that a sheath does not have a catheter protruding from it, as an exposed sheath end may lacerate coronary vessels during normal cardiac motion. We use an angiographic catheter as a “place holder” if an ablation catheter is not in the epicardial sheath for mapping or ablation.
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