Abstract
Ventricular tachycardia (VT) originating from the subepicardium is an important cause of failure of endocardial approaches to VT ablation. Mapping arrhythmia foci or circuits that are deep within the myocardium or in the subepicardium can be attempted via the coronary sinus or pericardial space. The coronary sinus approach has been particularly useful in idiopathic focal VTs; however, this approach 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 (assuming no areas of pericardial adhesions), and has been used most commonly for VT mapping and ablation. However, pericardial adhesions resulting from previous cardiac surgery or pericarditis can significantly limit the feasibility of percutaneous cannulation of the pericardial sac.
Catheter ablation from the epicardium is often required for elimination of VTs due to nonischemic cardiomyopathy and is occasionally useful for VTs in a variety of other diseases. Additionally, epicardial mapping and ablation is necessary in patients in whom endocardial ablation cannot be performed (e.g., left ventricular thrombus, mechanical aortic and mitral valve prosthesis).
Keywords
ventricular tachycardia, pericardium, coronary sinus, epicardial ablation, pericardial adhesions
Outline
Electrophysiological Substrate, 907
Ischemic Cardiomyopathy, 907
Arrhythmogenic Right Ventricular Cardiomyopathy, 908
Nonischemic Dilated Cardiomyopathy, 908
Idiopathic Ventricular Tachycardia, 908
Electrocardiographic Features, 908
Ventricular Tachycardia in Nonischemic Dilated Cardiomyopathy, 909
Ventricular Tachycardia in Arrhythmogenic Cardiomyopathy, 909
Idiopathic Ventricular Tachycardia, 909
Postinfarction Ventricular Tachycardia, 910
Clinical Considerations, 910
Anticoagulation, 911
Contrast-Enhanced Magnetic Resonance Imaging, 911
Contrast-Enhanced Computed Tomography, 912
Navigating the Pericardial Space, 912
Anatomical Considerations, 912
Technical Considerations, 912
Pericardial Adhesions, 914
Epicardial Fat, 914
Transthoracic Epicardial Mapping, 915
Transthoracic Epicardial Ablation, 916
Radiofrequency Ablation, 916
Cryoablation, 918
Complications of Transthoracic Epicardial Ablation, 918
Outcome, 920
Transvenous Epicardial Mapping and Ablation, 920
Ventricular tachycardia (VT) originating from the subepicardium is an important cause of failure of endocardial VT 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. However, the CS approach 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 (assuming no areas of pericardial adhesions), and has been used most commonly for VT mapping and ablation (far less so for supraventricular arrhythmias). Nevertheless, mapping within 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 focal VTs.
Electrophysiological Substrate
Mapping and ablation of arrhythmogenic substrates have traditionally been performed via the endocardial approach. Often, however, the site of origin of a focal tachycardia or a portion of the critical isthmus or even the entire circuit of a macroreentrant VT is located intramurally or in the subepicardium and cannot be identified or ablated from the endocardium. In these settings, the epicardial approach to mapping and ablation can be a valuable strategy for elimination of the arrhythmia.
The importance of epicardial VT circuits was first highlighted in Chagas disease, which classically results in an epicardial involvement in approximately 70% of patients. Epicardial substrates also have been increasingly recognized in the setting of scar-related VT in patients with nonischemic dilated cardiomyopathy (DCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), post–myocardial infarction (MI) VT, as well as in patients with idiopathic VT. Among patients with VT, an arrhythmogenic substrate requiring epicardial ablation is seen more commonly in patients with nonischemic DCM (25% to 50%), ARVC (30% to 40%), and less frequently in ischemic cardiomyopathy (10% to 16%).
Ischemic Cardiomyopathy
MI produces a predictable wavefront of necrosis progressing from subendocardium to epicardium, resulting in a wedge-shaped, primarily subendocardial scar with variable epicardial extension (depending on the transmurality of the infraction), usually confined to a specific coronary vascular territory. Therefore, unlike VT substrates in patients with nonischemic cardiomyopathy, the arrhythmogenic tissue can be accessed from the endocardium in the majority of post-MI patients. Even when the arrhythmogenic substrate is located epicardially, elimination of the overlying epicardial substrate is often successful by endocardial ablation through the thinned transmural scar, minimizing the need for epicardial ablation in this population. Nonetheless, VT originating from the subepicardium remains an important cause of failure of endocardial ablation approaches. In tertiary centers, epicardial ablation has been required in approximately 10% to 25% of post-MI VTs, and seems to be more common with inferior than anterior wall MI. However, epicardial access frequently is not feasible for patients who have undergone prior cardiac surgery (which is the case in more than half of post-MI patients undergoing VT ablation).
Arrhythmogenic Right Ventricular Cardiomyopathy
In ARVC, fibrofatty replacement usually begins in the subepicardium or midmural layers and progresses to the subendocardium. Thus the arrhythmogenic substrate in patients with ARVC is more extensive epicardially, predominantly located in the subtricuspid and right ventricular outflow tract (RVOT) regions. Although epicardial ablation is required in a significant proportion of these patients, the often-thinned right ventricular (RV) wall often allows for successful elimination of the epicardial substrate by endocardial ablation.
Nonischemic Dilated Cardiomyopathy
Myocardial scarring in nonischemic DCM has been shown to have a predilection for the midmyocardium and epicardium. The epicardial left ventricular (LV) scar areas in nonischemic DCM are typically larger than the endocardial scar and have a typical distribution similar to that for endocardial LV scars, usually located in basal lateral areas of the LV adjacent to the mitral valve annulus. Often, the epicardial substrate can exist with no significant endocardial scarring or ventricular wall thinning (unlike the substrate in post-MI and ARVC patients), rendering endocardial ablation alone ineffective in eliminating epicardial targets. As a result, epicardial ablation is needed more often in patients with VT associated with nonischemic DCM than in patients with prior MI.
Idiopathic Ventricular Tachycardia
Idiopathic focal VTs requiring epicardial ablation are observed in up to 14% of patients, and they typically arise in close proximity to the coronary venous system in the LV summit and cardiac crux. On the other hand, the anterior and lateral portions of the RVOT are fairly thin; thus ablation from the endocardium is usually effective, even when VT foci occur on the epicardial surface. The posterior RVOT (infundibulum) is much thicker, but the epicardial surface of the posterior infundibulum is the left ventricular outflow tract (LVOT), and thus ablation may be effective from either the LVOT or the RVOT for arrhythmias arising deep in the myocardium of the posterior RVOT. For the supravalvular aortic region there is no true epicardial location because the RVOT lies anterior to the right and left coronary cusps and the atria lie posterior to the noncoronary cusp.
For epicardial idiopathic VT, a combined approach from the coronary venous system and adjacent anatomical sites has been most effective, with a success rate around 70%. The outcome of the subxiphoid epicardial ablation is poor in the majority of cases due to the close proximity of the coronary arteries and the thick layer of epicardial fat that overlies the ablation targets.
Electrocardiographic Features
Various electrocardiogram (ECG) characteristics have been used to predict whether an epicardial approach may be required based on the VT morphology ( Box 27.1 ). Those ECG methods are mainly based on the concept that when ventricular activation starts at the epicardial level, the initial part of the wavefront progresses slowly through the myocardial wall until reaching the Purkinje system, which is located only at the subendocardium. This slow transmural activation is reflected as slurred onset of the QRS on the surface ECG. Furthermore, propagation of ventricular activation from the epicardial surface results in a QS pattern in the ECG leads over that region. This is in contrast to endocardial VT exit sites, which produce an initial “r” wave in the corresponding ECG leads, reflecting transmural ventricular activation in an endocardial-to-epicardial direction (towards the overlying ECG lead).
LV VT in Nonischemic Dilated Cardiomyopathy
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Pseudo-delta wave >34 msec
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Long R-wave peak time (≥85 msec) in lead V 2
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Shortest precordial RS complex duration >120 msec
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QRS duration >200 msec
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The presence of a Q wave in lead I (for basal superior and apical superior VTs)
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The absence of a Q wave in any of the inferior leads (for basal superior VTs)
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The presence of a Q wave in the inferior leads (for basal inferior and apical inferior VTs)
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Maximum deflection index ≥0.59 (for basal-superior/lateral VTs)
RV VT in Arrhythmogenic Cardiomyopathy
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The presence of an initial Q wave in lead I and QS in lead V 2 (for anterior sites in the RV).
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The presence of an initial Q wave in leads II, III, and aVF (for inferior sites in the RV)
LV Summit Idiopathic VT
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Pseudo-delta wave >34 msec
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Long R-wave peak time (≥85 msec) in lead V 2
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Shortest precordial RS complex duration >120 msec
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Delayed shortest precordial maximal deflection index (≥0.55)
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Peak deflection index >0.6
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R wave amplitude ratio in leads III/II ratio of >1.25
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R wave amplitude ratio in leads aVL/aVR >1.75
LV, Left ventricle; RV, right ventricle; VT, ventricular tachycardia.
It is important to understand that in the setting of scar-related VT, the QRS morphology is related solely to the VT exit site and this does not imply that some other component of the circuit (such as the critical isthmus or entrance site) cannot be ablated from the endocardium, even when an epicardial exit is indicated by the ECG characteristics. Therefore it is unlikely that the surface ECG by itself will ever be entirely predictive of the need for epicardial access for mapping and ablation for any given VT. In addition, large areas of conduction delay often present in patients with myocardial scar can produce misleading activation sequences and confound ECG prediction.
Furthermore, ECG criteria for identifying an epicardial origin of VT appear to be region and substrate specific. The published ECG criteria have very limited accuracy (40% to 60%) for differentiating epicardial from endocardial VT sites of origin when applied indiscriminately to all ventricular locations. The development of region-specific criteria has significantly improved the sensitivity and specificity (up to the 90% range). However, these criteria were validated only for a single region in the heart and only for patients with nonischemic cardiomyopathy.
A computerized algorithm was recently reported to improve ECG utility for identifying epicardial sites of origin of VT, with an accuracy of 80%. The algorithm has been validated for all regions of the endocardium and epicardium in patients with and without structural heart disease, and it performed better in most regions than previously described criteria. However, this will require further validation in large clinical studies.
Ventricular Tachycardia in Nonischemic Dilated Cardiomyopathy
Several ECG findings can suggest an epicardial origin of the LV VT with right bundle branch block (RBBB)-like configuration, and all generally rely on the late engagement of the rapidly conducting His-Purkinje fibers by exits on the epicardium, resulting in intramyocardial delay of conduction and a slurred initial part of the QRS complex. These ECG criteria include: (1) pseudo-delta wave (so called because of its similarity to the slurred upstroke delta wave observed during ventricular preexcitation) greater than 34 milliseconds (measured from the earliest ventricular activation to the earliest fast deflection in any precordial lead), which has a sensitivity of 83% and a specificity of 95%; (2) long R-wave peak time in lead V 2 (i.e., interval from the beginning of the QRS complex to the time of initial downstroke of the R wave after it has peaked [previously known as the intrinsicoid deflection ]) greater than 85 milliseconds, which has a sensitivity of 87% and a specificity of 90%; (3) shortest RS complex duration (measured from the earliest ventricular activation to the nadir of the first S wave in any precordial lead) greater than 120 milliseconds, which has a sensitivity of 76% and a specificity of 85%; and (4) QRS duration greater than 200 milliseconds ( see Fig. 22.11 ). However, all of these interval criteria suffer from being absolute numbers, which can be modified by effects of antiarrhythmic drugs; that is, an unmedicated patient’s pseudo-delta interval of 28 milliseconds (i.e., not epicardial) may be nonspecifically prolonged to 38 milliseconds (i.e., epicardial) by the effect of a sodium channel blocking antiarrhythmic drug. Morphological criteria and the maximum and peak deflection indices (see below) are not subject to this limitation.
However, these criteria do not seem to apply uniformly to all LV regions or to VTs originating from the RV. Other site-specific criteria have been suggested for identifying an epicardial origin for LV VTs: (1) the presence of a Q wave in lead I for basal superior and apical superior VTs; (2) the absence of a Q wave in any of the inferior leads for basal superior VTs; and (3) the presence of a Q wave in the inferior leads for basal inferior and apical inferior VTs. Also, measurement of the maximal deflection index (defined as the time from QRS onset to maximal deflection in precordial leads divided by the QRS duration) can help identify epicardial VT originating in the LVOT region.
Given the limited predictive value of ECG criteria when applied individually, a multistep algorithm that incorporates several criteria (two morphology criteria and two adjusted interval criteria) was proposed to predict the site of origin of VTs from the basal-superior/lateral epicardium in patients with nonischemic DCM. The criteria included, in a stepwise fashion: (1) the absence of Q waves in inferior leads; (2) a pseudo-delta wave greater than or equal to 75 milliseconds; (3) maximum deflection index (defined as the interval measured from the earliest ventricular activation [or from the stimulation artifact] to the peak of the largest amplitude deflection in each precordial lead [taking the lead with shortest time] divided by the QRS duration) greater than or equal to 0.59; and (4) the presence of a Q wave in lead I. This four-step algorithm had a 95% specificity and at least 20% sensitivity for identifying basal-superior/lateral epicardial origin of VTs in nonischemic cardiomyopathy. The morphological criteria (presence of a q wave in lead I and absence of q waves in the inferior leads) appear to be the most specific criteria. In particular, the presence of a q wave in lead I is a very specific (88%) and a very sensitive criterion (88%) for identifying an epicardial site of origin.
Ventricular Tachycardia in Arrhythmogenic Cardiomyopathy
Ventricular ectopy in ARVC usually arises from the “triangle of dysplasia” in the RV and therefore has a left bundle branch block (LBBB) pattern with superior, inferior, or indeterminate axis. Most sustained VTs arise from the RV free wall, and most VTs display LBBB configuration with poor R-wave progression in the precordial leads. Nonetheless, VT with RBBB morphology can be observed in patients with LV disease or when advanced structural RV disease distorts normal ventricular geometry within the thorax ( see Fig. 29.7 ). For VTs originating from the RV, the presence of an initial Q wave in lead I and QS in lead V 2 for anterior sites in the RV strongly predicts an epicardial origin. Similarly, an initial Q wave in leads II, III, and a VF is observed with pace mapping from the inferior epicardial locations in the RV.
Idiopathic Ventricular Tachycardia
The LV summit is the most superior aspect of the “epicardial” LVOT. Hence, VTs originating from this region exhibit the classic slower spread of activation from a focus on the epicardial surface relative to the endocardium and delayed global ventricular activation resulting from later engagement of the His-Purkinje network. Several ECG characteristics can help distinguish epicardial idiopathic VTs from endocardial arrhythmias, including: (1) pseudo-delta wave ≥34 milliseconds, (2) long R-wave peak time (≥85 milliseconds) in lead V 2 , and (3) shortest precordial RS complex of greater than 120 milliseconds.
Furthermore, the degree of initial QRS slurring, as measured by the maximal deflection index (defined as the product of the time from QRS onset to maximal deflection [i.e., the largest positive or negative amplitude deflection] in precordial leads divided by the total QRS duration), can help identify epicardial LV summit VTs. A delayed shortest precordial maximal deflection index (≥0.55) discriminates LV summit VTs from those originating within the aortic sinuses of Valsalva. Similarly, a peak deflection index (determined in the inferior lead presenting the tallest R wave by dividing the time from the QRS onset to the peak QRS deflection by a total QRS duration) of greater than 0.6 predicts an epicardial LV summit origin. This observation is consistent with slower spread of activation from a focus on the epicardial surface relative to the endocardium and delayed global ventricular activation resulting from later engagement of the His-Purkinje network.
Because of its superior location in the LV, VTs originating from the LV summit uniformly exhibit large R wave amplitudes in the inferior leads. However, R wave amplitude ratio in leads III/II can vary according to the location of VT focus within the LV summit. As the site of origin shifts progressively more laterally (from the superior region of the summit towards the inferior region, then towards the lateral mitral annulus), R wave amplitude becomes progressively larger in lead III compared to lead II (concurrent with progressively more steeply negative complexes in lead I). R wave amplitude ratio in leads III/II ratio of greater than 1.25 can predict the requirement of a pericardial approach for VT ablation (i.e., origins from the inferior aspect of the LV summit).
Similarly, the aVL/aVR Q-wave ratio was strongly correlated with the anatomical distance between the successful site and the apex of the LV summit; the longer distances away from the apex of the LV summit the larger the aVL/aVR Q-wave ratio. This indicates that the ECG vectors would shift laterally and inferiorly if the distance between the VT and the apex of the LV summit increased. Also, the aVL/aVR Q-wave ratio was found to predict the approach to successful ablation; the aVL/aVR Q-wave ratio was significantly higher for VTs requiring an epicardial approach, followed by VTs arising from the coronary venous system, subvalvular area, and aortic sinuses of Valsalva. An aVL/aVR Q-wave ratio of less than 1.45 predicted successful ablation from aortic sinuses of Valsalva or subvalvular approaches, whereas an aVL/aVR Q-wave ratio of greater than 1.75 indicated the need for a pericardial approach.
VTs originating from the superior region of the LV summit (the “inaccessible region” close to the apex of the summit) typically exhibit LBBB pattern, larger R wave amplitudes in the inferior leads, and absence of an S wave in leads V 5 to V 6 . When LV summit VTs exhibit an RBBB pattern, transition zone earlier than lead V 1 , aVL/aVR amplitude ratio of greater than 1.1, and S waves in V 5 to V 6 , those VTs are likely to be cured by catheter ablation within the great cardiac or anterior interventricular veins. As noted, when LV summit VTs exhibit lead III/II amplitude ratio of greater than 1.25 and lead aVL/aVR amplitude ratio of greater than 1.75, those VTs are likely to require a pericardial approach for ablation.
Postinfarction Ventricular Tachycardia
The proposed 12-lead ECG features for differentiation of epicardial versus endocardial VT exit sites were assessed in patients without MI, and their utility for localization of post-MI VTs has not been validated. In fact, in a recent report, those QRS characteristics failed to reliably identify post-MI VTs requiring epicardial ablation. Slow initial forces can be present during tachycardia at the MI scar region and, hence, are not specific for epicardial origins. Furthermore, the presence of typical Q waves in the VT ECGs of patients with previous MI precludes the use of morphological ECG criteria, and when present in the precordial leads, Q waves can interfere with the measurement of all interval criteria.
As noted earlier, epicardial VT exits are uncommon in post-MI VT because of the subendocardial nature of the underlying substrate. Furthermore, the VT 12-lead ECG provides information about the VT exit site from the scar border, which generally is not the target of ablation. The critical isthmus of the VT circuit, which constitutes the ablation target, often is complex, and can have an endocardial and epicardial trajectory permitting successful ablation from the endocardium (especially in the presence of wall thinning caused by the infract scar) even in the setting of VT with an epicardial exit. Therefore endocardial mapping should be the first approach to catheter ablation for VTs in patients with ischemic heart disease, even when the surface ECG suggests an epicardial origin of the tachycardia.
Clinical Considerations
Catheter ablation from the epicardium is often required for elimination of VTs due to nonischemic cardiomyopathy and is occasionally useful for VTs in a variety of other diseases, as well as some idiopathic VTs. In addition, epicardial mapping and ablation is necessary in patients in whom endocardial ablation cannot be performed (e.g., LV thrombus, mechanical aortic and mitral valve prosthesis). However, there are several conditions that can significantly limit the feasibility of percutaneous epicardial mapping and ablation. Previous cardiac surgery or pericarditis 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 can be extremely limited.
The need for epicardial ablation, however, is often difficult to determine at the beginning of a procedure. Although percutaneous epicardial VT ablation frequently is pursued after extensive endocardial mapping or ablation fails in achieving the desired procedural endpoint, the epicardial approach should be considered early in the procedure in patients known to have high propensity of epicardial substrates (including those with DCM and ARVC).
Combined endocardial and epicardial mapping during the initial procedure is increasingly being utilized in selected VT patients. Such an approach allows for performing pericardial puncture before initiating systemic anticoagulation and offers a better chance to map and ablate all inducible VTs during the index procedure ( eFig. 27.1 ). However, this strategy inevitably leads to unnecessary pericardial punctures in some patients. In fact, 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. Therefore epicardial access should be obtained at the beginning of a procedure only when an epicardial origin of the VT circuit is strongly suspected based on a thorough preprocedural assessment.
Several preprocedural clues can potentially help select VT patients in whom a combined endocardial-epicardial approach is appropriate as a first-line approach ( Box 27.2 ), including: (1) the presence of a predominantly epicardial underlying disease substrate (e.g., nonischemic DCM, ARVC, Chagas disease); (2) previously failed endocardial ablation; (3) predominantly epicardial location of myocardial scar on preprocedural cardiac imaging studies (cardiac magnetic resonance [CMR] or computed tomography [CT]); or (4) ECG criteria suggesting an epicardial VT exit site. As noted previously, while ECG characteristics can help predict an epicardial exit site, they alone are not reliably predictive of the need for epicardial access and mapping for any given VT. QRS morphology is related solely to the VT exit site and this does not imply that the critical isthmus of the VT circuit cannot be ablated from the endocardium, even when an epicardial exit is implied by the ECG characteristics.
Preprocedural Factors
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Intracavitary thrombus
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Mechanical aortic and mitral valves
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Prior failed endocardial ablation
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Predominantly epicardial underlying disease substrate (nonischemic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy)
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Predominantly epicardial scar on preprocedural cardiac magnetic resonance
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Electrocardiographic criteria suggesting an epicardial VT exit site
Intraprocedural Factors
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Inability to identify the reentry circuit isthmus on the endocardium
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Failed or late VT termination with endocardial radiofrequency ablation
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Endocardial activation mapping demonstrating a focal point of earliest endocardial activation with unfavorable results of entrainment or pace mapping
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Endocardial activation mapping demonstrating diffusely endocardial area of equally earliest activation, with unfavorable unipolar electrogram characteristics or paced mapping results
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Endocardial bipolar voltage mapping demonstrating small areas of abnormalities
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Abnormal endocardial unipolar voltage mapping suggestive of greater extent of epicardial scar
VT, Ventricular tachycardia.
During endocardial VT mapping and ablation, several findings should prompt early consideration of the epicardial approach: (1) the inability to identify the reentry circuit isthmus on the endocardium; (2) endocardial activation mapping demonstrating a focal point of earliest endocardial activation with unfavorable results of entrainment or pace mapping techniques; or (3) large endocardial area (>2 cm 2 region) of equally earliest activation, with no single site showing favorable unipolar electrogram characteristics or paced mapping results; (4) failed or late VT termination with endocardial radiofrequency (RF) energy application; (5) limited endocardial substrate, as indicated by endocardial bipolar voltage mapping demonstrating small areas of abnormalities; and (6) endocardial unipolar voltage mapping is suggestive of greater extent of epicardial bipolar signal abnormalities compared to the bipolar voltage abnormalities.
On the other hand, it is probably more appropriate to defer epicardial intervention in patients with ischemic cardiomyopathy and those anticipated difficult epicardial access (due to prior cardiac surgery) until an endocardial approach has failed ablation.
Anticoagulation
Epicardial access is generally avoided in patients on therapeutic doses of oral or IV anticoagulation. In patients requiring both endocardial and epicardial LV mapping, the pericardial access is typically obtained before endocardial mapping and before administering anticoagulation. When the decision to proceed to the epicardial approach is made after the patient has already received IV heparin during endocardial LV mapping, reversal of anticoagulation effects of heparin with protamine is generally recommended prior to pericardial puncture to reduce the risk of intrapericardial or access-related bleeding. Heparin may be started (if additional endocardial LV mapping is required) after safe epicardial access has been obtained without significant bleeding complications.
Of note, a recent report found that percutaneous pericardial access could be performed safely in anticoagulated patients. This approach obviates the need for temporary reversal of systemic anticoagulation (and potential difficulties in reestablishing therapeutic anticoagulation following protamine administration) in patients who already had endocardial LV ablation, which can potentially increase the risk of systemic thromboembolism. Furthermore, this approach obviates obtaining epicardial access until its value is confirmed based on findings of endocardial mapping.
Contrast-Enhanced Cardiac Magnetic Resonance
Delayed contrast-enhanced CMR delineates regions of scar tissue potentially forming part of the arrhythmia substrate in patients with ischemic and nonischemic cardiomyopathy, 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. 27.1 ).
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 CMR was found to be predictive of failure of the endocardial approach and of the need for the epicardial approach for VT ablation.
CMR can also help determine the underlying etiology of nonischemic cardiomyopathy in some patients, such as myocarditis, sarcoidosis, and ARVC, which can be associated with a higher susceptibility for epicardial VTs. Furthermore, in patients undergoing epicardial mapping and ablation procedures, the registration of preacquired CMR images with real-time electroanatomic mapping allows visualization of the 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 vs. scar).
One potential disadvantage concerns the safety and quality of CMR imaging in patients with implanted cardiac devices. However, recent studies have consistently demonstrated the feasibility and safety of CMR in patients with pacemakers and defibrillators, and evolving technologies have further improved the CMR imaging compatibility of some devices. Also, the device hardware introduces significant artifacts, especially in the basal anterior free LV wall, which degrades the image quality and often limit interpretation of CMR in VT patients. Nonetheless, the interventricular septum, and the LV lateral and inferior walls are mostly free of artifact in most patients. Recently, a wideband late gadolinium enhanced CMR technique has been reported to reduce hyper-intense artifacts from the cardiac device generator. When CMR cannot be obtained, cardiac CT may be used for scar and fat imaging.
Contrast-Enhanced Computed Tomography
Contrast-enhanced CT scanning enables detailed and comprehensive evaluation of LV myocardium using triple multimodality imaging based on anatomical, dynamic, and perfusion parameters to identify abnormal substrate (myocardial scar and border zone) with high spatial (≤1 mm) and temporal resolution. Areas of CT hypoperfusion correlate best with areas of abnormal voltage (<1.5 mV) rather than scar alone (<0.5 mV). Perfusion imaging from CT enables characterization of the transmural extent and intramyocardial location of scar tissue and visualization of surviving mid- and epicardial myocardium in the regions of the scar, which can help identify areas potentially involved in the VT substrate. Such preprocedural information can help the operator to plan an appropriate mapping and ablation strategy, and better inform the patient about the risks, benefits, and chances of procedural success.
The three-dimensional (3-D) CT-defined abnormal myocardium can be accurately extracted and embedded in clinical mapping systems displaying areas of abnormal anatomical, dynamic, and perfusion parameters for substrate-guided VT ablations. In addition, CT epicardial fat imaging can be used to characterize the extent of fat tissue by extracting and integrating epicardial fat information into the 3-D electroanatomic voltage map, thereby helping to distinguish epicardial fat from scar tissue.
Navigating the Pericardial Space
Anatomical Considerations
The pericardium is a double-walled sac that contains the heart and the roots of the great arteries, the 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.
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 (0.8 to 2.5 mm in thickness) consists of fibrous tissue and forms a flask-shaped bag, the neck of which is closed by its fusion with the adventitia of the great vessels, while its base is attached by loose fibro-areolar 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 the superior and inferior sterno-pericardial ligaments. 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 [RA] and ventricle), and to serve as direct protection against injuries.
The fibrous pericardium extends up to 5 to 6 cm along the great vessels, including 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 pericardium. Nerve fibers from the parietal layer of the pericardium transmitted by the phrenic nerve are sensitive to pain (e.g., during pericarditis). In contrast, the visceral pericardial layer on the cardiac surface is insensitive to pain.
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 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 tube-like 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.
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 ( eFig. 27.2 ). There are three sinuses in the pericardial space: superior, transverse, and oblique. The two pericardial space sinuses that can be accessed in electrophysiological (EP) procedures are the transverse and oblique sinuses. The superior sinus (superior aortic recess), which lies anterior to the upper ascending aorta and main pulmonary artery, is irrelevant to the EP procedure.
