Tachycardia
E. S
OSA, M. S
CANAVACCAIntroduction
Epicardial ventricular tachycardia (VT) is defined as VT in which the critical sites of the reentrant circuit (or the ‘sites of origin’) are located exclusively in the subepicardial tissue, as shown by entrainment manoeuvres or VT that is terminated within 10 s with standard radiofrequency (RF) pulses, or both.
This arbitrary definition is based on data obtained in our electrophysiology (EP) laboratory. Until now, the epicardial origin of a given VT has been sus- pected in those patients with nonischaemic VT, a QRS complex duration longer than 200 ms (specificity of 86% and sensitivity of 69% for epicardial circuits), and a delta-wave-like pattern (sensitivity and specificity of 80% for epicardial circuits). Berruezo et al. [1] recently reported similar ECG find- ings. At our centre, determination of the prevalence of an epicardial circuit is based on our experience using the above-mentioned criteria obtained at the EP lab. In our initial series of 215 consecutive patients, epicardial VT was systematically identified using a percutaneous subxiphoid approach.
Epicardial VTs were identified in 32% of patients with post-myocardial- infarction (MI) VT, 36% of patients with Chagas heart disease, and 25% of patients with idiopathic dilated cardiomyopathy [2].
Despite innovations in mapping techniques, the standard endocardial ablation of VT remains an enormous challenge especially in VT associated with structural heart disease. In this subset of patients, results following the use of an conventional endocardial approach have not been consistent [3, 4].
The presence of epicardial circuits has been considered as one of the reasons for the failure of endocardial ablation, and these circuits have been described
Clinical Arrhythmia and Pacemaker Units, Heart Institute – InCor –, University of São Paulo Medical School, São Paulo, Brazil
in several types of cardiac disease treated by surgical and nonsurgical tech- niques [5, 6].
The existent of epicardial VTs has been previously reported. Littmann et al. [7], using epicardial laser photocoagulation during surgical ablation of 25 VTs in 10 patients, observed that post-MI VT may result from epicardial macroreentry. Slow conduction within the reentry circuit can be localised by epicardial mapping, and epicardial ablation interrupts epicardial post-MI VT. In patients with non-ischaemic VT, Cassidy [8] and Perlman [9] suggest- ed that abnormal, fractionated, or late endocardial electrograms, or both, are less frequently seen in patients with dilated cardiomyopathy than in patients with post-MI VT, and the incidence of abnormal epicardial electrograms roughly equals that of abnormal electrograms. Svenson et al. [10] described the existence of epicardial circuits in post-MI VT, suggesting that they are particularly important in inferior-wall infarcts. More recently, other authors have described patients with epicardial VT [11-14].
Methods
Technique for Mapping and Ablating Epicardial VTs
Several techniques for mapping the epicardial surface of the heart in the EP laboratory by the electrophysiologist have been described. The transeptal [15] and coronary cusp approaches [16] can be useful to map specific forms of idiopathic VT, originating in the left ventricular outflow tract. Coronary veins can be used to carry out epicardial mapping, but manipulation of the catheter is limited by the anatomical distribution of these vessels [17]. To the best of our knowledge, the subxiphoid percutaneous approach to the epicar- dial space is the only technique currently available that allows extensive and unrestricted mapping of the epicardial surfaces of both ventricles [2, 18-23].
The Subxiphoid Percutaneous Approach
The epicardial subxiphoid percutaneous approach has been previously
described in detail [2, 18]. Approaching the pericardial space is easy and can
be done after positioning multipolar catheters in the coronary sinus and right
ventricular apex through the femoral venous approach, and before starting
anticoagulation. The pericardial space is reached by using a commercially
available needle, originally developed to perform a spinal tap (Fig. 1) (epidur-
al needle: 17 Gox 3–7/8’ (9.84 cm) and 17Gox 5’ (12.5 cm) TW with cm
markings; Arrow International; Reading, PA]. Other types of needles can be
used; however, the operator must be aware of the higher risk of perforation
of the heart.
The puncture must be done at the angle between the left border of the subxiphoid process and the lower left rib. The spatial orientation of the nee- dle will determine what portion of the ventricles will be reached. The needle usually has to point toward the left shoulder, and it must be introduced more horizontally if the target is the anterior portion of the ventricles and more vertically if the diaphragmatic portion of the heart is the area of interest.
After crossing the subcutaneous tissue, needle movement should be moni- tored by fluoroscopy in the left anterior oblique view, 35–40° (Fig. 2). The needle must be carefully moved toward the heart silhouette until the surgeon can detect movement of the heart.
The injection of a small amount (~1 ml) of contrast demonstrates whether the needle tip is pushing against or passing through the tissue. If the diaphragm has not been reached, the contrast will be seen in the subdi- aphragmatic area. When the needle reaches the pericardial sac, the contrast will spread around the heart, restricted to its silhouette (Fig. 2a). The appearance of a ‘sluggish’ layering of contrast medium indicates that the nee- dle is correctly positioned in the pericardial space. A soft floppy-tipped guidewire is then passed through the hollow, an #8F introducer is advanced, and a regular ablation catheter is then introduced into the pericardial space (Fig. 2b–d).
Once the catheter is inside the pericardial space, epicardial ventricular electrograms can be readily recorded during sinus rhythm and during VT.
The entire surface of the heart can be mapped and eventually ablated.
Fig. 1.Left-anterior oblique view of the heart and catheter position in coronary sinus (CS) and right ventricular (RV) apex. Observe the location of the con- trast medium, injected soon after feel- ing heart movement, to determine whether the needle tip is pushing against or passing through the tissue
Results
From the initial report in 1996 [18] to December 2003 [2], we have used this approach to treat 215 consecutive patients with VT. In 138 of these patients, VT was associated with Chagas disease, while 50 patients were post-inferior- MI, and 15 had VT associated with idiopathic dilated cardiomyopathy (IDCM). Twelve patients had idiopathic VT. The number of episodes of inducible VT ranged from 1.8 to 2.2. Nonmappable VT were observed in 40–44% of patients. Only one episode of endocardial VT was induced in an average of 5% of the patients, and only one episode of epicardial VT was induced in an average of 3.5% of patients. Regarding mappable VT, epicar- dial VT was present in 25% of IDCM-related VT, 32% of post-MI-related VT, and 36% of the episodes of VT associated with Chagas disease. Successful RF ablation (interruption and no reinduction) was obtained from the epicardi- um in 50% of post-MI VT patients, 60% of Chagas VT patients, and 55% of IDCM VT patients.
We are aware that, at least theoretically, critical epicardial sites could have been entrained or interrupted within 10 s from both the endocardial and the epicardial surfaces, making it difficult to demonstrate the presence of a
Fig. 2a–d.Left-anterior oblique views during a subxipfoid epicardial approach. a Note the appearance of a ‘sluggish’ layering of the contrast medium indicating that the needle is correctly positioned in the pericardial space. b A soft floppy-tipped guidewire is passed through the hollow and a #8F introducer is advanced. c, d Once the catheter is inside the pericardial space, the epicardial atrial and ventricular surfaces of the heart can be mapped and eventually ablateda
c d
b
truly epicardial circuit in a given case. In addition, it is not known how often this occurs. Epicardial VTs may occur in patients with idiopathic VT [22] and in those with VT associated with ischaemic [20] and non-ischaemic [6, 19]
VT (Fig. 3).
Problems Related to the Subxiphoid Epicardial Approach
Puncture
Several concerns exist regarding the use of this approach. The first is related to the possibility of inducing puncture accidents. Predictable and avoidable accidents were related to a ‘dry’ right ventricular puncture in 4.5% of 215 consecutive patients who underwent epicardial ablation. A drainable haemopericardium containing 200 ± 98 ml of blood was observed in 7% of the patients. These predictable accidents are mostly related to the learning curve. One patient in this series had bleeding in the abdominal cavity from an injured diaphragmatic vessel, which required blood transfusion and laparotomy to control. This is an unpredictable and difficult to avoid compli- cation.
Fig. 3a–c.a12-lead ECG during ventricular tachycardia (VT). b Best mid-diastolic elec- trogram during a recording of VT at the pericardial surface of the left ventricle. c Interruption of VT soon after epicardial RF delivery
a
b
c
Coronary Artery Damage
One of the main concerns during epicardial mapping and ablation is the avoidance of coronary artery damage. In this regard, d’Avila et al. [24]
reported experimental data from nine mongrel dogs in which linear and sin- gle RF lesions were applied on or near the coronary artery. The authors con- cluded that, in an acute model, RF application delivery above the artery may result in intimal hyperplasia and thrombosis. However, susceptibility to damage was inversely proportional to vessel size, and no endothelial lesions were present in vessels with an internal perimeter > 2 mm.
The long-term effects of RF lesions on the epicardial coronary artery were analysed by Miranda el al. [25] in seven young pigs observed for a least 70 days after RF ablation. The results suggested that RF pulse delivery in the vicinity of the epicardial vessels does not provoke either MI or vascular thrombosis. The endothelium was preserved in most of the animals, but intense intimal thickening was seen in a few. The presence of fat and veins interposed between the epicardial coronary arteries and the catheter tip was related to much less intimal thickening, but the long-term significance of intimal thickening is still unknown.
Our current approach to minimise the risk of damaging the coronary vessels is to obtain an angiogram before ablation in all patients. Based on the analysis of the anatomy of the coronary arteries, safe areas for epicardial ablation can be selected. Depending on the area where the ablation site is located, another angiogram can be obtained during the procedure, immedi- ately before starting ablation, although we do not routinely do this. As a gen- eral rule, we assume that a safe application can be delivered when the dis- tance between the catheter tip and a visible coronary vessel is > 1 cm.
However, if a putative critical site of the tachycardia circuit can only be iden- tified close to a coronary artery despite extensive mapping, then, as in all clinical scenarios, a risk–benefit analysis should be undertaken.
RF application resulted in coronary artery occlusion of a marginal branch causing non-Q-wave MI with a CKMB peak of 35 U/l in only one of 215 consecutive patients.
Effects of Epicardial Fat on Epicardial Mapping and Ablation
The presence of epicardial fat interposed between the catheter tip and an
epicardial target also deserves special mention. Depending on its location
and amount, the fat tissue may reduce the efficacy of epicardial catheter
ablation. D’Avila et al. [26] compared bipolar epicardial electrograms and
ventricular epicardial stimulation thresholds obtained with a 4-mm ablation
catheter from 44 areas without and 45 areas with epicardial fat in ten patients during open-chest surgery. The authors observed that epicardial fat thickness of up to 5 mm interposed between the ablation catheter and the epicardium does not change the amplitude and duration of the bipolar epi- cardial electrogram or the epicardial ventricular stimulation threshold. In areas with a layer of epicardial fat thickness > 5 mm, ventricular capture was not possible even at 10-mA pulses.
The role of epicardial fat in RF lesion formation was analysed in animal models by using standard and cooled-tip RF catheters [27]. This study sug- gested that fat attenuates epicardial lesion formation. The absence of blood flow in the epicardial space causes the catheter tip to heat up too quickly.
The use of a cool-tipped ablation catheter allows more energy to be delivered and a larger lesion to be created despite the presence of fat interposed between the catheter tip and the epicardium. Similar results [28] could be extrapolated to epicardial cryoablation, which can create very deep lesions;
however, the presence of a fat layer of > 5 mm strongly attenuates this type of lesions. These data are important and may help to explain failures during epicardial RF ablation.
Pericarditis
Another potential complication seen after epicardial catheter ablation is post-procedure pericarditis. In the experimental laboratory, animals mapped and ablated intrapericardially may develop intense postpericarditis [29], which can be eliminated by the per icardial infusion of 2 mg triamcinolone/kg at the end of the procedure. Such intense pericarditis was not seen in patients in our series. Precordial distress and pain were observed in approximately 30% of our patients; however, pericardial effusion was min- imal and the symptoms were easily controlled with regular anti-inflammato- ry drugs. All 29 patients in our series who had more than one epicardial pro- cedure, ranging from 1 week to 10 months after the first procedure, were free of pericardial effusion, neither were pericardial adhesions present.
Pericardial Adhesions
Postoperative pericardial adhesions may represent a limitation of the percu-
taneous transthoracic epicardial approach. In our series, five patients had
monomorphic VT 7–10 years after open-chest surgery [23]. The ejection
fraction was around 40%. Despite the presence of postoperative adhesions,
all patients underwent the endocardial and epicardial approach simultane-
ously. Pericardial puncture was directed to the inferior wall of the heart, where pericardial adhesions are thought to be less important than in the anterior wall. The pericardial space was entered in all patients. Fourteen VTs were induced, and eight VTs were unmappable. Three of six mappable VTs were successfully ablated from the endocardium, and two were successfully ablated from the epicardium.
Phrenic Nerve Injury
Injury of the phrenic nerve is a rare complication of endocardial atrial RF ablation. The phrenic nerves course through the upper chest, medial to the mediastinal pleura, and the apex of the right or left lung. The right phrenic nerve lies laterally to the right brachiocephalic vein and the superior vena cava. The left phrenic nerve courses along the lateral aspect of the transverse arch of the aorta. The two nerves subsequently pass anteriorly to their respective pulmonary hila and then inferiorly in a broad vertical plane along the margin of the heart, between the fibrous pericardium and the mediasti- nal pleura. While the application of RF pulses in the lateral aspect of the heart silhouette can theoretically induce phrenic nerve injury [30-32], we have never observed this complication. Nonetheless, we are aware that the incidence of this complication could be underestimated because unilateral diaphragmatic paralysis usually does not cause significant shortness of breath unless other underlying pulmonary disease is present.
For prevention of phrenic nerve injury, high output pacing (15 mA, 5-ms pulse duration) at the eventual ablation site (theoretically near the phrenic course) before RF delivery and even during RF application may be of use.
This is not a problem at our centre, because usually we do not apply many pulses to ablate epicardial VT.
When To Perform the Epicardial Approach?
This question has not been answered, and it depends on the preference of
the electrophysiologist. It is not clear whether one should use the epicardial
approach only after an endocardial failure or only when the ECG of a patient
with clinical VT suggests an epicardial origin of VT. As a matter of fact, the
simultaneous approach may have several advantages, such as reduction in
cost, better chance of mapping and ablating all inducible VTs, and an oppor-
tunity to acquire more expertise with the technique.
Conclusions
Epicardial VT may occur in ischaemic, non-ischaemic, and idiopathic VT.
Truly subepicardial VT can preferentially be ablated from the epicardial sur- face. The percutaneous subxiphoid approach to the pericardial space is easy and can be done safely in the EP laboratory by an electrophysiologist. This approach may improve the results of the catheter ablation procedure.
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