Key Points
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The regional anatomy of the superior vena cava is an important arrhythmogenic substrate for various arrhythmias.
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Cryoablation has unique attributes to prevent collateral damage when ablating in or near the superior vena cava.
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Techniques are available to avoid phrenic nerve damage during superior vena caval ablation.
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There are appropriate end points to ablation when isolating the superior vena cava with cryoenergy.
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The potential for complications exists when energy delivery is needed for pericaval tachyarrhythmias.
Introduction
The superior vena cava (SVC) has recently been recognized as an important arrhythmogenic substrate for various arrhythmias including atrial fibrillation (AF) and atrial tachycardia. In addition, because of the proximity of the sinus node region, ablation near the SVC is performed to manage patients with refractory inappropriate sinus tachycardia (IST). Cryoablation is uniquely suited for ablation in this region given the proximity of the phrenic nerve and the importance of avoiding SVC stenosis after circumferential ablation.
This chapter describes the clinical characteristics and relevant anatomic details for the arrhythmias that require peri-superior vena caval ablation. After a brief description of the specific use of cryoablation for venous ablation, a detailed approach to using cryoablative techniques to avoid collateral damage and superior vena caval stenosis when managing these arrhythmias ensues. Finally, an integrated approach combining information from the biophysics of cryoablation, fluoroscopic anatomy, and phrenic nerve function assessment when managing pericaval arrhythmias is described.
The SVC may need to be targeted for ablation for a variety of arrhythmias. Following the observation that the pulmonary veins harbor the triggers that initiate AF, it was soon realized that other thoracic veins, particularly the SVC, may also be the source of paroxysmal AF. As with pulmonary vein ablation, stenosis of the SVC may occur with increased energy delivery within the vein itself. Relatively unique to the SVC is the need to avoid phrenic nerve injury when ablating within or at the ostium of this vein.
Atrial tachycardias may arise from the crista terminalis. When such tachycardias arise from the superior limit of the crista terminalis, ablation is needed at the ostium of the SVC.
IST is a complex disorder where, occasionally, ablation is used to modify the sinus node and control symptoms. Because the sinus node is a cluster of cells located epicardially around the sulcus terminalis at the junction with the SVC, the extensive ablation frequently needed to control symptoms in this arrhythmia involves ablation within or close to the SVC-right atrial (RA) junction.
Cryoablation has several unique features that lend itself for SVC-related ablation procedures. Cryoenergy applications can be done at relatively lower levels (less negative temperatures) as a diagnostic prelude to complete ablation. Furthermore, cryoablation may be delivered circumferentially and is possibly associated with less risk for stenosis, even when energy is delivered within the vein.
Superior Vena Cava: Relevant Anatomy
The SVC has been shown to harbor electrically active tissue that, in some cases, represents the substrate for initiating atrial tachyarrhythmias including AF. This section reviews the unique anatomy of the SVC, particularly the relation with the phrenic nerve, azygos vein, sinus node and ridges, and continuation of the crista terminalis onto and near the SVC-RA junction.
The SVC drains blood from the upper body, measures 6 to 8 cm in length, and is formed by the junction of the innominate veins. Located in front of the SVC are the anterior margins of the right lung and pleura, with pericardial reflections seen inferiorly. Behind the SVC is the right lung and right vagus nerve. To the right are the phrenic nerve and pleura, and to the left is the commencement of the innominate artery and the overlapping ascending aorta. The SVC is endowed with muscular extensions from the right atrium. In human embryos and young children, these muscular extensions are more extensive than those seen in the adult. Electrical activity within these sleeves could trigger arrhythmias, including AF and atrial tachycardia.
The crista terminalis is the junction between the smooth (venous) and muscular right atrium. The crista terminalis crosses anterior and medial to the SVC at the SVC-RA junction to its inferior extent, where it becomes continuous with the eustachian valve anterior to the inferior vena cava. The crista terminalis is an area of marked anisotropy caused by poor transverse cell-to-cell coupling. Such anisotropy, by creating a region of slow conduction, favors the development of reentry. In addition, the normal sinus pacemaker complex is distributed along the long axis of the crista terminalis. The presence of automatic tissue, together with relative cellular uncoupling, may be a requirement for abnormal automaticity such that normal atrium is prevented from electrotonically inhibiting abnormal phase 4 depolarization. Kalman et al. have shown that approximately two thirds of focal RA tachycardias occurring in the absence of structural heart disease will arise along the crista terminalis. The superior margin of the crista terminalis did not end at the junction of the SVC and right atrium, but rather continued in a distinct arclike continuation of the ridge on to the interatrial septum (a superior arcuate ridge) in 7.3% of individuals. This finding is of relevance in patients who have atrial arrhythmias arising from this location. Ablation at this site could cause phrenic nerve damage.
Phrenic Nerve
The phrenic nerve is a mixed somatic nerve that arises mainly from the anterior ramus of the fourth with contributions from the third and fifth cervical segments. The right phrenic nerve is covered by mediastinal pleura as it descends along the brachiocephalic vein and then along the right anterolateral border of the SVC. The nerve is separated from the SVC at its RA junction by the pericardium. It continues inferiorly along the same line over the RA wall. Histologic reports have shown a close relation between the SVC and the right phrenic nerve, separated by variable amounts of fatty tissue. The right phrenic nerve appears to be closest to the SVC superiorly and as it curves posteriorly approaching the superior cavoatrial junction. The phrenic nerve crosses the ostium of the SVC ( Figure 17–1 ).
Azygous Vein
The azygous vein begins opposite the first lumbar vertebra and, via the ascending lumbar vein, enters the aortic hiatus in the diaphragm passing along the right side of the vertebrae, and arches forward over the root of the right bronchus before draining into the SVC. The entrance of the azygous vein marks the junction of the two SVC segments. The upper is directed posteroinferiorly, paralleling the trachea; the lower is directed anteroinferiorly and medially. Like in the SVC, there are muscular sleeves that extend from the right atrium into the azygous vein, which could be the focus of arrhythmias.
Sinus Node
In humans, the sinus node is a spindle-shaped structure composed of a fibrous matrix with closely packed cells. It is 10 to 20 mm long and 2 to 3 mm wide and thick, tending to narrow caudally. It lies less than 1 mm from the epicardial surface and laterally in the RA sulcus terminalis at the junction of the SVC and right atrium.
Arrhythmias Associated with Superior Vena Cava
Atrial Fibrillation
Effective ablation-related management of AF may require attention to the SVC ( Figure 17–2 ). The myocardial extension into the vein may house the trigger or reentrant circuit that subsequently causes global AF. Isolation of the SVC may also be needed as part of a RA maze procedure. The aortocaval ganglion housed between the SVC and the adjacent ascending aorta may also be targeted by transmural ablation to modify the atrial substrate. Finally, because of the proximity of this vein to the right superior pulmonary vein (RSPV), ablation or pacing in the SVC may be required to manage connections between these two veins or defining the true nature of far-field electrograms recorded in one or the other vein ( Figure 17–3 ).
Although ablation can be done within the SVC, the risk for stenosis or venous trauma is significant. Superior vena caval stenosis as a result of SVC isolation has been poorly reported, but systematic imaging assessment for SVC stenosis is seldom done. Besides after the procedure, computed tomography scans cannot exclude subclinical or minor SVC stenosis. Typically, the vein is isolated in a similar fashion to circumferential atrial ablation performed for the pulmonary veins. Isolation of the vein, however, can be challenging because of the proximity of the phrenic nerve.
Inappropriate Sinus Tachycardias
IST is also known as nonparoxysmal sinus tachycardia. The occurrence of an unexplained sinus tachycardia was reported as early as 1939 by Codvelle and Boucher. In 1979, Bauernfeind et al. described the syndrome of IST in seven patients with no other explanation for their tachycardia. They further showed that the underlying mechanism for this arrhythmia was one of abnormal autonomic control on the heart rate. Patients have palpitations, shortness of breath, chest pain, dizziness or near syncope, and the finding of resting tachycardia on a 12-lead electrocardiogram. The tachycardia, similar to sinus tachycardia, will be minimally affected by vagal maneuvers, such as Valsalva or carotid sinus pressure. The usual rate of the tachycardia is between 100 and 160 beats/min.
The delivery of multiple radiofrequency (RF) ablation lesions, often necessary for curing IST, can cause considerable atrial swelling and resultant narrowing of the SVC-RA junction. Animal studies have shown that RA tissue thickening after RF application persists for at least 150 minutes. Multiple ablations done for IST usually result in irreversible SVC stenosis and florid SVC syndrome.
Atrial Tachycardias
RF ablation has a high success rate with few complications in patients with focal atrial tachycardias. However, RF ablation of arrhythmia substrates originating from the vicinity of the sinus node and superior portion of the crista terminalis pose specific challenges to electrophysiologists, including the risk for sinus node dysfunction and phrenic nerve palsy ( Figure 17–4 ). A common site for symptomatic atrial tachycardias requiring ablation is the crista terminalis. When the origin is the myocardium in the superior portion of the crista terminalis, SVC ablation is required. Care must again be given to avoid injury to the phrenic nerve or venous trauma. Importantly, the fear of these complications may have biased the published data regarding complication risks and treatment failure with RF ablation. In many reports, success rates of RF therapy in atrial tachycardia are calculated from the patients who actually underwent ablation, whereas it is not specified how often RF therapy was avoided because of an estimated high risk for complications.
Cryoablation
Unlike heat that destroys cells by coagulation and tissue necrosis with potential for thrombus formation and aneurysmal dilatation, cryoablation involves a distinct pathophysiologic process. These devices all rely on the Joule–Thomson effect, whereby a refrigerant at high pressure, for example, liquid N 2 O, flows down the central lumen of an injection tube and then evaporates at the tip of the catheter into the outer shaft at lower pressure, causing cooling of the catheter tip. Cooling first occurs at the distal catheter tip in contact with endocardial tissue. Freezing then extends radially into the tissues, establishing a temperature gradient. The lowest temperature and fastest freezing rate are generated at the point of contact, with slower tissue cooling rates more peripherally. Of importance, as distant tissue achieves a temperature in the order of −20°C to −30°C, a “dynamic cryomap” is obtained. Catheter tip temperatures of −30°C or slightly higher cause reversible suppression of local electrical activity useful for cryomapping, whereas tip temperatures of −60°C result in irreversible damage of the target tissue, the desired effect during cryoablation. Longer duration of freezing and lower temperatures produce larger lesions, although a plateau is reached within 5 minutes.
Cryoenergy may be particularly valuable in ablating focal sources within venous structures. Theoretical advantages of cryoenergy over RF ablation for perivenous or intravenous applications include a decreased propensity for thrombosis and transmural necrosis. Because cryoablation does not cause endothelial disruption or collagen shrinkage, it is advantageous when used in the veins. Suppression of local cardiac electrical activity by cooling a site briefly to approximately −30°C can be used to predict whether cryoablation at that site will be effective at eliminating the ablation target. When undesirable effects occur during cryomapping or cryoablation, the tissue is allowed to rewarm, and the catheter is then moved to another mapping site. The utility of this approach is based on the observation that effects seen during cryomapping are typically reversible as long as catheter tip temperatures are maintained at or greater than −30°C and the time of application is limited to less than 80 seconds.
To date, thromboembolism or pulmonary vein stenosis has yet to be reported as a complication of cryoablation. One approach, much like RF ablation, is point-by-point ablation to disconnect pulmonary veins or create linear lesions, or both. This has been shown to be feasible and safe with successful pulmonary vein isolation in a high proportion of patients. A second novel approach uses an expandable cryoablation balloon catheter, 18 to 30 mm in diameter, specifically designed for this purpose (Arctic Front; CryoCath Technologies, Point Claire, Quebec, Canada). The balloon is deployed at the ostium of targeted veins and curvilinearly freezes a 64-mm distal segment of the pulmonary vein shaft.
Phrenic Nerve Injury during Radiofrequency Ablation Procedures
Before the advent of thoracic vein-related ablation for AF, reports of phrenic nerve injury with ablation were rare. These typically involved ablation in the right atrium close to the SVC junction as was performed to modify the sinus node (IST), atrial tachycardias arising from the superior crista terminalis, and ablation of RA flutters. Once electrical isolation targeting the triggers in the thoracic veins became an integral part of AF ablation, phrenic nerve injury was increasingly recognized.
The most common site where phrenic nerve-related injury arises when ablating is the SVC ( Figure 17–5 ). This vein is a well-established site for triggers of AF initiators. Perhaps more so than ablation at any other site, precise knowledge on the course of this nerve is essential to avoid injury when attempting to electrically isolate this vein. RF energy to isolate the SVC or to tackle arrhythmias such as IST that arise in its proximity entails a risk for causing SVC stenosis besides phrenic nerve injury. Cryoablation may be superior to RF energy on both these counts, but phrenic nerve injury may still occur with any energy source.
