DOI: 10.1148/rg.23si035513
(Radiographics. 2003;23:S19-S33.)
© RSNA, 2003
PERIOPERATIVE CROSS-SECTIONAL IMAGING |
Percutaneous Ablation for Atrial Fibrillation: The Role of Cross-sectional Imaging
Benoit Ghaye, MD,
David Szapiro, MD,
Jean-Nicolas Dacher, MD,
Luz-Maria Rodriguez, MD, PhD,
Carl Timmermans, MD, PhD,
David Devillers, MD and
Robert F. Dondelinger, MD
1 From the Department of Medical Imaging, Liège University Hospital, Sart Tilman B 35, B-4000 Liège, Belgium (B.G., D.S., D.D., R.F.D.); the Department of Medical Imaging, Rouen University Hospital, France (J.N.D.); and the Department of Cardiology, Maastricht Academic Hospital, the Netherlands (L.M.R., C.T.). Presented as an education exhibit at the 2002 RSNA scientific assembly. Received February 28, 2003; revision requested April 22 and received May 19; accepted May 29. Address correspondence to B.G. (e-mail: bghaye@chu.ulg.ac.be).
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Abstract
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Percutaneous ablation is a well-established technique for treating cardiac arrhythmia by removing or isolating tissue at the site of the abnormal impulse formation. Various forms of energy for ablation procedures may be delivered via a catheter with fluoroscopic guidance. The procedures most commonly performed are radiofrequency ablation and cryotherapy. Atrial fibrillation, the most frequently occurring supraventricular tachyarrhythmia, may be initiated by ectopic beats that originate in the ostia of the pulmonary veins. The clinical efficacy of isolation (or focal ablation) of the pulmonary veins for treatment of atrial fibrillation has been well demonstrated. Pre- and postprocedural examinations with computed tomography (CT) or magnetic resonance (MR) imaging are frequently performed to depict the anatomy and to obtain baseline measurements of the pulmonary veins to enable early detection of complications from ablation. Venous stenosis or thrombosis and pulmonary hypertension may occur after radio-frequency ablation. Familiarity with the appearance of normal anatomic variants at CT and MR imaging and with the normal range of pulmonary vein diameters is essential for preoperative management and early detection of procedure-related complications.
© RSNA, 2003
Index Terms: Cryotherapy • Heart, arrhythmia, 50.91 • Heart, CT, 50.12116 • Heart, interventional procedures, 50.1269 • Heart, MR, 50.12142
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Introduction
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Since the first use of percutaneous ablation in 1986, the technique has developed into an effective therapy for supraventricular and ventricular tachycardias (1–3). More than 90% of ectopic beats that lead to atrial fibrillation originate in the pulmonary veins (PVs) (4). Atrial fibrillation can be treated effectively with targeted ablation of foci in or near the ostia of the PVs, although the technique is associated with cardiopulmonary complications including PV stenosis and thrombosis. Because this procedure is performed with increasing frequency, radiologists should be familiar with the normal and abnormal appearances of PVs at cardiac and chest imaging and should be able to recognize complications of ablation therapy whether they are discovered during postoperative follow-up or incidentally (5).
In this article, we discuss the use of percutaneous ablation in treatment of atrial fibrillation. We also review and illustrate the normal and abnormal anatomy of PVs, the pathophysiology of atrial fibrillation, and the technique, results, and potential complications of percutaneous ablation performed with use of radio-frequency (RF) energy or cryoenergy.
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Atrial Fibrillation
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Cardiac arrhythmias are distortions in the heart rate and rhythm such that the ability of the heart to efficiently deliver blood to the body is affected. Atrial fibrillation is characterized by rapid and uncoordinated atrial electric activity and an irregular ventricular response (6). The prevalence of atrial fibrillation increases with age; it has been estimated at 0.4% in the general population and at 5% in individuals older than 65 years (7). A rapid, irregular ventricular response may result in decreased ventricular efficacy and output. Symptoms include discomfort, anxiety, palpitations, dizziness, shortness of breath, exercise intolerance, difficulties with sleep, and generalized fatigue. Atrial fibrillation is the most common form of cardiac arrhythmia that causes substantial morbidity and mortality. It is a major cause of ischemic stroke, the incidence of which is 5% per year in patients older than 65 years. Factors contributing to risk of atrial fibrillation include smoking, diabetes, hypertension, congestive heart failure, coronary artery disease, previous myocardial infarction, left ventricular hypertrophy, rheumatic heart disease, and valvular disease (8).
Diagnosis of atrial fibrillation has been based traditionally on electrocardiographic (ECG) tracings showing irregular atrial electric activity associated with an irregular ventricular response. Electrophysiologic studies are essential for determining the mechanisms and physiologic characteristics of the arrhythmia and the most appropriate type of treatment (9).
Drug Therapy
Atrial fibrillation is usually treated first with antiarrhythmic medications (10). However, the use of antiarrhythmic drugs is limited by relatively low efficacy and by potential for proarrhythmic side effects. Anticoagulants, in turn, increase the risk of hemorrhagic complications (11).
Cardioversion, Pacemakers, and Defibrillation
Cardioversion has a high initial success rate for treatment of atrial fibrillation, especially in patients with a recent onset, but it is associated with a recurrence rate of 60% at 6 months after treatment (12). Pacemakers can be used to regulate the activity of the atrium or ventricle, or to synchronize the two; these devices also can be used in combination with ablation of the atrioventricular conduction system to regulate the ventricular response. Implanted atrial defibrillators may obviate repeated external cardioversion.
Surgical Treatment
Surgical treatment of arrhythmia consists of either removal or isolation of tissue at the site of the abnormal impulse formation; the anatomic pathways involved in the conduction of arrhythmia are thereby dissected and interrupted. The so-called maze procedure involves the creation of long, superficial surgical incisions in the atrium that eventually will form scars that block the electric conduction that sustains atrial fibrillation. The procedure is most often performed in patients undergoing concomitant valve replacement (13). Cryoablation also has been used successfully during surgery (14).
Percutaneous Ablation
Since the 1980s, various energy sources have been used for percutaneous ablation via catheter. A side benefit of ablation in atrial fibrillation is that it enables the discontinuation of antiarrhythmic and anticoagulant drug therapy.
RF Ablation.—
RF ablation is performed by using an electric current with alternating frequencies of 500–1,000 kHz (15). This procedure involves the creation of myocardial lesions by resistive heating that occurs at the tip of the catheter during the transmission of RF energy (16). RF energy is considered the standard for catheter ablation in tachyarrhythmia (3,14,17). RF energy has been used to create linear lesions in the right or left atrium in patients with atrial fibrillation, similar to the surgical incisions created in the so-called maze procedure (18,19). Because atrial fibrillation is often initiated by ectopic beats that originate in the ostia of PVs, the isolation or focal ablation of the implicated PVs has proved clinically effective therapy, although additional ablation in the right atrium is sometimes necessary (11,20–25).
Cryoablation.—
Cryoablation is the most recently developed technique for percutaneous ablation of supraventricular tachyarrhythmias (26,27). Cryosurgery has been a safe and effective technique for managing cardiac arrhythmias since the late 1970s (14). Transvenous cryotherapy was introduced in 1991 for cryoablation of the His bundle (28). The procedure currently used for percutaneous cryoablation in atrial fibrillation involves the mapping and ablation of tissue in or around the PVs by means of catheters placed in the left atrium.
Other Techniques.—
The use of direct-current ablation by means of high-energy (160–360 J) shocks has been limited in atrial fibrillation by several potential complications and a low efficacy rate (16,29). Ablation performed with ultrasound, laser, or microwave energy sources also has been reported rarely (30).
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Anatomic Variations in the Pulmonary Veins
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The entire network of PVs originates from a single common PV during the 4th week of gestation, before the separation of the right and left atria. The common PV progresses inside the dorsal mesenchyma of the mesocardium, bridging the heart and the mediastinum, toward the concomitantly forming lung buds. The common PV ostium is then displaced leftward by the development of the left valve of the sinus venosus, and takes up its permanent location on the left side of the septum primum, initiating atrial septation. Subsequently, as the apex of the heart rotates leftward and as the left atrium takes up a dorsal midline position and the right atrium adopts an anterior position farther to the right, the common PV is incorporated into the left dorsal atrium. This complex remodeling of the heart is not complete until the 7th week of gestation. The further incorporation of the common PV takes place as the atrial chamber continues to grow (31).
Knowledge of the anatomy of the main PVs is required for the proper planning of ablation therapy in atrial fibrillation (32). Modal anatomy, found in approximately 70% of the general population, consists of four PVs, two superior and two inferior, with four independent ostia (33) (Fig 1). The superior PVs enter the mediastinum downward and anterior to their accompanying pulmonary arteries, the left superior PV being longer than the right. The inferior PVs are oriented upward and located below their homonymous bronchi. Anatomic variations in the number, branching patterns, and length of preostial portions of the PVs, which occur during gestation, result from the under- or overincorporation of the common PV into the left dorsal atrium (33). Both under- and overincorporation are illustrated in Figure 2.
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Figure 1a. Posterior (a) and superoinferior (b) views of the modal anatomy of the PVs, from a three-dimensional volume-rendered image data set obtained with contrast-enhanced multisection computed tomography (CT) (four sections, 2.5-mm collimation, 1.25-mm reconstruction interval) in a 45-year-old man prior to ablation therapy. Four independent ostia are visible in the dorsal aspect of the left atrium. Note that the right middle PV has a normal drainage into the central part of the right superior PV and that the lingular PV drains into the left superior PV. LI = left inferior, LS = left superior, RI = right inferior, RM = right middle, RS = right superior.
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Figure 1b. Posterior (a) and superoinferior (b) views of the modal anatomy of the PVs, from a three-dimensional volume-rendered image data set obtained with contrast-enhanced multisection computed tomography (CT) (four sections, 2.5-mm collimation, 1.25-mm reconstruction interval) in a 45-year-old man prior to ablation therapy. Four independent ostia are visible in the dorsal aspect of the left atrium. Note that the right middle PV has a normal drainage into the central part of the right superior PV and that the lingular PV drains into the left superior PV. LI = left inferior, LS = left superior, RI = right inferior, RM = right middle, RS = right superior.
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Figure 2. Schematic shows three variant configurations of the atrial-venous junction. The left PV branches are represented in blue and pink, and the left atrial wall is shown in orange. The normal pattern is pictured in B. Under- and overincorporation of pulmonary veins into the left atrial wall are shown in C and A, respectively. Divergent development of the cardiac anatomy results in variable lengths of the common trunk and variable numbers and morphology of ostia and PV branches.
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Underincorporation may be asymmetric and involve the confluence of both superior PVs or both inferior PVs (Fig 3) or of the superior and inferior PVs on one side. The latter variant, the most common, is found in 12%–25% of the general population, usually on the left side (Fig 4) (34). A rare and extreme manifestation of underincorporation involves the persistence of the common PV, which results in a narrowing of the common chamber opening into the left atrium (cor triatriatum).
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Figure 3a. Preoperative single-section CT scans (5-mm collimation, 1-mm reconstruction interval, pitch of 2) obtained in a 53-year-old man with a type A dissecting thoracic aneurysm. Two-dimensional axial CT sections obtained from inferior (a) to superior (c) show a common retroatrial chamber formed by the confluence of the two inferior PVs. Note the clear delineation from the main left atrium. Compare this structure with the uniformly smooth posterior left atrial wall shown in Figure 1b. LI = left inferior, LS = left superior, RI = right inferior, RS = right superior.
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Figure 3b. Preoperative single-section CT scans (5-mm collimation, 1-mm reconstruction interval, pitch of 2) obtained in a 53-year-old man with a type A dissecting thoracic aneurysm. Two-dimensional axial CT sections obtained from inferior (a) to superior (c) show a common retroatrial chamber formed by the confluence of the two inferior PVs. Note the clear delineation from the main left atrium. Compare this structure with the uniformly smooth posterior left atrial wall shown in Figure 1b. LI = left inferior, LS = left superior, RI = right inferior, RS = right superior.
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Figure 3c. Preoperative single-section CT scans (5-mm collimation, 1-mm reconstruction interval, pitch of 2) obtained in a 53-year-old man with a type A dissecting thoracic aneurysm. Two-dimensional axial CT sections obtained from inferior (a) to superior (c) show a common retroatrial chamber formed by the confluence of the two inferior PVs. Note the clear delineation from the main left atrium. Compare this structure with the uniformly smooth posterior left atrial wall shown in Figure 1b. LI = left inferior, LS = left superior, RI = right inferior, RS = right superior.
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Figure 4. Preablation baseline contrast-enhanced multisection CT scan (four sections, 2-mm collimation, 1-mm reconstruction interval) obtained in a 60-year-old woman shows the confluence of the left PVs. Volume-rendered posterior view shows a single ostium on the left side (*) and three distinct ostia on the right. LI = left inferior, LS = left superior, RI = right inferior, RM = right middle, RS = right superior.
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Overincorporation beyond the first division is responsible for supernumerary or accessory PVs with independent ostia leading into the left atrium. An increase in number of PVs occurs more frequently on the right side (35,36). An occurrence of three isolated left PVs also has been reported. The occurrence of more than three PVs on the same side has been described rarely in the literature. In most such instances, one or more of the PVs manifested an abnormal return (36). Variants are encountered frequently in the right middle lobe PV connection, the most common of which involve drainage from the right middle lobe PV into the right superior PV (in 53%–69% of the general population), into the left atrium via an independent ostium (in 17%–23% of the general population), or into the right inferior PV (in 3%–8% of the general population) (37,38) (Fig 5). Similarly, the lingular vein has been reported to drain into the left inferior PV in 2.5% of patients (39). These ectopic variants may be responsible for atrial fibrillation foci that have been successfully ablated (37), and the imaging specialist should be able to recognize them.
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Figure 5a. The most common variations in right middle lobe PV draining patterns are shown in volume-rendered posterior views obtained with single-section CT (2-mm collimation, 1-mm reconstruction interval, pitch of 2) before ablation in a 48-year-old woman (a) and a 51-year-old man (c) and obtained with contrast-enhanced multisection CT (four sections, 2.5-mm collimation, 1.25-mm reconstruction interval) before ablation in a 40-year-old man (b). In a, the drainage pathway from the right middle PV to the central portion of the right superior PV is visible; note the independent ostium in a right middle subsegmental vein, which drains into the left atrium (arrowhead). In b, the drainage pathway from the right middle PV to the left atrium via an independent ostium is shown. In c, drainage pathways from the right middle PV to the central portion of the right inferior PV, and from the lingular vein to the central portion of the left inferior PV, are depicted. LI = left inferior, LS = left superior, RI = right inferior, RM = right middle, RS = right superior.
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Figure 5b. The most common variations in right middle lobe PV draining patterns are shown in volume-rendered posterior views obtained with single-section CT (2-mm collimation, 1-mm reconstruction interval, pitch of 2) before ablation in a 48-year-old woman (a) and a 51-year-old man (c) and obtained with contrast-enhanced multisection CT (four sections, 2.5-mm collimation, 1.25-mm reconstruction interval) before ablation in a 40-year-old man (b). In a, the drainage pathway from the right middle PV to the central portion of the right superior PV is visible; note the independent ostium in a right middle subsegmental vein, which drains into the left atrium (arrowhead). In b, the drainage pathway from the right middle PV to the left atrium via an independent ostium is shown. In c, drainage pathways from the right middle PV to the central portion of the right inferior PV, and from the lingular vein to the central portion of the left inferior PV, are depicted. LI = left inferior, LS = left superior, RI = right inferior, RM = right middle, RS = right superior.
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Figure 5c. The most common variations in right middle lobe PV draining patterns are shown in volume-rendered posterior views obtained with single-section CT (2-mm collimation, 1-mm reconstruction interval, pitch of 2) before ablation in a 48-year-old woman (a) and a 51-year-old man (c) and obtained with contrast-enhanced multisection CT (four sections, 2.5-mm collimation, 1.25-mm reconstruction interval) before ablation in a 40-year-old man (b). In a, the drainage pathway from the right middle PV to the central portion of the right superior PV is visible; note the independent ostium in a right middle subsegmental vein, which drains into the left atrium (arrowhead). In b, the drainage pathway from the right middle PV to the left atrium via an independent ostium is shown. In c, drainage pathways from the right middle PV to the central portion of the right inferior PV, and from the lingular vein to the central portion of the left inferior PV, are depicted. LI = left inferior, LS = left superior, RI = right inferior, RM = right middle, RS = right superior.
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Size assessment of PV ostia is mandatory for the optimal selection of circular or balloon catheter gauges (40). Small ostia, in which the risk of stenosis is greater, should be identified at imaging for isolation outside the ostial zone. The ostial diameters of supernumerary PVs are significantly smaller than those of normal PVs. Most PV ostia on the left side are oval (unlike the PV ostia on the right side, which tend to be circular) and are therefore better measured with cross-sectional imaging than with projection imaging (41). The diameters of ostial and more proximal portions of the PVs are larger in the superior PVs than in the inferior PVs and larger in patients with atrial fibrillation than in the general population (40). PVs with large ostia may be prime targets for ablation even without any other evidence of atrial fibrillation foci (41). We measured PV diameters on preablation cross-sectional CT images in 28 patients. Mean ostial diameters were 1.71 cm ± 0.24 for the right superior PV, 1.59 cm ± 0.25 for the right inferior PV, 1.76 cm ± 0.41 for the left superior PV, and 1.39 cm ± 0.29 for the left inferior PV. Mean PV diameters at locations 1 cm from the ostium were 1.40 cm ± 0.21 for the right superior PV, 1.16 cm ± 0.25 for the right inferior PV, 1.45 cm ± 0.32 for the left superior PV, and 1.23 cm ± 0.24 for the left inferior PV.
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Pathophysiology of Arrhythmogenic Ectopic Foci
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During the embryonic development of PVs, the incorporation of the PV confluence into the dorsal left atrium is followed by the muscularization or atrialization of the venous part of the atrial wall (31). The resultant myocardium that surrounds atrial-venous junctions extends from the left atrium 1–2 cm into the adventitia of the PVs (34,42). These myocardial sleeves are distinct from the smooth muscle in the media of the PVs and are circularly or spirally oriented, forming sphincter-like structures. They are more developed and longer around the superior PVs than around the inferior ones (42). The sleeves are thickest at the atrial-venous junctions in the left superior PV. Antigen expression of myocardium similar to that of the developing cardiac conduction system has been shown to occur around the common PV, from which the four PVs originate (43).
Ectopic foci, which are commonly found inside or around the PVs in the left atrium, also can be found in the right atrium, around the crista terminalis and the orifice of the coronary sinus (43), in the interatrial septum, and at the atrial free wall (20). The most common sites of ectopic foci implicated in the triggering of atrial fibrillation are the left superior PV (47%), the right superior PV (37%), the right inferior PV (8%), and the left inferior PV (5%), either near the ostium (39%) or located more distally inside the vein (61%) (20,23). Multiple sources of atrial fibrillation in the same PV or in multiple PVs of the same patient (69%) have been described frequently (21,23). Depolarization in specialized ectopic myocardial cells, like that in the sinus node, accounts for abnormal automaticity found in PVs. It has been suggested that a stretch mechanism occurring in dilated PVs also may trigger activity in these ectopic foci (40,44,45). After ablation, gradual reversal in atrial size and consequently in PV ostial diameters could be an important factor contributing to the maintenance of sinus rhythm (11).
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Imaging Modalities for Morphologic Assessment of PVs
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Pulmonary angiography performed with multiple wedge injections into the pulmonary arteries and selective PV angiography performed after transseptal puncture are the standard diagnostic techniques for identification of PV abnormalities but are invasive and may provide inaccurate measurement due to projection errors. Echocardiography is suboptimal for proper atrial-venous junction evaluation and inadequate for visualization of more proximal portions of the PVs. Magnetic resonance (MR) imaging and multidetector CT of the left atrium and PVs are the most appropriate techniques with which to define the morphology and size of PVs before ablation procedures and to obtain baseline images for reference in subsequent evaluations of acute or delayed complications. To our knowledge, no studies have been published that compare the relative merits of CT versus MR imaging in this context.
Contrast medium–enhanced spiral CT of the PVs ideally should be performed with a multidetector CT scanner and with the patient in sustained deep inspiration. Collimation of 1.5–2.5 mm is appropriate for demonstration of all PVs on axial or reformatted sections. Acquisition should begin 20 seconds after intravenous injection of 100 mL of 30% iodine-based contrast medium at a flow rate of 3 mL/sec. A bolus test or bolus monitoring with triggering may be used to reduce the amount of contrast medium needed. Three-dimensional or multiplanar reformations are useful for analysis of the atrial-venous junction. ECG gating is not mandatory.
In our experience, morphologic evaluation of the PV wall can be performed with the use of a 1.5-T MR imager (Magnetom Symphony; Siemens, Erlangen, Germany), ECG gating, and fat-suppressed dark-blood two-dimensional fast spin-echo sequences at the very end of the cardiac cycle, since atrial systole occurs before ventricular systole. Three-dimensional gadolinium-enhanced MR angiography performed with a fast low-angle shot, or FLASH sequence, during a single patient breath hold provides angiogram-like images that can be rotated in any direction. The initial image set should be acquired in the coronal plane centered on the left atrium. Image acquisition should begin as soon as possible after intravenous bolus injection of gadolinium-based contrast material containing 0.2 mmol of gadolinium per kilogram of body weight at a flow rate of 4 mL/sec, followed by a 30-mL saline solution flush at 3 mL/sec. Alternatively, bolus monitoring may be used and a two-dimensional perfusion image may be acquired that shows the bifurcation of the pulmonary trunk with a temporal resolution of 500 msec. A three-dimensional FLASH sequence with centric reordering should be performed at the beginning of pulmonary trunk enhancement, while the aorta is still unenhanced and the PVs and left atrium are optimally enhanced. A high spatial resolution setting should be used. A bright-blood single-section cine mode true-FISP pulse sequence (ie, true fast imaging with steady-state precession) can be used to demonstrate the morphologic modifications in PV luminal diameters that occur cyclically along with normal flow variations during the cardiac cycle. Flow quantification can be achieved with images acquired with a two-dimensional FLASH sequence, which in normal individuals depict normal pulmonary venous flow peaks during ventricular systole and diastole and a small backflow during atrial systole. PV stenosis also is distinguishable on these images by its effect on blood flow. Postprocessed images are useful adjuncts to source images.
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Catheter Ablation Procedures
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The performance of CT or MR imaging of the PVs prior to ablation may be desirable for visualization of the PV anatomy and for baseline measurements of the ostia (32). Patients must receive anticoagulant drug therapy for at least 3 weeks prior to ablation, and such therapy must be discontinued 2 days before the procedure. Catheter ablation is performed with fluoroscopic guidance. After femoral venous access, catheterization of the left side of the heart is achieved via a patent foramen ovale (20%) or with a transseptal puncture (80%). PVs are selected for ablation on the basis of clinical and electrophysiologic assessment. According to the distribution of the PV potentials, ablation is applied at a series of sites around the ostium of the PV (Fig 6d). Selective PV angiography is performed for measurement of PV diameter and to assess acute PV spasm, thrombosis, or stenosis. Heparin should be administered to maintain an activated clotting time of more than 250 seconds during the procedure (22,27).
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Figure 6a. Percutaneous cryoablation in atrial fibrillation. (a) The cardiac catheter is inserted via the femoral vein and guided to the heart. (b) The catheter is inserted through the septum and into the left atrium. (c) The catheter enters the left upper pulmonary vein. (d) The cryoablation catheter is shown below the mapping Lasso catheter.
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Figure 6b. Percutaneous cryoablation in atrial fibrillation. (a) The cardiac catheter is inserted via the femoral vein and guided to the heart. (b) The catheter is inserted through the septum and into the left atrium. (c) The catheter enters the left upper pulmonary vein. (d) The cryoablation catheter is shown below the mapping Lasso catheter.
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Figure 6c. Percutaneous cryoablation in atrial fibrillation. (a) The cardiac catheter is inserted via the femoral vein and guided to the heart. (b) The catheter is inserted through the septum and into the left atrium. (c) The catheter enters the left upper pulmonary vein. (d) The cryoablation catheter is shown below the mapping Lasso catheter.
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Figure 6d. Percutaneous cryoablation in atrial fibrillation. (a) The cardiac catheter is inserted via the femoral vein and guided to the heart. (b) The catheter is inserted through the septum and into the left atrium. (c) The catheter enters the left upper pulmonary vein. (d) The cryoablation catheter is shown below the mapping Lasso catheter.
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RF Ablation
The predominant mechanism of tissue injury in RF ablation presumably is the accumulation and transfer of thermal energy, but the precise mechanism remains undefined (15). The resulting lesions are irreversible and involve some degree of permanent tissue disruption (14) that may result in postprocedural complications. Lesions show inhomogeneous dense fibrous tissue with scattered strands of viable myocardium within the scar, chronic inflammation, and cartilage formation (46).
Cryoablation
This technique results in minimal tissue disruption and preserves the basic underlying tissue architecture (14). The lesions are well delineated and show homogeneous dense fibrous tissue without interspersed strands of viable myocardium (46). The size of the lesion depends on the temperature and size of the probe and on the duration and number of applications (14).
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Complications
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RF-based treatments for cardiac arrhythmia, such as atrioventricular junction ablation, modification of atrioventricular conduction, ablation of accessory pathways, and others, have an overall clinical complication rate of 1.67%–5.1% (2,17,47). The risk of complications is higher, however, in ablation of the atrioventricular junction or of accessory pathways; ventricular arrhythmia, myocardial infarction, and sudden death have been reported (48,49). Complications related to RF catheter ablation in atrial fibrillation are listed in the Table.
PV Stenosis
The most frequently reported complication of ablation for atrial fibrillation is PV stenosis. The reported prevalence varies from 1.5% to 42%, depending on the definition of PV stenosis and the diagnostic method used (20–23,25,50). PV stenosis can develop in the first days after RF ablation (50,51). Early stenosis is caused by tissue swelling, which may either subside gradually or progress to fibrosis and contraction of the venous wall. Investigators in a long-term follow-up study using transesophageal ultrasonography (US) and color Doppler US reported that stenoses were observed frequently at the lesion sites but that most lesions did not cause significant hemodynamic changes (50). If a single PV is obstructed, the clinical symptoms may be mild and go unrecognized (25). The most frequent symptoms include progressive or exertional dyspnea, orthopnea, nonproductive cough, chest discomfort, recurrent pulmonary infection, and hemoptysis (20,22,23). Pulmonary hypertension is unlikely to develop unless a substantial portion of the pulmonary venous drainage is affected (25,50). Multiple PV stenoses may be life-threatening (25). Successful balloon dilation of the stenosis and instances of stent-graft placement have been reported (23,25,51). The long-term results of these treatments are unknown.
Chest radiography may depict focal pulmonary edema (25,51). Transesophageal echocardiography may reveal elevated pulmonary pressure; increased PV flow velocity; turbulence in the left atrium, at the junction of the stenosed PV and the atrium; and in some instances, stenosis (20,25, 51). However, transesophageal echocardiography is often limited to the superior PVs (50). A ventilation-perfusion scan may show absence of perfusion and a normal or diminished pattern of ventilation in one lobe or lung (23,25,51). Contrast-enhanced CT or MR images may reveal one or more focal reductions in the diameter of the abnormal PV (Figs 7, 8). Pulmonary angiography may demonstrate pruning of the small pulmonary arteries, delayed transit of contrast material through the lung to the left atrium, and PV stenosis (25,51). Cardiac catheterization and venous angiography also can be used for direct visualization of PV stenosis (23,25,51).
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Figure 7a. Asymptomatic PV stenoses in a 59-year-old man who underwent two sessions of RF ablation for atrial fibrillation. (a) Coronal maximum-intensity projection image, obtained with a three-dimensional gradient-echo MR angiographic sequence 9 months after the first session of RF ablation for atrial fibrillation in three PVs, shows slight stenosis (arrow) at the origin of the left superior PV. Note the normal origins (arrowheads) of the right superior and inferior PVs. (b) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence 3 months after the second session of RF ablation, this time involving all four PVs, shows moderate stenoses (arrows) at the origins of the left superior and right superior and inferior PVs.
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Figure 7b. Asymptomatic PV stenoses in a 59-year-old man who underwent two sessions of RF ablation for atrial fibrillation. (a) Coronal maximum-intensity projection image, obtained with a three-dimensional gradient-echo MR angiographic sequence 9 months after the first session of RF ablation for atrial fibrillation in three PVs, shows slight stenosis (arrow) at the origin of the left superior PV. Note the normal origins (arrowheads) of the right superior and inferior PVs. (b) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence 3 months after the second session of RF ablation, this time involving all four PVs, shows moderate stenoses (arrows) at the origins of the left superior and right superior and inferior PVs.
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Figure 8a. PV stenosis in a 40-year-old man who presented with mild chest discomfort and who had undergone RF ablation for atrial fibrillation in the left superior pulmonary vein 6 months earlier. Axial (a), axial oblique (b), and coronal oblique (c) views obtained with contrast-enhanced spiral CT show severe stenosis of the left superior pulmonary vein (arrow), associated with soft-tissue infiltration of surrounding fat. Note the multiple small lymph nodes (arrowhead in a and b). (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC.)
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Figure 8b. PV stenosis in a 40-year-old man who presented with mild chest discomfort and who had undergone RF ablation for atrial fibrillation in the left superior pulmonary vein 6 months earlier. Axial (a), axial oblique (b), and coronal oblique (c) views obtained with contrast-enhanced spiral CT show severe stenosis of the left superior pulmonary vein (arrow), associated with soft-tissue infiltration of surrounding fat. Note the multiple small lymph nodes (arrowhead in a and b). (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC.)
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Figure 8c. PV stenosis in a 40-year-old man who presented with mild chest discomfort and who had undergone RF ablation for atrial fibrillation in the left superior pulmonary vein 6 months earlier. Axial (a), axial oblique (b), and coronal oblique (c) views obtained with contrast-enhanced spiral CT show severe stenosis of the left superior pulmonary vein (arrow), associated with soft-tissue infiltration of surrounding fat. Note the multiple small lymph nodes (arrowhead in a and b). (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC.)
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PV Thrombosis and Pulmonary Infarction
Patients are given heparin systematically during RF ablation and warfarin afterward for a variable period of time. Several investigators have reported instances of endocardial thrombus formation after RF ablation, with a resultant risk of systemic embolism despite adequate prior therapy with anticoagulant drugs (52,53). To our knowledge, only one case of PV thrombosis has been reported (5). The thrombosis occurred 4 months after ablation was performed, and the corresponding lobe had to be resected. PV stenosis frequently is associated with thrombosis.
Chest radiographs also may depict focal pulmonary edema (Fig 9), and ventilation-perfusion scans may indicate absence of perfusion and a normal pattern of ventilation in one lobe or lung (5). In such instances, contrast-enhanced CT scans and MR images typically show occlusion of the PV with perivenous infiltration and occasionally show regional lymphadenopathy, reflecting mediastinal inflammation and fibrosis caused by thermal injuries. Nodules and wedge-shaped parenchymal consolidation also may be observed in locations of venous infarction (5). In addition, CT scans may show septal thickening and ground-glass attenuation—visual signs of localized pulmonary venous hypertension (Figs 9, 10). Cardiac catheterization and venous angiography provide direct visualization of PV thrombosis (5).
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Figure 9a. Thrombosis of the left upper PV in a 31-year-old man presenting with hemoptysis and transient discomfort of 3 months duration in the left side of the chest. RF ablation in the left superior PV had been performed for refractory atrial fibrillation 4 months earlier. The patient also received anticoagulant drug therapy. (a) Posteroanterior chest radiograph shows poorly demarcated opacities suggestive of asymmetric edema in the left upper lobe. (b, c) Axial contrast-enhanced CT scans (lung window) show diffuse ground-glass attenuation (arrows in b) and focal peripheral consolidation (arrow in c) in the left upper lobe, consistent with pulmonary venous infarction. Note the thickened interlobular septum (arrowhead in b) and the small pleural effusion. (d) Axial contrast-enhanced CT scan (mediastinal window) shows occlusion of the left superior PV (arrow), with soft-tissue attenuation surrounding the expected location of the vein. (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC. Reprinted, with permission, from reference 5.)
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Figure 9b. Thrombosis of the left upper PV in a 31-year-old man presenting with hemoptysis and transient discomfort of 3 months duration in the left side of the chest. RF ablation in the left superior PV had been performed for refractory atrial fibrillation 4 months earlier. The patient also received anticoagulant drug therapy. (a) Posteroanterior chest radiograph shows poorly demarcated opacities suggestive of asymmetric edema in the left upper lobe. (b, c) Axial contrast-enhanced CT scans (lung window) show diffuse ground-glass attenuation (arrows in b) and focal peripheral consolidation (arrow in c) in the left upper lobe, consistent with pulmonary venous infarction. Note the thickened interlobular septum (arrowhead in b) and the small pleural effusion. (d) Axial contrast-enhanced CT scan (mediastinal window) shows occlusion of the left superior PV (arrow), with soft-tissue attenuation surrounding the expected location of the vein. (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC. Reprinted, with permission, from reference 5.)
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Figure 9c. Thrombosis of the left upper PV in a 31-year-old man presenting with hemoptysis and transient discomfort of 3 months duration in the left side of the chest. RF ablation in the left superior PV had been performed for refractory atrial fibrillation 4 months earlier. The patient also received anticoagulant drug therapy. (a) Posteroanterior chest radiograph shows poorly demarcated opacities suggestive of asymmetric edema in the left upper lobe. (b, c) Axial contrast-enhanced CT scans (lung window) show diffuse ground-glass attenuation (arrows in b) and focal peripheral consolidation (arrow in c) in the left upper lobe, consistent with pulmonary venous infarction. Note the thickened interlobular septum (arrowhead in b) and the small pleural effusion. (d) Axial contrast-enhanced CT scan (mediastinal window) shows occlusion of the left superior PV (arrow), with soft-tissue attenuation surrounding the expected location of the vein. (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC. Reprinted, with permission, from reference 5.)
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Figure 9d. Thrombosis of the left upper PV in a 31-year-old man presenting with hemoptysis and transient discomfort of 3 months duration in the left side of the chest. RF ablation in the left superior PV had been performed for refractory atrial fibrillation 4 months earlier. The patient also received anticoagulant drug therapy. (a) Posteroanterior chest radiograph shows poorly demarcated opacities suggestive of asymmetric edema in the left upper lobe. (b, c) Axial contrast-enhanced CT scans (lung window) show diffuse ground-glass attenuation (arrows in b) and focal peripheral consolidation (arrow in c) in the left upper lobe, consistent with pulmonary venous infarction. Note the thickened interlobular septum (arrowhead in b) and the small pleural effusion. (d) Axial contrast-enhanced CT scan (mediastinal window) shows occlusion of the left superior PV (arrow), with soft-tissue attenuation surrounding the expected location of the vein. (Case courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC. Reprinted, with permission, from reference 5.)
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Figure 10a. Pulmonary venous thrombosis and pulmonary infarction in a 48-year-old woman presenting with hemoptysis and pain in the left side of the chest. The patient had undergone successful RF ablation for recurring paroxysmal atrial fibrillation in the left superior pulmonary vein 4 months earlier. Fiber-optic bronchoscopy demonstrated hypervascular mucosa in the left upper lobe bronchus. A transesophageal echocardiogram was unremarkable. Chest radiographs (not shown) depicted alveolar areas of increased opacity in the left upper lobe. (a) Anterior perfusion lung scan shows hypoperfusion of the left lung. (The ventilation lung scan, which is not shown, was normal.) (b) Axial CT section shows increased attenuation, septal thickening (arrowhead), and rounded areas of consolidation (arrow) in the left upper lobe. (c) Axial contrast-enhanced CT scan shows stenosis and thrombosis in the left superior PV (arrow). (d) Coronal three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung during the arterial phase. (e) Coronal venous phase three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung, absence of venous flow in the left upper lobe, and thrombosis (arrow) of the left superior pulmonary vein. (f) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence shows hypoperfusion of the left lung and absence of venous flow in the left upper lobe.
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Figure 10b. Pulmonary venous thrombosis and pulmonary infarction in a 48-year-old woman presenting with hemoptysis and pain in the left side of the chest. The patient had undergone successful RF ablation for recurring paroxysmal atrial fibrillation in the left superior pulmonary vein 4 months earlier. Fiber-optic bronchoscopy demonstrated hypervascular mucosa in the left upper lobe bronchus. A transesophageal echocardiogram was unremarkable. Chest radiographs (not shown) depicted alveolar areas of increased opacity in the left upper lobe. (a) Anterior perfusion lung scan shows hypoperfusion of the left lung. (The ventilation lung scan, which is not shown, was normal.) (b) Axial CT section shows increased attenuation, septal thickening (arrowhead), and rounded areas of consolidation (arrow) in the left upper lobe. (c) Axial contrast-enhanced CT scan shows stenosis and thrombosis in the left superior PV (arrow). (d) Coronal three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung during the arterial phase. (e) Coronal venous phase three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung, absence of venous flow in the left upper lobe, and thrombosis (arrow) of the left superior pulmonary vein. (f) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence shows hypoperfusion of the left lung and absence of venous flow in the left upper lobe.
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Figure 10c. Pulmonary venous thrombosis and pulmonary infarction in a 48-year-old woman presenting with hemoptysis and pain in the left side of the chest. The patient had undergone successful RF ablation for recurring paroxysmal atrial fibrillation in the left superior pulmonary vein 4 months earlier. Fiber-optic bronchoscopy demonstrated hypervascular mucosa in the left upper lobe bronchus. A transesophageal echocardiogram was unremarkable. Chest radiographs (not shown) depicted alveolar areas of increased opacity in the left upper lobe. (a) Anterior perfusion lung scan shows hypoperfusion of the left lung. (The ventilation lung scan, which is not shown, was normal.) (b) Axial CT section shows increased attenuation, septal thickening (arrowhead), and rounded areas of consolidation (arrow) in the left upper lobe. (c) Axial contrast-enhanced CT scan shows stenosis and thrombosis in the left superior PV (arrow). (d) Coronal three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung during the arterial phase. (e) Coronal venous phase three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung, absence of venous flow in the left upper lobe, and thrombosis (arrow) of the left superior pulmonary vein. (f) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence shows hypoperfusion of the left lung and absence of venous flow in the left upper lobe.
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Figure 10d. Pulmonary venous thrombosis and pulmonary infarction in a 48-year-old woman presenting with hemoptysis and pain in the left side of the chest. The patient had undergone successful RF ablation for recurring paroxysmal atrial fibrillation in the left superior pulmonary vein 4 months earlier. Fiber-optic bronchoscopy demonstrated hypervascular mucosa in the left upper lobe bronchus. A transesophageal echocardiogram was unremarkable. Chest radiographs (not shown) depicted alveolar areas of increased opacity in the left upper lobe. (a) Anterior perfusion lung scan shows hypoperfusion of the left lung. (The ventilation lung scan, which is not shown, was normal.) (b) Axial CT section shows increased attenuation, septal thickening (arrowhead), and rounded areas of consolidation (arrow) in the left upper lobe. (c) Axial contrast-enhanced CT scan shows stenosis and thrombosis in the left superior PV (arrow). (d) Coronal three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung during the arterial phase. (e) Coronal venous phase three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung, absence of venous flow in the left upper lobe, and thrombosis (arrow) of the left superior pulmonary vein. (f) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence shows hypoperfusion of the left lung and absence of venous flow in the left upper lobe.
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Figure 10e. Pulmonary venous thrombosis and pulmonary infarction in a 48-year-old woman presenting with hemoptysis and pain in the left side of the chest. The patient had undergone successful RF ablation for recurring paroxysmal atrial fibrillation in the left superior pulmonary vein 4 months earlier. Fiber-optic bronchoscopy demonstrated hypervascular mucosa in the left upper lobe bronchus. A transesophageal echocardiogram was unremarkable. Chest radiographs (not shown) depicted alveolar areas of increased opacity in the left upper lobe. (a) Anterior perfusion lung scan shows hypoperfusion of the left lung. (The ventilation lung scan, which is not shown, was normal.) (b) Axial CT section shows increased attenuation, septal thickening (arrowhead), and rounded areas of consolidation (arrow) in the left upper lobe. (c) Axial contrast-enhanced CT scan shows stenosis and thrombosis in the left superior PV (arrow). (d) Coronal three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung during the arterial phase. (e) Coronal venous phase three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung, absence of venous flow in the left upper lobe, and thrombosis (arrow) of the left superior pulmonary vein. (f) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence shows hypoperfusion of the left lung and absence of venous flow in the left upper lobe.
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Figure 10f. Pulmonary venous thrombosis and pulmonary infarction in a 48-year-old woman presenting with hemoptysis and pain in the left side of the chest. The patient had undergone successful RF ablation for recurring paroxysmal atrial fibrillation in the left superior pulmonary vein 4 months earlier. Fiber-optic bronchoscopy demonstrated hypervascular mucosa in the left upper lobe bronchus. A transesophageal echocardiogram was unremarkable. Chest radiographs (not shown) depicted alveolar areas of increased opacity in the left upper lobe. (a) Anterior perfusion lung scan shows hypoperfusion of the left lung. (The ventilation lung scan, which is not shown, was normal.) (b) Axial CT section shows increased attenuation, septal thickening (arrowhead), and rounded areas of consolidation (arrow) in the left upper lobe. (c) Axial contrast-enhanced CT scan shows stenosis and thrombosis in the left superior PV (arrow). (d) Coronal three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung during the arterial phase. (e) Coronal venous phase three-dimensional gradient-echo MR angiogram shows hypoperfusion of the left lung, absence of venous flow in the left upper lobe, and thrombosis (arrow) of the left superior pulmonary vein. (f) Coronal maximum-intensity projection image obtained with a three-dimensional gradient-echo MR angiographic sequence shows hypoperfusion of the left lung and absence of venous flow in the left upper lobe.
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PV Dissection
PV dissection may occur during ablation via catheter, particularly during insertion of the mapping catheter. One case that has been reported illustrates the need for careful placement of the mapping and ablation catheters within the PVs. Because the authors were unable to insert the catheter into the vein, spasm was suspected. Angiography revealed a persistent "radiopaque patch," confirming PV dissection (54).
Embolism
Embolic complications can occur from day 1 to 3 months after the procedure. Patients are systematically treated with heparin during the procedure and subsequently with warfarin for variable lengths of time. An embolism rate of 2% was reported despite anticoagulation therapy (52).
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Postprocedural Outcomes
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Abstract
Introduction
