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Cardiopulmonary Imaging |
1 Department of Radiology, Division of Thoracic Radiology, University of
Michigan Health Systems, B1 132F Taubman Center, 1500 E Medical Center Dr., TC
2910, Ann Arbor, MI, 48109.
2 Department of Internal Medicine, Division of Cardiology, University of
Michigan Health Systems, Ann Arbor, MI.
Received October 22, 2003; accepted after revision March 3, 2004.
Address correspondence to P. Cronin
(pcronin{at}med.umich.edu).
Atrial fibrillation, the most common sustained cardiac arrhythmia, is a major cause of stroke [1] and the most common cardiac arrhythmia requiring hospitalization [2]. It may occur in patients with normal hearts in times of stress, such as after surgery, after strenuous exercise, or with stimulants such as coffee or alcohol [2]. Atrial fibrillation is more frequent in patients with structural heart disease such as hypertension, valvular heart disease (especially rheumatic), and coronary artery disease [2]. A strong association exists with other arrhythmias, such as Wolff-Parkinson-White syndrome, atrioventricular nodal reentrant tachycardias, and sick sinus syndrome. In addition, it may also occur in patients with cardiopulmonary disease resulting in hypoxia or hypercapnia, such as chronic obstructive pulmonary disease or hypertension, or in patients with metabolic or electrolyte disturbances, such as diabetes mellitus and hyperthyroidism [2].
Atrial fibrillation usually begins as paroxysmal atrial fibrillation, with approximately 60% of patients converting spontaneously to normal sinus rhythm. Approximately 40% of patients develop persistent atrial fibrillation requiring medical or procedural intervention to restore normal sinus rhythm. Up to 50% of patients develop recurrent atrial fibrillation within the first year of initial onset [2]. Patients with atrial fibrillation have a mortality rate twice that of control subjects and are exposed to considerable morbidity, such as stroke [2].
The main symptoms associated with atrial fibrillation are related to the rapid ventricular rate. This may cause hypotension or induce angina because patients often have coincidental ischemic heart disease. A rapid ventricular rate may also lead to the loss of atrioventricular synchrony, as well as to an impaired cardiac response to exercise. The major complication of atrial fibrillation is the formation of atrial thrombi with the risk of systemic embolization, placing these patients at considerable risk for stroke.
The electrocardiographic characteristics of atrial fibrillation are an undulating or sawtooth baseline with absent P waves, an atrial rate of 300–600 beats per minute, and an irregularly irregular ventricular response. Paroxysmal atrial fibrillation is usually found in the absence of structural heart disease. Over years it may progress to persistent atrial fibrillation if substantial atrial remodeling has occurred. Atrial fibrillation is considered persistent if it lasts for more than 30 days and requires cardioversion for termination.
Management
The management of atrial fibrillation includes removing any precipitating factors or treating the primary cardiovascular abnormality. Treatment has three major objectives: controlling the ventricular response, preventing thromboembolism, and maintaining normal sinus rhythm [2]. If a patient is severely compromised hemodynamically, electrical cardioversion is the treatment of choice. In hemodynamically stable patients, pharmacologic agents, such as ß-blockers or calcium channel antagonists, are used to slow the ventricular response. Chemical cardioversion may be performed with various antiarrhythmic agents. Normal sinus rhythm can also be restored with direct current cardioversion, which is successful in 80% of patients [2]. Cardioversion restores mechanical atrial contraction over time; therefore, the risk of stroke is increased after cardioversion. Patients receive anticoagulation with an international ratio of 2.0–3.0 for up to 3 weeks before and 4 weeks after cardioversion if the duration of atrial fibrillation is greater than 48 hr to reduce this risk.
It may not be possible to perform cardioversion in some patients or to maintain normal sinus rhythm. Such patients require long-term pharmacologic agents and longterm anticoagulation because of the risk of systemic embolization. The American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines recommend anticoagulation for newly discovered atrial fibrillation, recurrent paroxysmal atrial fibrillation, and recurrent persistent or permanent atrial fibrillation [3]. The American College of Chest Physicians guidelines recommend anticoagulation in nonrheumatic atrial fibrillation in all patients older than 65 years and in patients with any single risk factor associated with increased thromboembolism. Aspirin is recommended as thromboembolic prophylaxis in patients with no risk factors who are younger than 65 years [2].
Various antiarrhythmics have been used to maintain normal sinus rhythm. However, a meta-analysis has questioned the safety of some class I antiarrhythmics. Certain class III drugs have been shown to be efficacious with no adverse affects. Amiodarone has been shown to be superior in maintaining normal sinus rhythm and reducing the incidence of atrial fibrillation after cardiac surgery. However, amiodarone has potentially serious organ toxicity [2]. For this reason, nonpharmacologic approaches have been developed to maintain sinus rhythm. These include atrioventricular junction ablation, atrioventricular node modification, atrial pacing, surgical treatments, and endoluminal catheter ablation.
Transvenous atrioventricular junction ablation involves applying radiofrequency energy to the atrioventricular junction. Success rates approach 100%. However, this procedure results in the lifelong need for a pacemaker and the ongoing risk of thromboembolic disease. Atrioventricular node modification involves the application of radiofrequency energy to the right posterior or mid septal regions of the atrioventricular node. This procedure avoids the need for a pacemaker but has a high recurrence rate [4]. Atrial pacing to prevent atrial fibrillation is particularly efficacious in patients with atrial fibrillation of vagal origin or sick sinus syndrome. Other treatment options, including surgery and pulmonary vein ablation, will be discussed next.
Surgical Treatment
Surgical treatment for atrial fibrillation includes the Cox-Maze procedure, in which a series of atrial incisions are made to reduce the number of circulating wavelets necessary to sustain atrial fibrillation [4]. This procedure is best performed in patients who require open heart surgery for another reason such as coronary artery bypass or mitral valve surgery. Endoluminal equivalents of the Cox-Maze procedure have also been attempted and have shown mixed results. Surgical cryoablation of the posterior left atrium has also been tried [4].
Ectopic Foci of Atrial Fibrillation in Pulmonary Veins
Jais et al. [5] were first to document that paroxysmal atrial fibrillation could be initiated by ectopic beats originating from the pulmonary veins. Recently, it has been discovered that paroxysms of atrial fibrillation are initiated by trains of spontaneous activity originating from the pulmonary veins in 90–96% of patients [1, 6], with almost half arising in the left superior pulmonary vein. In most individuals, sleeves of the left atrial myocardium extend into the pulmonary veins for a distance of 2–17 mm [7]. The myocardial sleeves are longest in the superior pulmonary veins and thickest at the venoatrial junction of the left superior vein, which may explain why the ectopic foci of atrial fibrillation most commonly arise from the left superior pulmonary vein [8]. Successful ablation of all electric connections to these veins can eliminate paroxysmal atrial fibrillation.
Radiofrequency Ablation Technique
Ablation of the pulmonary veins is performed to electrically disconnect
them from the left atrium. Several techniques exist, and details of our
institutional procedures are included here. Typically, access to the pulmonary
veins and left atrium is gained via a percutaneous transluminal approach.
Under fluoroscopic guidance, the foramen ovale cordis is probed or a
transseptal puncture is made if a patent foramen ovale is absent. Two
guidewires are introduced (through the transseptal puncture or patent foramen
ovale), followed by catheters and sheaths. These include a deflectable,
decapolar catheter with a distal ring configuration (Lasso, Biosense Webster)
and a deflectable, quadripolar 7-French catheter with 2-5-2-mm interelectrode
spacing and a 4-mm distal electrode with an embedded thermistor (EP
Technologies). After access to the left atrium is achieved, anticoagulation
with heparin is started and the heparin is titrated until the prothrombin time
is more than twice the patient's control value (activated partial thrombosin
time ratio 
2.0). During the procedure an antiarrhythmic agent is infused,
such as 4 µg/min isoproterenol. One or two catheters may be used, usually 7
or 8 French. Once the catheters are in the left atrium, the sheath is usually
withdrawn into the inferior vena cava to minimize the risk of emboli. Ablation
is usually performed during normal sinus rhythm.
The anatomy of the left atrium and position of the pulmonary vein ostia are identified by selective angiography. The pulmonary veins are mapped with the circular Lasso catheter to identify electrically conducting myocardial fasicles. These fasicles are then ablated using radiofrequency energy up to 52°C, with a maximum power output of 30–35 W for 30–45 sec (Model EPT-1000-TC, EP Technologies) [8]. To reduce the need for a repeated procedure for the development of recurrent atrial fibrillation, we perform empiric ablation of all pulmonary vein ostia when feasible. Ablation is performed at or within 5 mm of the pulmonary vein ostia to reduce the risk of pulmonary vein stenosis. Ablation inside the pulmonary veins increases the risk of stenosis and increases the difficulty in treating the stenosis.
Patients are observed for 24 hr after the procedure in a monitored bed and given anticoagulation. Low-molecular heparin is administered for 4 days after discharge. Patients are given anticoagulation with warfarin for 1–3 months after the procedure [5, 8]. Patients are routinely seen in the outpatient clinic 4–6 weeks after the ablation procedure and again at 3–4 months, with CT performed after ablation.
Justification for Mapping Before Ablation
Four pulmonary veins compose the common pulmonary vein anatomy. However, pulmonary vein anatomy is commonly variable, such as common ostia or extra veins. Because radiofrequency energy is preferably applied at the venoatrial junction of all the pulmonary veins to avoid stenoses and eliminate ostial remnants that may contribute to recurrent atrial fibrillation, knowledge of how many pulmonary veins are present, and their ostial locations, is important to ensure that all the ostia are ablated. However, it is difficult and time-consuming to locate the ostia with conventional angiography at the time of ablation (Fig. 1).
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It is also important to know ostial orientation and distance from each ostium to the bifurcation of each pulmonary vein, because pulmonary vein narrowing seems to be critically dependent on catheter position and not on duration of radiofrequency energy application [9], and to avoid ablation and damage to pulmonary vein branches. Helical CT before ablation is a noninvasive method for delineating this anatomy. In addition, CT may also be performed after ablation to noninvasively evaluate for pulmonary vein stenosis after the procedure. Scanning is also important before ablation to exclude atrial or atrialappendage thrombi, which are an absolute contraindication to the procedure [10].
We have performed pulmonary vein mapping on helical CT scanners, including LightSpeed QX/i 4-MDCT, LightSpeed Ul-tra 8-MDCT, and LightSpeed and Light-Speed plus 16-MDCT scanners (GE Healthcare). We use 120–150 mL of Omnipaque 300 ([iohexol] Nycomed) nonionic IV contrast material administered with a power injector at a rate of 4 mL/sec through an antecubital vein. Scanning is initiated with a delay time of 30 sec after beginning the IV contrast material injection. We use 1.25-mm collimation and a 0.625-mm reconstruction interval. Pitch depends on the scanner used. For the LightSpeed 16, we use a pitch of 1.375 and ECG gating. For the LightSpeed QX/i 4-MDCT scanner, we use 7.5 pitch high-speed mode. We scan from the lung bases to the apices during a single breath-hold. This bottom-up direction minimizes respiratory motion should the patient inhale or exhale toward the end of the scan and minimizes streak artifact from contrast material in the superior vena cava and brachiocephalic veins. It is important to include the superior thorax, not just the left atrium and central veins, because aberrant pulmonary venous drainage to the brachiocephalic veins or superior vena cava may occur. For an average-sized adult male patient, the effective radiation dose for a pulmonary vein scan using 16-MDCT, assuming a 320-mA tube current, is approximately 10 mSv (1 rem). The dose is proportional to the milliampere-seconds, which is adjusted for the patient's size (i.e., for the same time per rotation and 300 mA, the effective dose would be 10 mSv x [300/320] = 9.4 mSv).
ECG gating improves the quality of 3D images. However, most of the information regarding pulmonary vein location and ostia can be gleaned from axial images and multiplanar reconstructions (Figs. 2A, 2B, 2C, 2D and 3A, 3B). ECG gating becomes more important when performing cardiac CT to delineate the coronary venous anatomy before planning for biventricular pacemaker placement. These scans are obtained as just described but using an additional 5- to 15-sec delay after beginning contrast material injection and ECG gating. Treatment with biventricular pacing has been shown to increase cardiac output and can increase exercise tolerance in patients with dilated cardiomyopathy and intraventricular conduction delay [11].
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Pulmonary Vein Advanced Processing
We obtain maximum-intensity-projection multiplanar reconstruction images at the workstation. These images allow a more accurate measurement of the ostial diameter of pulmonary veins obliquely oriented to the axial imaging plane.
We routinely reconstruct 3D models of the left atrium and pulmonary veins to guide electrophysiologists before atrial fibrillation ablation (Figs. 4A, 4B, 4C, 4D, 4E and 5A, 5B, 5C, 5D, 5E). Surface-rendered views of the left atrium and the pulmonary veins are obtained. These 3D models are reconstructed to exclude surrounding structures such as the aorta, vertebral column, ribs, lung parenchyma, and peripheral pulmonary arteries, using Card EP software and a left atrium volume-rendered protocol on a GE Advantages Windows workstation (all GE Healthcare products). These views give the electrophysiologists an "angiographic" view of the left atrium and the pulmonary veins. The pulmonary veins are best visualized from a dorsocranial view with right posterior oblique and left posterior oblique angulation to overcome overlap by the proximal pulmonary arteries. This posterior view allows better visualization of the left atrium and the pulmonary veins because these are posterior structures. The surface-rendered views are shaded to appear as if illuminated from above, which allows excellent visualization of the superior pulmonary veins but poor visualization of the inferior pulmonary veins. To better visualize the inferior pulmonary veins, we view the surface-rendered images of the left atrium and the pulmonary veins upside down. The pulmonary vein ostial diameters and length to the first bifurcation can be measured.
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We also routinely render endoluminal views using Card EP software and Navigator protocol on Advantages Windows workstations (all GE Healthcare products). Theses views allow visualization of the pulmonary vein ostia but also give a better sense of pulmonary vein orientation, distance to first branch, geometry of pulmonary vein branches, and common ostia.
Software is currently under development to superimpose the 3D CT reconstructions with the electrophysiologic mapping software to improve registration of the two data sets (Figs. 6A, 6B, and 6C).
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Normal Pulmonary Vein Anatomy
During embryologic development, the pulmonary vein confluence is incorporated into the dorsal wall of the left atrium. This is followed by musculization or atrialization of the venous part of the atrial wall. Myocardium is found around atriovenous junctions and within the media of the pulmonary veins. These myocardial sleeves are more developed around the superior pulmonary veins than around the inferior. Normally, two superior pulmonary veins are present, one right and one left, and two inferior pulmonary veins, one right and one left. The right superior vein drains the right upper and middle lobes. The left superior vein drains the left upper lobe, including the lingula. The inferior veins drain their respective lower lobes.
The course of the pulmonary veins is distinct from the course of the pulmonary arteries and bronchi. The superior veins take an oblique course caudally as they pass medially, whereas the inferior veins take virtually a horizontal course centrally and a vertical course distally. The right superior pulmonary vein is usually the largest pulmonary vein. It passes posterior in relation to the superior vena cava and anterior in relation to the right pulmonary artery. As it courses caudally, it passes under the right pulmonary artery to enter the most superior and lateral aspect of the left atrium. The left superior pulmonary vein runs anterior to but in close relationship with the left pulmonary artery. It joins the left atrium near the left atrial appendage (Figs. 2A, 2B, 2C, 2D and 3A, 3B). As well as coursing horizontally, the inferior pulmonary veins pass forward as they pass medially to enter the left atrium at its most inferior and lateral aspect. They lie in a plane considerably posterior to the superior pulmonary veins. On a lateral chest radiograph, the pulmonary vein confluence is sometimes seen as what appears to be a lung nodule or outpouching of the left atrium at the mid posterior heart border.
The superior pulmonary vein ostia are significantly larger than the inferior pulmonary vein ostia. Scharf et al. [12] reported 42 patients with atrial fibrillation and found the mean diameter of the right superior pulmonary vein ostia was 19.8 mm, the mean diameter of the left superior pulmonary vein ostia was 19.2 mm, compared with 16 mm for the right inferior pulmonary vein ostia and 17.3 mm for the left inferior pulmonary vein ostia. No significant difference was seen between the average diameters of right and left pulmonary vein ostia. The pulmonary vein trunk is defined as the distance from the ostium to the first-order branch. The superior pulmonary veins tend to have a longer trunk (21.6 ± 7.5 mm) than the inferior pulmonary veins (14.0 ± 6.2 mm). The superior veins are also overlapped by the descending proximal pulmonary artery, which may make visualization of the first branch difficult. Scharf et al. found greater variation in pulmonary vein length than in diameter.
Pulmonary Vein Anatomic Variants
Pulmonary vein anatomy is more variable than pulmonary artery anatomy, and developmental anomalies are common. Common anomalies (Table 1) include a common left or right pulmonary vein in 2.4–25% of individuals [10, 12] (Figs. 7A and 7B). A single common left vein is much more frequently seen than a common right vein. In our experience with several hundred patients, we have not yet come across a common right vein. When present, a common pulmonary vein trunk has a significantly larger diameter than the other pulmonary veins.
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Supernumerary veins are frequently seen. The most common is a separate right middle pulmonary vein, which drains the middle lobe (Figs. 8A, 8B and 9A, 9B). This is estimated to occur in 1.6–19% of individuals [11, 13, 14]. Tsao et al. [14] reported that the right middle lobe vein may drain directly into the left atrium in 23% of patients, share a common ostium to the proximal part of the right superior pulmonary vein in 69% of patients, and share a common ostium to the proximal right inferior pulmonary vein in 8% of patients. The ostial diameter of the right middle pulmonary vein is also smaller than other veins (mean, 9.9 ± 1.9 mm) [14]. Given its small size, the vein is often difficult to identify at fluoroscopy and may be overlooked and therefore untreated as a possible focus of atrial fibrillation.
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Several anomalous pulmonary and systemic connections exist, and drainage can be partial or total (Figs. 10A, 10B and 11). These abnormal pulmonary–systemic venous connections are best classified on the basis of their embryologic derivation and the anatomy of the anomalous connection. On the basis of this classification, four types are described: The supracardiac type is composed of derivatives of the right cardinal system (superior vena cava or azygos vein) or derivatives of the left cardinal system (a persistent left superior vena cava, vertical vein, or left brachiocephalic vein). The cardiac type is composed of derivatives of the left cardinal system (the coronary sinus) or the right atrium. The infracardiac type is composed of the unbilicovitelline system (the portal vein or ductus venosus) or the inferior vena cava. The mixed type is a combination of two or more of the anomalies [13].
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Reporting Pulmonary Vein CT Examinations
Before reviewing the left atrium and pulmonary vein axial or reconstructed images, the radiologist must review all lung and soft-tissue images to identify any potentially significant incidental findings [10].
The electrophysiologists need to know four things from mapping before ablation. First, is there normal anatomy (i.e., four pulmonary veins)? Second, what is the ostial diameter of each vein and the length to the first-order branch? These facts influence the selection of circular catheter size used. Third, is there an extra pulmonary vein such as a right middle pulmonary vein, where does it drain, and what is its size and length to the first bifurcation? Fourth, are there major anomalies, such as a common ostium to the superior and inferior veins or an anomalous pulmonary venous return?
Complications After Ablation
Ablation is associated with complications, as listed in Appendix 1. Complications immediately after the procedure include pericardial effusion and embolic events in 1% of patients [6, 15]. The radiologist may encounter these complications on chest radiographs or head CT scans after the procedure. Pulmonary dysfunction and bleeding resulting from anticoagulation may also occur [16]. These complications are unlikely to be seen by radiologists.
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Electric isolation of pulmonary vein ostia is shown to be safe and rarely causes symptomatic stenosis [12]. Pulmonary vein stenosis after the procedure may occur in 40–100% of patients [17]. Scharf et al. [12] showed that 3% of patients have stenosis of up to 65% luminal diameter narrowing but are asymptomatic. They also showed some patients have pulmonary vein dilatation after radiofrequency ablation. Severe pulmonary vein stenosis is described in 11% of patients [16] and has been reported to cause pulmonary venoocclusive disease in three patients [17, 18]. Clinically, pulmonary vein stenosis may present with dyspnea on exertion or manifest as focal pulmonary edema on chest radiographs or CT scans or as pulmonary vein luminal narrowing on CT pulmonary vein images (Figs. 12A and 12B).
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Electric isolation of pulmonary vein ostia is shown to be safe and rarely causes symptomatic stenosis. Pulmonary vein stenosis after the procedure may occur in 40–100% of patients however, only 11% of patients have severe pulmonary vein stenosis. Three percent of patients have stenosis of up to 65% luminal diameter narrowing but are usually asymptomatic. Some patients may have pulmonary vein dilatation after radiofrequency ablation. Pulmonary venoocclusive disease in three patients has been reported. Clinically, this disease may present with dyspnea on exertion, manifest as focal pulmonary edema on chest radiographs or CT or pulmonary vein luminal narrowing on CT pulmonary vein imaging. Ablation is performed at or within 5 mm of pulmonary vein ostia to reduce risk of pulmonary vein stenosis. Ablation inside pulmonary veins increases the risk of stenosis and increases the difficulty in treating stenosis.
Robbins et al. [16] describe two patients with venoocclusive disease after the procedure, one with severe stenosis of all four pulmonary veins 3 months after ablation and another patient with severe stenosis of three pulmonary veins and complete occlusion of one pulmonary vein several months after radiofrequency ablation. Although congenital pulmonary vein stenosis has a poor prognosis unless treated, pulmonary vein stenosis acquired after ablation shows a different course. Both patients with severe stenoses described by Robbins et al. were successfully treated with angioplasty, followed by resolution of symptoms. Scanavacca et al. [18] also described severe venoocclusive disease of the left pulmonary veins in a patient 10 days after radiofrequency ablation that was treated with angioplasty with complete resolution of symptoms. Ravenel et al. [17] described a patient with hemoptysis and chest pain developing 1 month after radiofrequency ablation and progressing over 3 months. This patient had asymmetric left-sided pulmonary edema on chest radiography and an occluded left superior pulmonary vein on IV contrast-enhanced CT, confirmed at venography. Ventilation–perfusion scanning showed absent perfusion to the left upper lobe. A left upper lobectomy was required because of pulmonary ischemia. At our institution, patients routinely undergo 3- and 12-month pulmonary vein CT after the procedure to identify pulmonary vein stenoses.
Stenosis after ablation is not predicted by the initial pulmonary vein size or total duration of radiofrequency energy application delivered to the vein, but by catheter position. The more distal the catheter from the ostium, the greater the degree of narrowing created [9]. The left inferior pulmonary vein is most susceptible to the development of narrowing because of the more medial location of its ostia, located more posteriorly and therefore inside the cardiac silhouette on standard imaging and fluoroscopic projections. As a consequence, more energy may be delivered inside the vein distal to the ostium. CT before the procedure is helpful to clearly identify the position of the left inferior pulmonary vein ostium.
Pulmonary vein stenosis may be associated with pulmonary vein thrombosis [17]. Thrombus formation has been reported to occur from 1 day to 3 months after radiofrequency ablation, with an embolism rate of 2% despite adequate anticoagulation therapy. Therefore, patients receive anticoagulation during the procedure and for approximately 1 month after [8]. Chest radiographs may show evidence of focal pulmonary edema distal to the occluded vein. CT angiography or MR angiography can be used to noninvasively show pulmonary vein occlusion. Infarction may result in wedge-shaped parenchymal consolidation. CT may also show interlobular septal thickening and ground-glass opacity as a result of localized pulmonary venous hypertension. Reactive regional mediastinal lymph node enlargement may occur as a result of mediastinal inflammation and fibrosis from thermal injury [19]. In our experience with more than 300 cases over the last 3 years, we have not experienced any cases of pulmonary vein thrombosis, severe stenosis, or symptomatic pulmonary vein occlusive disease.
One case of pulmonary vein dissection has been described. This case highlights the need for careful placement of mapping and ablation catheters within the pulmonary veins [20].
Conclusion
Electric isolation of pulmonary veins by the application of radiofrequency energy at the venoatrial junction is a new technique for the treatment of paroxysmal atrial fibrillation. Because atrial fibrillation is the most common cardiac arrhythmia, an increasing number of ablations are being performed at many centers. CT of the pulmonary veins can be used to guide the electrophysiologist by providing anatomic details noninvasively before the procedure, including the number, location, and size of pulmonary veins and pulmonary vein branching anomalies, and is used to select the size of catheters for the procedure. Preprocedural mapping has been shown to reduce radiofrequency ablation procedure time. Mapping is also used to evaluate for pulmonary vein stenosis or thrombosis after the procedure. Therefore, radiologists need to be familiar with how to perform and interpret pulmonary vein-mapping examinations, whether done with CT or MRI. An understanding of normal anatomy and anomalous pulmonary vein anatomy and where to take measurements is important.
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