ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Overview of catheter ablation of cardiac arrhythmias

Overview of catheter ablation of cardiac arrhythmias
Literature review current through: Jan 2024.
This topic last updated: Feb 14, 2022.

INTRODUCTION — Pharmacologic therapy of arrhythmias, while frequently effective, is limited by high failure rates, potential for proarrhythmia, and drug toxicity. Nonpharmacologic therapy for symptomatic and life-threatening cardiac arrhythmias includes the use of catheter ablation, the implantable cardioverter-defibrillator for ventricular arrhythmias, and, at times, cardiac surgery. The clinical role of catheter ablation in the treatment of arrhythmias will be reviewed here. A discussion of invasive cardiac electrophysiology studies and cardiac mapping, both precursors to catheter ablation, is presented separately. (See "Invasive diagnostic cardiac electrophysiology studies".)

INDICATIONS AND CLINICAL USE — Catheter ablation using radiofrequency or cryothermal energy has become an important therapy in the management of patients with various types of tachyarrhythmia (table 1), including [1-3]:

Atrioventricular reentrant tachycardia (AVRT) associated with the Wolff-Parkinson-White (WPW) syndrome or a concealed accessory pathway (see "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Treatment to prevent recurrent arrhythmias')

AV nodal reentrant tachycardia (AVNRT) (see "Atrioventricular nodal reentrant tachycardia", section on 'Catheter ablation')

Atrial tachycardia (see "Focal atrial tachycardia", section on 'Catheter ablation')

Atrial flutter (see "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter ablation')

Atrial fibrillation, either in a curative attempt, or AV nodal ablation with pacemaker implantation (see "Atrial fibrillation: Catheter ablation")

Frequent ventricular ectopy with refractory symptoms or associated cardiomyopathy (see "Arrhythmia-induced cardiomyopathy", section on 'Frequent ventricular ectopy')

Ventricular tachycardia (VT), both idiopathic and in some patients with structural heart disease, particularly if there are recurrent implantable cardioverter-defibrillator therapies (see "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Radiofrequency catheter ablation' and "Ventricular tachycardia in the absence of apparent structural heart disease" and "Bundle branch reentrant ventricular tachycardia")

Persistent, frequent, or incessant tachycardia with tachycardia-induced cardiomyopathy (see "Arrhythmia-induced cardiomyopathy")

Triggering premature ventricular contractions (PVCs) in rare patients with polymorphic VT and ventricular fibrillation

The indications for catheter ablation of a cardiac arrhythmia generally revolve around the treatment of a recurrent or persistent symptomatic arrhythmia which has been refractory to medical therapy or for which medical therapy is not tolerated or preferred.

Atrial tachycardia may be unifocal or multifocal; some unifocal tachycardias originate in or around the sinus node.

Unifocal (or ectopic) atrial tachycardia may have an automatic or reentrant mechanism, and a paroxysmal or incessant pattern (waveform 1 and waveform 2). Most varieties of unifocal atrial tachycardia are amenable to catheter ablation. (See "Intraatrial reentrant tachycardia" and "Focal atrial tachycardia" and "Atrial fibrillation: Catheter ablation".)

Sinoatrial node reentrant tachycardia (SNRT) is a specific type of unifocal atrial tachycardia in which sinoatrial (SA) nodal or peri-SA nodal tissue is part of the reentry circuit; this results in P waves during tachycardia which may be indistinguishable from normal sinus P waves [4,5]. (See "Sinoatrial nodal reentrant tachycardia (SANRT)".)

Intraatrial reentrant tachycardia (IART) is a macroreentrant atrial tachycardia that does not utilize the cavotricuspid isthmus (figure 1) as a critical pathway for the reentry to perpetuate. Catheter ablation, however, has relatively high success rates for the acute termination of IART and for the long-term prevention of recurrences. (See "Intraatrial reentrant tachycardia", section on 'Catheter ablation'.)

Inappropriate sinus tachycardia (IST), also known as chronic nonparoxysmal sinus tachycardia, is a distinct syndrome in which the resting sinus rate is elevated and there is an exaggerated chronotropic response to exercise [6]. Although IST is most often treated with beta blockers or ivabradine, ablation may be considered in refractory patients. (See "Sinus tachycardia: Evaluation and management", section on 'Inappropriate sinus tachycardia'.)

Occasionally, patients with more than one discrete ectopic atrial focus are candidates for curative ablation. Multifocal atrial tachycardia (MAT), however, is due to abnormal automaticity or triggered activity throughout the atria, and is therefore not curable with standard catheter techniques (waveform 3). Refractory patients with MAT may benefit from complete atrioventricular junctional ablation and permanent pacemaker implantation or AV nodal modification [7]. (See "Multifocal atrial tachycardia".)

In some select indications for arrhythmias known to have a high cure rate with ablation therapy (eg, atrial flutter, paroxysmal supraventricular tachycardia, WPW, idiopathic PVCs/VT), catheter ablation may be indicated as a first-line treatment (class I indication). Catheter ablation is considered preferable to medical therapy in patients with symptomatic WPW syndrome. (See "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter ablation' and "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Catheter ablation'.)

CONTRAINDICATIONS — The absolute contraindications to catheter ablation, performed as part of an invasive cardiac electrophysiology (EP) study, are generally similar to the contraindications of the EP study itself and include [8]:

Unstable angina

Bacteremia or septicemia

Acute decompensated congestive heart failure not caused by the arrhythmia

Major bleeding diathesis

Acute lower extremity venous thrombosis if femoral vein cannulation is desired

Intracardiac mass or thrombus

PREPROCEDURE EVALUATION, PREPARATION, AND INTRAPROCEDURE MONITORING — Because catheter ablation is performed as part of an invasive electrophysiology (EP) study, the preprocedure evaluation, preparation, and intraprocedure monitoring for patients undergoing catheter ablation is essentially identical to that for an invasive EP study. This information is discussed in detail separately. (See "Invasive diagnostic cardiac electrophysiology studies", section on 'Preprocedural evaluation' and "Invasive diagnostic cardiac electrophysiology studies", section on 'Preparation and monitoring'.)

MAPPING AND LOCALIZATION OF THE ARRHYTHMIA — Cardiac mapping refers to careful movement of a mapping or ablation catheter in the area of interest, probing for the site at which radiofrequency or cryothermal ablation will be successful at curing the arrhythmia. Cardiac mapping during electrophysiologic testing identifies the temporal and spatial distributions of electrical potentials generated by the myocardium during normal and abnormal rhythms. This process allows description of the spread of activation from its initiation to its completion within a region of interest and, in its usual application, is focused toward the identification of the site of origin or a critical site of conduction for an arrhythmia. Multiple techniques for mapping have been developed [9].

Electrogram recordings — Recorded electrograms can provide two important pieces of information:

The local activation time (ie, the time of activation of myocardium immediately) adjacent to the recording electrode relative to a reference.

The complexity of myocardial activation within the "field of view" of the recording electrode.

Recording electrodes may be either unipolar (one pole in contact with the tissue whose electrical activity is being recorded and the second, an indifferent electrode located on the same catheter far from the first electrode, or independent from the catheter altogether) or bipolar (two poles in contact with the tissue and adjacent to each other separated by a few millimeters). In actuality, both types of recordings are bipolar, except that the two poles are much more widely spaced in unipolar electrodes. Unipolar recordings more accurately represent the timing of local activation but are fraught with the detection of far-field signals due to the wide separation of the two poles. Bipolar signals do not suffer from the problem of recording far-field signals, and that is why they are more widely employed in mapping. Since extracellular potential decreases inversely with the square of the distance from a point source [10], far-field events generate relatively low amplitude signals compared with electrogram components generated by near-field sources in unipolar recordings.

Establishing electrogram criteria, which permits accurate determination of the moment of myocardial activation at the recording electrode, is critical for construction of an area map of the activation sequence.

Unipolar recording — For unipolar recording, the point of maximum amplitude, the zero crossing, the point of maximum slope (maximum first derivative), and the minimum second derivative of the electrogram have been proposed as indicators for underlying myocardial activation [11,12]. Most studies have suggested that local activation is best determined from the unipolar electrogram by the point with maximum slope (maximum change in potential, or dV/dt) [13,14]. Using this fiducial point, errors in determining the local activation time as compared with intracellular recordings have been typically less than 1 millisecond [12].

Bipolar recording — Algorithms for detecting local activation time from bipolar electrograms have been more problematic, due in part to generation of the bipolar electrogram by two spatially separated recording poles. Among several options, the absolute maximum electrogram amplitude appears to most consistently correlate with local activation time determined by other means [12].

Equipment — The necessary equipment for mapping includes special catheters and an appropriate recording device. A large number of multipolar electrode catheters have been developed to facilitate desired catheter positioning and to fulfill various recording requirements. These include, among others, bipolar or quadripolar electrode catheters, multipolar recording electrode catheters, "halo" catheters used for mapping, small caliber electrode catheters, circular/spiral electrode catheters, a "flower" catheter (which has 20 electrodes on five radiating spines in a branching configuration), basket electrodes which can conform to the size and shape of the chamber, and steerable catheters [15-19]. For digital recording systems, the sampling rate should be at least twice as fast as the highest frequency component of the signal in order to avoid aliasing (the Nyquist limit). For practical purposes of activation mapping, however, sampling rates of 1000 Hz are generally adequate.

Endocardial mapping techniques — The simplest form of mapping is achieved by moving the single electrode sequentially to various points of interest on the endocardium in order to measure local activation. The success of roving single point mapping is predicated upon the sequential beat-by-beat stability of the activation sequence being mapped and the ability of the patient to tolerate the sustained arrhythmia. However, this situation may not be present in certain settings such as mapping of polymorphic ventricular tachycardia (VT) or a monomorphic VT that has a repetitive sequence of endocardial activation, but is hemodynamically too unstable to allow time for complete roving of the endocavitary catheter in the electrophysiology laboratory. Mapping simultaneously from as many sites as possible greatly enhances the precision, detail, and speed of identifying regions of interest. The more sites that are simultaneously mapped, the less roving of a single point is required.

Other types of mapping are available for use depending on the clinical situation and type(s) of arrhythmias being investigated. These include activation sequence mapping, pace mapping (waveform 4A-B), entrainment mapping (waveform 5), voltage mapping, and use of the dominant frequency and fractionated local electrogram. A detailed discussion of these techniques is beyond the scope of this topic but is discussed elsewhere [20].

Limitations of endocardial mapping — The site of origin of the tachycardia may not be reachable from the endocardial approach. As an example, animal and human studies have shown that approximately one-third of VTs due to ischemic heart disease are generated within midmyocardial, subepicardial, or intraseptal regions; critical sites of VT origin in patients with inferior infarction without aneurysms are more likely to be located in the subepicardium [21-24]. Another limitation is that focal and presumably nonreentrant mechanisms of VT are not infrequent, even in the setting of ischemic heart disease with aneurysms.

Epicardial ventricular mapping — In a subset of patients in whom an endocardial approach is unsuccessful, the critical portion of the arrhythmia circuit may be located epicardially [25-27]. VT that cannot be successfully mapped by an endocardial approach, suggesting an epicardial origin, appears to be more common in patients with a nonischemic dilated cardiomyopathy.

Epicardial ventricular mapping can be performed with special recording catheters that can be steered in the branches of the coronary sinus. It may be particularly important in identifying right ventricular outflow tract VTs, which may be difficult to ablate with the endocardial approach only. Another epicardial mapping technique using a subxiphoid percutaneous approach for accessing the epicardial surface has been used to map ventricular arrhythmias [27,28].

Electroanatomical mapping — Electroanatomical (or electromagnetic) mapping, which is available in many electrophysiology (EP) laboratories, is based upon the use of a special catheter with a locatable sensor tip, connected to a mapping and navigation system [29,30]. The system can generate isochrones of electrical activity as color-coded static maps or animated dynamic maps of activation wavefront. These pictures can define reentrant circuits as well as the site of origin or breakthrough of an ectopic activity with centrifugal, monoregional, or asymmetric spread of electrical activity (image 1A-C and image 2).

A major advantage of three-dimensional electroanatomical mapping is its ability to allow the catheter to anatomically and accurately "revisit" a critically important recording site, identified previously during the study, even if the tachycardia is no longer present or inducible and map-guided catheter navigation is no longer possible. This accurate repositioning can allow pace mapping from or further application of radiofrequency current to critically important sites that otherwise cannot be performed with a high degree of accuracy and reproducibility.

The electroanatomical map can be integrated with other imaging modalities. In order to reduce the need for point-by-point reconstruction of the cardiac anatomy, systems have been developed to import and merge a three-dimensional computed tomography (CT) or magnetic resonance (MR) image of the heart obtained pre-procedurally with the electroanatomical map generated during the procedure [31]. Future mapping systems will likely use real-time imaging to create an accurate dynamic chamber image during intracardiac mapping [32].

Noncontact mapping — The noncontact catheter available for clinical use is a multielectrode array mounted on a balloon tipped catheter. The balloon can be filled with contrast dye, permitting it to be visualized fluoroscopically [18,19,33]. The location of any conventional mapping catheter with respect to this multielectrode array can be determined by passing a high frequency, low current locator signal by a process described and validated previously [33].

The multielectrode array has been deployed in all four cardiac chambers using a transvenous, transseptal, or retrograde transaortic approach in order to map atrial tachyarrhythmias and VT [19,34,35]. Systemic anticoagulation is critical to avoid thromboembolic complications. It has been argued that the biggest advantage of noncontact endocardial mapping is its ability to recreate the endocardial activation sequence from simultaneously acquired multiple data points over a few (theoretically one) tachycardia beats, obviating the need for prolonged tachycardia episodes that the patient may tolerate poorly.

Anatomic localization — Mapping of the arrhythmia prior to performing an ablation is not required for all arrhythmias. Anatomic approaches to ablation are used when the arrhythmia has a known anatomic course. As an example, in typical or common type I atrial flutter, the wave front must proceed through the isthmus of tissue between the tricuspid annulus (TA) and inferior vena cava (IVC). Thus, ablation is directed largely anatomically, with the goal of delivering a continuous series of RF lesions to create an ablation line of complete bidirectional conduction block between the TA and IVC (waveform 6A-B) [36]. (See "Electrocardiographic and electrophysiologic features of atrial flutter".)

There are several approaches to ablation for management atrial fibrillation (AF). All of these approaches incorporate an understanding of left atrial anatomy, and some are entirely anatomically based. Ablation for AF focuses on the elimination of triggers for AF via electrical isolation of the pulmonary vein ostia from the body of the left atrium, and sometimes also includes additional lesions made in the body of the left atrium to modify arrhythmic substrate. Advanced imaging techniques (eg, intracardiac echo, electroanatomic mapping, and three-dimensional CT reconstructions) are generally used to facilitate this procedure. The approach to AF ablation is discussed in greater detail separately. (See "Atrial fibrillation: Catheter ablation".)

ENERGY SOURCES USED FOR ABLATION

DC energy — DC energy, delivered during general anesthesia, was the initial energy source used for catheter ablation. However, DC shock ablation, or fulguration, never achieved widespread use because of a high incidence of complications related to the high energy discharge. The procedure has not been used for many years and is of only historical interest.

RF energy — Radiofrequency (RF) energy, low voltage high frequency electrical energy (30 KHz to 1.5 MHz), is generally delivered from the tip of a catheter to the endocardial surface. RF energy produces controlled focal tissue ablation, as compared with the more extensive damage caused by DC fulguration. Initially, the magnitude and duration of RF ablation were limited by progressive heating of the catheter, leading to the formation of an insulating coagulum of denatured tissue proteins on the catheter tip. In 1995, RF ablation was further refined by the use of saline irrigation to cool the RF catheter tip [37]. This technique prevents tissue coagulum formation and makes larger RF lesions feasible. Saline cooling increased the efficacy of RF ablation in subsequent clinical studies [38-41]. In selected cases, RF energy may be applied to the epicardial surface via a pericardial approach.

Since RF energy does not directly stimulate nerves or myocardium, the procedure is usually relatively painless and general anesthesia is not necessary.

Cryothermal energy — Even though RF energy is vastly superior to and safer than DC energy, efforts continue to identify alternate energy sources for catheter ablation. Microwave energy has been tested in animal models [42]. Cryothermal ablation offers the potential benefit of reversible cold mapping; if mild cooling has the intended effect, more profound freezing can inflict permanent tissue damage [43-46]. If limited cooling has an untoward effect or no effect at all, the tissue is allowed to thaw without permanent damage.

Pulsed field ablation — A new ablation modality, pulsed field ablation (PFA) [47] holds promise for the treatment of AF [48] and perhaps other arrhythmias, such as VT. PFA uses a series of very brief, high-amplitude electrical pulses to desiccate tissue by electroporation of the sarcolemmal membrane without significantly heating the tissue. Moreover, this energy form seems to be specific to myocardial tissue, as other tissues seem to be resistant to this modality. PFA systems are approved for use in Europe (CE Mark), and are undergoing clinical trials in the United States.

COMPLICATIONS — The potential risks and benefits of the ablation procedure include those risks associated with an invasive electrophysiology study (EP study) alone (table 2). Generally, risks are lower in experienced operators and centers that perform larger numbers of procedures. These risks are discussed in greater detail separately. (See "Invasive diagnostic cardiac electrophysiology studies", section on 'Complications of invasive cardiac electrophysiology studies'.)

Incidence — The overall incidence of peri-procedural complications following catheter ablation is approximately 3 percent [9,49-51]. This was shown in a systematic review and meta-analysis of 192 studies including 83,236 patients undergoing catheter ablation for atrial fibrillation (AF) between 2000 and 2012, in which the overall incidence of periprocedural complications was 2.9 percent [51]. The acute complication rate declined over time, dropping to 2.6 percent on ablations performed from 2007 to 2012 compared with 4.0 percent from 2000 to 2006 [51]. Major complication rates can vary significantly depending on the type of ablation procedure (0.8 percent for supraventricular tachycardia, 3.4 percent for idiopathic ventricular tachycardia (VT), 5.2 percent for AF, and 6 percent for VT with structural heart disease) [50].

The potential risks and approximate incidences are similar in younger and older patients and include [52-54]:

Death (approximately 0.1 to 0.3 percent).

Heart block requiring permanent pacemaker (1 to 2 percent). (See 'Heart block' below.)

Thromboembolism, including stroke, systemic embolism, pulmonary embolism (<1 percent).

Complications related to vascular access (2 to 4 percent), including bleeding, infection, hematoma, and vascular injury. (See "Peripheral venous access in adults", section on 'Complications'.)

Cardiac trauma, including myocardial perforation, tamponade, infarction, coronary artery dissection or embolism, valvular damage (1 to 2 percent). (See 'Troponin I and BNP' below.)

New arrhythmias. (See 'New arrhythmias' below.)

Radiation exposure. (See 'Radiation exposure' below.)

Pulmonary hypertension due to pulmonary vein stenosis following pulmonary vein isolation for AF. (See "Atrial fibrillation: Catheter ablation", section on 'Pulmonary vein stenosis'.)

Phrenic nerve injury following sinus node modification for inappropriate sinus tachycardia (IST) or AF ablation, particularly cryoablation.

Esophageal injury following catheter ablation for AF. (See "Atrial fibrillation: Catheter ablation", section on 'Complications'.)

Heart block — Heart block requiring the placement of a permanent pacemaker is relatively rare, occurring in less than 1 to 2 percent of procedures [55,56]. Atrioventricular (AV) block may not be immediately observed but may progress following the procedure. However, this is extremely rare in patients who did not have transient AV block during the ablation. The use of cryothermal ablation of the slow pathway is an approach that may reduce the potential for AV block; the ability to test prospective ablation sites before permanent destruction can prevent this inadvertent complication [45].

Radiation exposure — Because of the risks of radiation exposure, clinicians and staff should be vigilant to try and minimize radiation exposure to the patient as well as the staff [57]. Newer imaging and mapping techniques have reduced fluoroscopy times, particularly during complex ablations as for AF. Pulse fluoroscopy and optimization of fluoroscopy exposure parameters also reduces the risk of radiation injury. Radiation exposure and its potential effects and manifestations are discussed in detail separately. (See "Radiation-related risks of imaging" and "Radiation dose and risk of malignancy from cardiovascular imaging".)

New arrhythmias — New arrhythmias are a potential concern, since radiofrequency lesions themselves might serve as arrhythmogenic foci. While this is a possibility, this problem has been seen clinically in only a few settings.

New AF has occurred in patients undergoing ablation for atrial flutter; it is possible, however, that this occurs primarily in patients predisposed to AF [58]. Incomplete ablation lines in patients treated for AF may lead to left atrial flutter, which in some cases can cause more severe symptoms than the original AF.

An inappropriate sinus tachycardia may be present in some patients after posteroseptal accessory pathway or AV nodal modification for AVNRT, suggesting disruption of the parasympathetic and/or sympathetic inputs into the sinus and AV nodes [59-61]. When this occurs, it is typically relatively mild and transient.

Ventricular fibrillation has been reported in up to 6 percent of patients with chronic AF after AV nodal ablation when the pacing rate is ≤70 beats per minute [62]. This complication can be minimized by post-ablation pacing for three months at a higher rate (ie, 90 beats per minute). A possible mechanism for post-ablation ventricular arrhythmia is activation of the sympathetic nervous system and a prolongation in action potential duration; pacing at a rate of 90 beats per minute decreases sympathetic nervous system activity [63].

Troponin I and BNP — The degree of myocardial injury is more accurately assessed by serum troponin levels than CK-MB [64,65]. Elevated troponin I, present in up to 68 percent of patients undergoing ablation, correlates with the number of radiofrequency lesions applied, the site of lesions (ventricular > atrial > annular), and the approach to the left side (transaortic > transseptal) [64]. The prognostic significance of asymptomatic elevations of troponin I remains unclear. As such, we do not routinely monitor cardiac enzymes following electrical cardioversion in asymptomatic patients.

Similarly, mild elevations of brain natriuretic peptide (BNP), also of uncertain clinical significance, have been noted following ablation procedures. In a series of 36 patients undergoing ablation for supraventricular tachycardia, a transient rise in BNP was noted [66]. From a baseline of 11.3 pg/mL, BNP peaked three hours post-procedure at 40 pg/mL and approached baseline 24 hours post-procedure. This rise correlated closely with modest troponin I elevations, as well as with the duration of ventricular stimulation and total RF energy application.

Iatrogenic atrial septal defect — Some catheter ablation procedures require crossing the atrial septum with placement of sheaths/catheters. An iatrogenic atrial septal defect may persist in 5 to 20 percent of patients 9 to 12 months after the procedure [67,68]. It is possible but unproven that the use of an oral anticoagulant may reduce the risk of paradoxical embolism, particularly in those with a cardiac implantable electronic device (eg, pacemakers and implantable cardioverter defibrillators).

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Catheter ablation for the heart (The Basics)")

Beyond the Basics topic (see "Patient education: Catheter ablation for abnormal heartbeats (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Catheter ablation either using radiofrequency or cryothermal energy has emerged as a major tool for the non-pharmacological management of the vast majority of arrhythmias that are refractory to antiarrhythmic drug therapy for arrhythmias that are symptomatic and/or may have an untoward effect on cardiac function. (See 'Introduction' above.)

In most supraventricular tachycardias (atrioventricular reentrant tachycardia [AVRT] or AV nodal reentrant tachycardia [AVNRT], in atrial flutter, and in macroreentrant or focal atrial tachycardias) and in idiopathic ventricular ectopy/tachycardia, the success rates are high. Catheter ablation of atrial fibrillation is increasingly offered to drug-refractory symptomatic patients with paroxysmal tachycardia and selected patients with persistent atrial fibrillation with the aim of isolating the pulmonary vein where most ectopic foci are located and/or to modify the anatomic left atrial substrate (table 1). (See 'Indications and clinical use' above.)

For life-threatening ventricular tachyarrhythmias (ventricular tachycardias and ventricular fibrillation), the mainstay treatment is the implantable cardioverter-defibrillator (ICD) alone or in combination of pharmacological therapy for the prevention of arrhythmia episodes. Catheter ablation may be useful in reducing the frequency of appropriate ICD discharges and to improve patient quality of life or to treat the arrhythmia storm in patients with ICD.

The potential risks and benefits of the ablation procedure include those risks associated with an invasive electrophysiology study (EP study) alone (table 2). Generally, risks are lower in experienced operators and centers that perform larger numbers of procedures. (See 'Complications' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Bradley Knight, MD, FACC, Mark Link, MD, Brian Olshansky, MD, and Leonard Ganz, MD, FHRS, FACC, who contributed to earlier versions of this topic review.

  1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2018; 72:e91.
  2. Calkins H, Hindricks G, Cappato R, et al. 2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation. Heart Rhythm 2017; 14:e275.
  3. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2016; 67:e27.
  4. Narula OS. Sinus node re-entry: a mechanism for supraventricular tachycardia. Circulation 1974; 50:1114.
  5. Gomes JA, Mehta D, Langan MN. Sinus node reentrant tachycardia. Pacing Clin Electrophysiol 1995; 18:1045.
  6. Krahn AD, Yee R, Klein GJ, Morillo C. Inappropriate sinus tachycardia: evaluation and therapy. J Cardiovasc Electrophysiol 1995; 6:1124.
  7. Ueng KC, Lee SH, Wu DJ, et al. Radiofrequency catheter modification of atrioventricular junction in patients with COPD and medically refractory multifocal atrial tachycardia. Chest 2000; 117:52.
  8. Tracy CM, Akhtar M, DiMarco JP, et al. American College of Cardiology/American Heart Association 2006 update of the clinical competence statement on invasive electrophysiologystudies,catheterablation,andcardioversion: a report of the American College of Cardiology/American Heart Association/American College of Physicians Task Force on Clinical Competence and Training developed in collaboration with the Heart Rhythm Society. J Am Coll Cardiol 2006; 48:1503.
  9. Tanawuttiwat T, Nazarian S, Calkins H. The role of catheter ablation in the management of ventricular tachycardia. Eur Heart J 2016; 37:594.
  10. Plonsey R. Bioelectric Phenomenon, McGraw-Hill, New York 1969.
  11. Biermann M, Shenasa M, Borggrefe M, et al. The interpretation of cardiac electrograms. In: Cardiac mapping, Shenasa M, Borggrefe M, Breithardt G (Eds), Futura, Mount Kisco, NY 1993. p.11.
  12. Anderson KP, Walker R, Fuller M, et al. Criteria for local myocardial electrical activation: effects of electrogram characteristics. IEEE Trans Biomed Eng 1993; 40:169.
  13. Damiano RJ Jr, Blanchard SM, Asano T, et al. Effects of distant potentials on unipolar electrograms in an animal model utilizing the right ventricular isolation procedure. J Am Coll Cardiol 1988; 11:1100.
  14. Claydon FJ 3rd, Pilkington TC, Ideker RE. Classification of heart tissue from bipolar and unipolar intramural potentials. IEEE Trans Biomed Eng 1985; 32:513.
  15. Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial fibrillation organized by prior ablation. Circulation 2006; 113:616.
  16. Rodriguez E, Man DC, Coyne RF, et al. Type I atrial flutter ablation guided by a basket catheter. J Cardiovasc Electrophysiol 1998; 9:761.
  17. Schmitt C, Zrenner B, Schneider M, et al. Clinical experience with a novel multielectrode basket catheter in right atrial tachycardias. Circulation 1999; 99:2414.
  18. Schilling RJ, Peters NS, Davies DW. Simultaneous endocardial mapping in the human left ventricle using a noncontact catheter: comparison of contact and reconstructed electrograms during sinus rhythm. Circulation 1998; 98:887.
  19. Schilling RJ, Peters NS, Davies DW. Feasibility of a noncontact catheter for endocardial mapping of human ventricular tachycardia. Circulation 1999; 99:2543.
  20. Josephson ME. Catheter and surgical ablation in the therapy of arrhythmias. In: Clinical Cardiac Electrophysiology, 4th, Lippincott, Philadelphia 2008. p.746.
  21. Downar E, Harris L, Mickleborough LL, et al. Endocardial mapping of ventricular tachycardia in the intact human ventricle: evidence for reentrant mechanisms. J Am Coll Cardiol 1988; 11:783.
  22. Downar E, Kimber S, Harris L, et al. Endocardial mapping of ventricular tachycardia in the intact human heart. II. Evidence for multiuse reentry in a functional sheet of surviving myocardium. J Am Coll Cardiol 1992; 20:869.
  23. Garan H, Fallon JT, Rosenthal S, Ruskin JN. Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction. Circ Res 1987; 60:879.
  24. Kramer JB, Saffitz JE, Witkowski FX, Corr PB. Intramural reentry as a mechanism of ventricular tachycardia during evolving canine myocardial infarction. Circ Res 1985; 56:736.
  25. Sosa E, Scanavacca M. Epicardial mapping and ablation techniques to control ventricular tachycardia. J Cardiovasc Electrophysiol 2005; 16:449.
  26. Desai AD, Burke MC, Hong TE, et al. Termination of epicardial left ventricular tachycardia by pacing without global capture. J Cardiovasc Electrophysiol 2005; 16:92.
  27. Schweikert RA, Saliba WI, Tomassoni G, et al. Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003; 108:1329.
  28. Sosa E, Scanavacca M, D'Avila A, et al. Endocardial and epicardial ablation guided by nonsurgical transthoracic epicardial mapping to treat recurrent ventricular tachycardia. J Cardiovasc Electrophysiol 1998; 9:229.
  29. Gepstein L, Hayam G, Ben-Haim SA. A novel method for nonfluoroscopic catheter-based electroanatomical mapping of the heart. In vitro and in vivo accuracy results. Circulation 1997; 95:1611.
  30. Ben-Haim SA, Osadchy D, Schuster I, et al. Nonfluoroscopic, in vivo navigation and mapping technology. Nat Med 1996; 2:1393.
  31. Pérez-Castellano N, Villacastín J, Moreno J, et al. Errors in pulmonary vein identification and ostia location in the absence of pulmonary vein imaging. Heart Rhythm 2005; 2:1082.
  32. Packer DL. Evolution of mapping and anatomic imaging of cardiac arrhythmias. J Cardiovasc Electrophysiol 2004; 15:839.
  33. Schilling RJ, Peters NS, Davies DW. Noncontact mapping of cardiac arrhythmias. J Electrocardiol 1999; 32 Suppl:13.
  34. Schneider MA, Ndrepepa G, Zrenner B, et al. Noncontact mapping-guided catheter ablation of atrial fibrillation associated with left atrial ectopy. J Cardiovasc Electrophysiol 2000; 11:475.
  35. Schilling RJ, Kadish AH, Peters NS, et al. Endocardial mapping of atrial fibrillation in the human right atrium using a non-contact catheter. Eur Heart J 2000; 21:550.
  36. Cosio FG, Arribas F, Lopez-Gil M, Gonzalez HD. Radiofrequency ablation of atrial flutter. J Cardiovasc Electrophysiol 1996; 7:60.
  37. Ruffy R, Imran MA, Santel DJ, Wharton JM. Radiofrequency delivery through a cooled catheter tip allows the creation of larger endomyocardial lesions in the ovine heart. J Cardiovasc Electrophysiol 1995; 6:1089.
  38. Jaïs P, Shah DC, Haïssaguerre M, et al. Prospective randomized comparison of irrigated-tip versus conventional-tip catheters for ablation of common flutter. Circulation 2000; 101:772.
  39. Yamane T, Jaïs P, Shah DC, et al. Efficacy and safety of an irrigated-tip catheter for the ablation of accessory pathways resistant to conventional radiofrequency ablation. Circulation 2000; 102:2565.
  40. Calkins H, Epstein A, Packer D, et al. Catheter ablation of ventricular tachycardia in patients with structural heart disease using cooled radiofrequency energy: results of a prospective multicenter study. Cooled RF Multi Center Investigators Group. J Am Coll Cardiol 2000; 35:1905.
  41. Soejima K, Delacretaz E, Suzuki M, et al. Saline-cooled versus standard radiofrequency catheter ablation for infarct-related ventricular tachycardias. Circulation 2001; 103:1858.
  42. Jumrussirikul P, Chen JT, Jenkins M, et al. Prospective comparison of temperature guided microwave and radiofrequency catheter ablation in the swine heart. Pacing Clin Electrophysiol 1998; 21:1364.
  43. Skanes AC, Klein G, Krahn A, Yee R. Cryoablation: potentials and pitfalls. J Cardiovasc Electrophysiol 2004; 15:S28.
  44. Rodriguez LM, Leunissen J, Hoekstra A, et al. Transvenous cold mapping and cryoablation of the AV node in dogs: observations of chronic lesions and comparison to those obtained using radiofrequency ablation. J Cardiovasc Electrophysiol 1998; 9:1055.
  45. Skanes AC, Dubuc M, Klein GJ, et al. Cryothermal ablation of the slow pathway for the elimination of atrioventricular nodal reentrant tachycardia. Circulation 2000; 102:2856.
  46. Rodriguez LM, Geller JC, Tse HF, et al. Acute results of transvenous cryoablation of supraventricular tachycardia (atrial fibrillation, atrial flutter, Wolff-Parkinson-White syndrome, atrioventricular nodal reentry tachycardia). J Cardiovasc Electrophysiol 2002; 13:1082.
  47. Bradley CJ, Haines DE. Pulsed field ablation for pulmonary vein isolation in the treatment of atrial fibrillation. J Cardiovasc Electrophysiol 2020; 31:2136.
  48. Reddy VY, Dukkipati SR, Neuzil P, et al. Pulsed Field Ablation of Paroxysmal Atrial Fibrillation: 1-Year Outcomes of IMPULSE, PEFCAT, and PEFCAT II. JACC Clin Electrophysiol 2021; 7:614.
  49. Calkins H, Yong P, Miller JM, et al. Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. The Atakr Multicenter Investigators Group. Circulation 1999; 99:262.
  50. Bohnen M, Stevenson WG, Tedrow UB, et al. Incidence and predictors of major complications from contemporary catheter ablation to treat cardiac arrhythmias. Heart Rhythm 2011; 8:1661.
  51. Gupta A, Perera T, Ganesan A, et al. Complications of catheter ablation of atrial fibrillation: a systematic review. Circ Arrhythm Electrophysiol 2013; 6:1082.
  52. Kay GN, Epstein AE, Dailey SM, Plumb VJ. Role of radiofrequency ablation in the management of supraventricular arrhythmias: experience in 760 consecutive patients. J Cardiovasc Electrophysiol 1993; 4:371.
  53. Chen SA, Chiang CE, Tai CT, et al. Complications of diagnostic electrophysiologic studies and radiofrequency catheter ablation in patients with tachyarrhythmias: an eight-year survey of 3,966 consecutive procedures in a tertiary referral center. Am J Cardiol 1996; 77:41.
  54. Scheinman MM, Huang S. The 1998 NASPE prospective catheter ablation registry. Pacing Clin Electrophysiol 2000; 23:1020.
  55. Katritsis DG, Zografos T, Siontis KC, et al. Endpoints for Successful Slow Pathway Catheter Ablation in Typical and Atypical Atrioventricular Nodal Re-Entrant Tachycardia: A Contemporary, Multicenter Study. J Am Coll Cardiol EP 2019; 5:113.
  56. Chrispin J, Misra S, Marine JE, et al. Current management and clinical outcomes for catheter ablation of atrioventricular nodal re-entrant tachycardia. Europace 2018; 20:e51.
  57. Heidbuchel H, Wittkampf FH, Vano E, et al. Practical ways to reduce radiation dose for patients and staff during device implantations and electrophysiological procedures. Europace 2014; 16:946.
  58. Paydak H, Kall JG, Burke MC, et al. Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course. Circulation 1998; 98:315.
  59. Kocovic DZ, Harada T, Shea JB, et al. Alterations of heart rate and of heart rate variability after radiofrequency catheter ablation of supraventricular tachycardia. Delineation of parasympathetic pathways in the human heart. Circulation 1993; 88:1671.
  60. Psychari SN, Theodorakis GN, Koutelou M, et al. Cardiac denervation after radiofrequency ablation of supraventricular tachycardias. Am J Cardiol 1998; 81:725.
  61. Hamdan MH, Page RL, Wasmund SL, et al. Selective parasympathetic denervation following posteroseptal ablation for either atrioventricular nodal reentrant tachycardia or accessory pathways. Am J Cardiol 2000; 85:875.
  62. Geelen P, Brugada J, Andries E, Brugada P. Ventricular fibrillation and sudden death after radiofrequency catheter ablation of the atrioventricular junction. Pacing Clin Electrophysiol 1997; 20:343.
  63. Hamdan MH, Page RL, Sheehan CJ, et al. Increased sympathetic activity after atrioventricular junction ablation in patients with chronic atrial fibrillation. J Am Coll Cardiol 2000; 36:151.
  64. Manolis AS, Vassilikos V, Maounis T, et al. Detection of myocardial injury during radiofrequency catheter ablation by measuring serum cardiac troponin I levels: procedural correlates. J Am Coll Cardiol 1999; 34:1099.
  65. Katritsis D, Hossein-Nia M, Anastasakis A, et al. Use of troponin-T concentration and kinase isoforms for quantitation of myocardial injury induced by radiofrequency catheter ablation. Eur Heart J 1997; 18:1007.
  66. Chen L, Wei T, Zeng C, et al. Effect of radiofrequency catheter ablation on plasma B-type natriuretic peptide. Pacing Clin Electrophysiol 2005; 28:200.
  67. Anselmino M, Scaglione M, Battaglia A, et al. Iatrogenic atrial septal defects following atrial fibrillation transcatheter ablation: a relevant entity? Europace 2014; 16:1562.
  68. Madhavan M, Yao X, Sangaralingham LR, et al. Ischemic Stroke or Systemic Embolism After Transseptal Ablation of Arrhythmias in Patients With Cardiac Implantable Electronic Devices. J Am Heart Assoc 2016; 5:e003163.
Topic 1007 Version 36.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟