Article

Technology Update for Mapping, Imaging, and Ablation

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Since the 1980s, dramatic advances in electrophysiology procedures have occurred. Catheter positioning is most often assisted by fluoroscopy. Sophisticated electroanatomical mapping systems can also display catheter position and create a 3D depiction of the anatomy. Magnetic resonance imaging (MRI) and computed tomography (CT) data can also be integrated, facilitating complex ablation procedures. Ablation is most commonly achieved with application of radiofrequency (RF) energy. Freezing with catheter-based cryoablation is also widely available. Serious complications of catheter ablation are infrequent and most often related to the catheterization procedure, most commonly including vascular injury, and cardiac perforation with tamponade.

Re-entrant Supraventricular Tachycardia
Atrioventricular Nodal Re-entrant Tachycardia

Catheter ablation for atrioventricular nodal re-entrant tachycardia (AVNRT) is recommended when episodes are poorly tolerated or resistant to medical therapy.1 In patients with AVNRT, tachycardia can be eliminated in more than 95% of patients by ablating a functional pathway for slow conduction between the os of the coronary sinus and the septal leaflet of the tricuspid valve.2 Heart block is the major risk, requiring a permanent pacemaker in 0.8% of patients. Cryoablation may be associated with a lower risk of heart block, but lower long-term success rates.3

Atrioventricular Reciprocating Tachycardia Due to Accessory Pathways

Patients with AV reciprocating tachycardia (AVRT) have an accessory pathway (AP). If the AP can conduct from atrium to ventricle, the electrocardiogram (ECG) shows pre-excitation, consistent with Wolff- Parkinson-White (WPW) syndrome. APs that are able to conduct only from ventricle to atrium are considered ‘concealed’ because during sinus rhythm pre-excitation is absent, but AVRT still can occur. Catheter ablation is the standard of care for symptomatic WPW syndrome, or for concealed accessory pathways causing symptomatic tachycardias when pharmacological therapy is ineffective or not desirable.1 AP location determines whether an arterial, venous, or trans-septal approach is required. Success rates are 90–95%, with a risk of recurrent pathway conduction after healing of 3–10%.1 Serious complications related to left or right heart catheterization can occur, but are uncommon.

Regular Atrial Arrhythmias
Focal Atrial Tachycardia

Focal atrial tachycardias (ATs) tend to occur in specific anatomical locations: along the crista terminalis, tricuspid or mitral annulus, coronary sinus musculature, atrial appendages, and in the pulmonary veins. Areas of earliest activation during the AT are targeted for ablation. Lack of inducibility at electrophysiology study is the most common cause of failure.4,5 Ablation is successful in more than 80% of patients, with a recurrence rate after successful ablation of approximately 8%.1 Significant complications occur in 1–2% of patients.

Atrial Flutter and Other Macro Re-entrant Atrial Tachycardias

Common atrial flutter is due to a large macro re-entrant circuit with a wave front revolving around the tricuspid annulus. In typical counterclockwise atrial flutter, the wave front proceeds up the atrial septum and down the right atrial free wall. Re-entry is dependent on conduction through the cavo-tricuspid isthmus bounded by the tricuspid valve annulus, inferior vena cava, Eustachian ridge, and coronary sinus os. Other atrial tachycardias can mimic atrial flutter. In patients with prior atrial surgery or ablation, common atrial flutter may also have an atypical ECG appearance. Once the diagnosis is confirmed by entrainment and activation mapping, a series of ablation lesions are placed across the cavo-tricuspid isthmus, creating a line of conduction block. Success is achieved in more than 95% of patients and recurrences are less frequent than in those managed with antiarrhythmic drug therapy.6 Approximately 20–30% of patients with successful atrial flutter ablation will present with atrial fibrillation (AF) in the next 20 months. A history of AF and depressed ventricular function increases the risk of subsequent AF.7 Other macro re-entrant circuits can occur in the left or right atrium. Arrhythmias are often due to re-entry around atrial scars from prior heart surgery or ablation, and are referred to as ‘lesion-related’ or ‘scar-related’ macro re-entrant ATs.1 Catheter ablation is more difficult, with success rates of 80–85% and more frequent late recurrences than are observed for common flutter.8

Atrial Fibrillation
Atrioventricular Junction Ablation for Rate Control

In patients with AF, rate control can be achieved with ablation of the AV junction to produce complete heart block. The procedure is generally reserved for older patients who may already have an implanted pacing system, cannot tolerate rate control medications, and are not candidates for other rhythm control strategies. Anticoagulation for thromboembolic risk is still required. For patients with previously uncontrolled AF rates, quality of life, exercise tolerance, and ejection fraction can improve.9 However, cases of sudden death have occurred, likely due to polymorphic ventricular tachycardia consequent to the abrupt decrease in heart rate. Pacing the ventricle at 90 beats per minute and then gradually reducing the rate over time mitigates the risk.10 Biventricular pacing may be required to reduce the risk of heart failure exacerbation in patients with impaired left ventricular (LV) function.9 AV junction ablation may be used to ensure delivery of biventricular pacing in patients with chronic AF and heart failure.

Atrial Fibrillation Ablation for Maintaining Sinus Rhythm

The majority of focal triggers for initiation of AF can be found originating from sleeves of myocardium extending along the pulmonary veins. 11 Atrial ablation, usually with pulmonary vein isolation, has the goal of electrically isolating those regions with additional lesions to address other atrial regions thought to promote AF.12–14 An extensive series of lesions is usually placed in the left atrium, though the exact lesion set varies from center to center (see Figure 1). Intra-cardiac echocardiography and 3D mapping systems that incorporate anatomy from MRI or CT images are helpful adjuncts to facilitate ablation strategies.15 Young patients with paroxysmal lone AF have the best outcome. More than 70–80% have sinus rhythm after the initial healing phase following ablation. Reported follow-up periods are still relatively short, with few studies reporting data beyond one year. Success rates are lower for patients with persistent or permanent AF or impaired LV function.12

Following ablation, recurrent ATs and AF can occur over a period of several weeks as ablation lesions heal and the atrium remodels. A second procedure is required in 20–50% of patients. Antiarrhythmic medications are often continued for one to three months after ablation. Anticoagulation with warfarin is required as well. Major procedural complications include myocardial perforation with tamponade (1–2%) and stroke (0.5–1%). Severe pulmonary vein stenosis has been reported in 2–6% of patients.16 Death from atrio-esophageal fistulae, presenting days to a few weeks after the procedure with endocarditis, septic emboli, or gastrointestinal bleeding, has been reported (<0.5% estimated).17 Phrenic nerve injury, particularly secondary to ablating near the right pulmonary veins, has also occurred.18 Appropriate patient selection requires adequate assessment of risks and benefits for each individual patient. The risks and benefits can be expected to improve as this relatively new procedure continues to evolve.

Ventricular Tachycardia
Idiopathic Ventricular Tachycardia

Idiopathic ventricular tachycardia (VT) occurs in the absence of structural heart disease and is often amenable to catheter ablation. The most common form originates from a focus in the right ventricular outflow tract, beneath the pulmonary valve, and may cause exercise-induced VT, repetitive bursts of monomorphic VT, or symptomatic premature ventricular contractions.19 Ablation is performed at the area of earliest activation in the outflow tract with successful elimination of tachycardia in more than 80% of patients. Occasionally, the aortic annulus, LV outflow tract, or epicardial areas can be sites of origin. Inducibility of the VT for mapping is essential for successful ablation, which is occasionally prevented by the proximity of the VT to vital structures such as the left main coronary artery. Idiopathic LV VT commonly originates from the LV apical septum.20 It often responds to verapamil and can be mistaken for SVT with aberrancy. It appears to be due to re-entry involving portions of the distal Purkinje system. Ablation targeting characteristic electrograms in the re-entry region is successful in more than 80% of patients. Significant complications are infrequent, although femoral arterial and retrograde aortic LV catheterization is usually required.

Ventricular Tachycardia after Myocardial Infarction and Scar-related Re-entry

Sustained VT with structural heart disease is associated with a risk of sudden death, necessitating placement of an implanted cardioverter–defibrillator (ICD). Catheter ablation is an important alternative to antiarrhythmic drug therapy for reducing the frequency of symptomatic VT and can be life-saving if VT becomes incessant.

Any ventricular scar can cause VT. Myocardial infarction is most common, but fibrosis from idiopathic dilated cardiomyopathy, sarcoidosis, arrhythmogenic right ventricular dysplasia, Chagas’ disease, or prior cardiac surgery for congenital heart disease can also result in VT substrate. Areas of conduction block with channels of slow conduction in the scar region support re-entry, producing monomorphic VT. The ECG morphology of the VT suggests the location of the scar and region where the re-entry wave front exits regions of the scar to produce the QRS complex.

During mapping, areas of scar are identified as regions with abnormal, low-voltage electrograms that can be highlighted on 3D anatomical maps.21–23 Pacing from the mapping catheter during sinus rhythm (‘pace-mapping’) also helps identify the exit region. Identification of the scar region during sinus rhythm, referred to as ‘substrate mapping,’ allows some VTs that are hemodynamically unstable to be mapped. Ablation then targets conducting channels through the scar region, or the border of the scar region that contains the exit (see Figure 2).

The goal is often to control the main clinical VT circuit, which can be achieved in more than 70% of patients.24,25 The scar region is typically large, usually containing multiple potential re-entry circuits causing multiple morphologies of VT inducible by electrical stimulation, and parts of the circuit can be deep within the myocardium or in the epicardium.26–28 Some epicardial VTs can be approached by a subxiphoid percutaneous puncture or surgical entry into the pericardial space for mapping and ablation. Procedure-related mortality is approximately 3%, some from uncontrollable VT when the procedure fails.29

Bundle branch re-entry VT is particularly susceptible to ablation, and is found in approximately 6% of patients with VT and structural heart disease. A diseased Purkinje system supports a re-entry circuit revolving up one bundle branch and down the contralateral bundle branch. These patients often have intraventricular conduction delay or a pattern of left bundle branch block during sinus rhythm and advanced ventricular dysfunction.30 Catheter ablation of the right bundle branch is curative.

Ablation for Electrical Storm and Ventricular Fibrillation

Repetitive episodes of ventricular fibrillation causing ‘electrical storm’ are sometimes initiated by ectopic foci in the Purkinje system or right ventricle (RV) outflow tract. Idiopathic ventricular fibrillation, acute and chronic myocardial infarction, long QT syndrome, and Brugada syndrome are commonly associated.31 Such cases are rare, but ablation targeting the initiating foci during periods of electrical storm with a strategy similar to that used for idiopathic VT can be life-saving.

Conclusion

Tremendous advances in the treatment of cardiac arrhythmias with catheter ablation have occurred in recent decades. Ablation is now a reasonably definitive treatment strategy for symptomatic SVT due to accessory pathways, atrial flutter, AV node re-entrant tachycardia, and idiopathic VT. Its use for atrial fibrillation is increasing and further studies will continue to define the risks and benefits. Catheter ablation is an important adjunctive therapy for patients with recurrent VT associated with structural heart disease, and can be life-saving for patients with incessant VT or electrical storms.

References

  1. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al., Circulation, 2003;108:1871–1909.
    Crossref | PubMed
  2. Wu J, Olgin J, Miller JM, et al., Circ Res, 2001;88:1189–95.
    Crossref | PubMed
  3. Friedman PL, Dubuc M, Green MS, et al., Heart Rhythm, 2004;1:129–38.
    Crossref | PubMed
  4. Dong J, Zrenner B, Schreieck J, et al., Heart Rhythm, 2005;2:578–91.
    Crossref | PubMed
  5. Badhwar N, Kalman JM, Sparks PB, et al., J Am Coll Cardiol, 2005;46:1921–30.
    Crossref | PubMed
  6. Natale A, Newby KH, Pisano E, et al., J Am Coll Cardiol, 2000;35:1898–1904.
    Crossref | PubMed
  7. Paydak H, Kall JG, Burke MC, et al., Circulation, 1998;98:315–22.
    Crossref | PubMed
  8. Delacretaz E, Ganz LI, Soejima K, et al., J Am Coll Cardiol, 2001;37:1665–76.
    Crossref | PubMed
  9. Doshi RN, Daoud EG, Fellows C, et al., J Cardiovasc Electrophysiol, 2005;16:1160–65.
    Crossref | PubMed
  10. Ozcan C, Jahangir A, Friedman PA, et al., J Am Coll Cardiol, 2002;40:105–10.
    Crossref | PubMed
  11. Haissaguerre M, Jais P, Shah DC, et al., N Engl J Med, 1998;339:659–66.
    Crossref | PubMed
  12. Verma A, Natale A, Circulation, 2005;112:1214–22; discussion 1231.
    Crossref | PubMed
  13. Oral H, Pappone C, Chugh A, et al., N Engl J Med, 2006;354:934–41.
    Crossref | PubMed
  14. Pappone C, Santinelli V, Heart Rhythm, 2004;1:326–8.
    Crossref | PubMed
  15. Dong J, Dickfeld T, Lamiy SZ, et al.,Heart Rhythm, 2005;2:1021–2.
    Crossref | PubMed
  16. Cappato R, Calkins H, Chen SA, et al., Circulation, 2005;111:1100–5.
    Crossref | PubMed
  17. Pappone C, Oral H, Santinelli V, et al., Circulation, 2004;109:2724–6.
    Crossref | PubMed
  18. Bunch TJ, Bruce GK, Mahapatra S, et al., J Cardiovasc Electrophysiol, 2005;16:1318–25.
    Crossref | PubMed
  19. Joshi S, Wilber DJ, J Cardiovasc Electrophysiol, 2005;16(Suppl. 1):S52–8.
    Crossref | PubMed
  20. Ouyang F, Cappato R, Ernst S, et al., Circulation, 2002;105: 462–9.
    Crossref | PubMed
  21. Marchlinski FE, Callans DJ, Gottlieb CD, et al., Circulation, 2000;101:1288–96.
    Crossref | PubMed
  22. Soejima K, Stevenson WG, Maisel WH, et al., Circulation, 2002;106:1678–83.
    Crossref | PubMed
  23. Brunckhorst CB, Stevenson WG, Soejima K, et al., J Am Coll Cardiol, 2003;41:802–9.
    Crossref | PubMed
  24. Calkins H, Epstein A, Packer D, et al., J Am Coll Cardiol, 2000;35:1905–14.
    Crossref | PubMed
  25. Stevenson W, Wilber D, Natale A, et al., Circulation, 2004;110 (Suppl.):1869.
  26. Soejima K, Stevenson WG, Sapp JL, et al., J Am Coll Cardiol, 2004;43:1834–42.
    Crossref | PubMed
  27. Berruezo A, Mont L, Nava S, et al., Circulation, 2004;109:1842–7.
    Crossref | PubMed
  28. Sosa E, Scanavacca M, d’Avila A, et al., J Am Coll Cardiol, 2000;35:1442–9.
    Crossref | PubMed
  29. Scheinman MM, Huang S, Pacing Clin Electrophysiol, 2000;23:1020–28.
    Crossref | PubMed
  30. Tchou P, Jazayeri M, Denker S, et al., Circulation, 1988;78:246–57.
    Crossref | PubMed
  31. Haissaguerre M, Extramiana F, Hocini M, et al., Circulation, 2003;108:925–8.
    Crossref | PubMed