Catheter ablation of hemodynamically compromising incessant atrioventricular tachycardia

Catheter Ablation of Hemodynamically Compromising Incessant Atrioventricular Tachycardia

Cynthia M. Tracy, MD, John F. Swartz, MD, Pamela Karasik, MD, Allen Solomon, MD, and Ross D. Fletcher, MD

Abstract:

A 27-year-old woman was admitted to the Georgetown University Hospital with refractory hemodynamically compromising incessant atrioventricular tachycardia. A single left-sided accessory pathway was identified and successfully modified acutely. Endocardial delivery of direct current energy provided an extremely effective therapeutic intervention resulting in termination of atrioventricular tachycardia and restoration of stable hemodynamic status. Although a second ablation procedure was necessary to permanently interrupt accessory pathway conduction, the patient has remained free of symptoms without medications for 13 months. Key words: catheter ablation, incessant atrioventricular tachycardia.

multiple pharmacologic cardioversion.

Acute therapy of symptomatic supraventricular tachycardia associated with the Wolff-ParkinsonWhite Syndrome has traditionally relied on inuavenous drug administration and electrical cardioversion. Due to the efficacy of these therapies, definitive accessory pathway (AP) interruption is rarely required for acute management of arrhythmias. Definitive accessory pathway interruption by surgical means has been the usual approach since its description by Sealy et al. in 1969.’ More recently, closed chest accessory pathway fulguration has been utilized by several investigators.2-5 Catheter ablation has typically been employed in patients with stable clinical condition.6 We describe successful endocardial direct current catheter ablation of a left free wall AP in a patient with hemodynamically compromising incessant atrioventricular tachycardia resistant to

interventions

and

repeat

Case Report A 2i’-year-old woman was referred for emergency therapy of incessant wide complex tachycardia with associated hemodynamic deterioration. The patient related a lifelong history of palpitations associated with shortness of breath and near syncope. Eight months prior to this admission, a diagnosis of WolffParkinson-White Syndrome was made after presentation for therapy of atria1 fibrillation with rapid anterograde accessory pathway conduction (Fig. 1) . Procainamide therapy was instituted. However, 2 weeks later, recurrent atrioventricular tachycardia led to the addition of flecainide ( 150 mg twice a day). Twenty-four hours later, she again presented with palpitations, chest pain, near syncope, and hypotension (systolic BP 100 mmHg). A procainamide level

From the Division of Cardiology, Georgetown University Hospital, Veterans Administration Medical Center, Washington, DC and Uniformed Services University, Bethesda, Maryland.

Reprintrequests: Cynthia M. Tracy, MD, Division of Cardiology, 4 North, Georgetown University Hospital, 3800 Reservoir Road NW, Washington, DC 20007.

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Fig. 1. Twelve-lead

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ECG obtained at the time of clinical presentation.

of 5.2 pg/ml and N-acetyl procainamide level of 3.9 pghl were documented at presentation. Intravenous verapamil, lidocaine, esmolol, and procainamide were administered without effect. Electrical cardioversion resulted in only a brief period of sinus rhythm, and oral quinidine therapy resulted in worsened hypotension (BP 80150 mmHg). After 3 days, all medications were discontinued. Sinus rhythm could not be maintained and the patient was referred to our institution for definitive therapy. On arrival, the patient was in moderate distress due to chest discomfort and shortness of breath. Vital signs were: BP 75/50, HR 148, RR 18, T 367°C. Physical examination was otherwise unremarkable. A regular wide complex tachycardia, rate 134 bpm, with middiastolic P waves (Fig. 2) was noted on the electrocardiogram. Echocardiography revealed normal chamber dimensions and functions without evidence of valvular dysfunction.

Ablation Procedure The patient was brought to the cardiac catheterization laboratory in a postabsorptive, mildly sedated state. Selective coronary angiography demonstrated a normal left dominant coronary tree. Electrophysiologic evaluation was accomplished using quadripolar catheters advanced to the high right atrium,

Shortest preexcited RR interval

= 220 ms.

His bundle, and ventricular apex positions from right and left femoral venous access sites. An orthogonal array coronary sinus catheter was used for accessory pathway localization. Orthodromic atrioventricular tachycardia with left bundle branch block was mediated by a single left free wall AP (Fig. 3). Anterograde AP refractory periods could not be determined due to the complete block induced by recent therapy with procainamide and flecainide. Incremental ventricular ramp pacing resulted in 1: 1 retrograde conduction via the AP to a cycle length of 290 ms. Atrioventricular reentrant tachycardia (AVRT) could only transiently be interrupted by overdrive pacing. During AVRT, the AH interval was 140 ms, HV was 70 ms, and the V to high right atrium was 200 ms (Fig. 3). Earliest retrograde atria1 activation was localized to a site 6 cm beyond the coronary sinus OS. An 8 F bipolar catheter with lumen (Bard Electrophysiology, Billerica, MA) was positioned on the endocardial aspect of the accessory pathway atria1 insertion using a transseptal approach. At the atria1 insertion, a presumed direct recording of an accessory pathway potential revealed local V-AP time of 30 ms and APA time of 25 ms. Surface QRS-A conduction time was 185 ms (Fig. 4). Endocardial delivery of 200 J cathodal direct current ablative energy resulted in complete retrograde dissociation and termination of the incessant AVRT (Fig. 5). A damped sinusoidal

Catheter Ablation for Incessant Tachycardia

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-_

-_ --.

_

_._.

-__-_

.

.

. _ _..___-_. - . _ _.--. -_.--

Fig. 2. Twelve-lead

ECG demonstrating orthodromic AVRT using the left free wall AP for retrograde conductic ,n. (Note middiastolic P waves that correlate with timing of atria1 activity as seen in Fig. 3).

HBE PCS MCS, MCSz DCS

Fig. 3. Surface and intracardiac

electrograms obtained during orthodromic AVRT. (Note earliest retrograde activation mediated by left-sided AP). Anterograde AV nodal and His-Purkinje slowing consistent with residual Flecainide effect. HBE = His bundle electrogram; PCS = proximal coronary sinus; MCS = mid coronary sinus; DCS = distal coronary sinus.

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I II III

V, V,

V‘ HBE ABL PCS MCS MCS

Fig. 4. Surface and intracardiac electrograms demonstrating positioning of ablation catheter. Bipolar ablation catheter electrograms clearly demonstrate atria1 and probable AP electrograms. HBE = His bundle electrogram; ABL = ablation catheter; PCS = proximal coronary sinus; DCS = distal coronary sinus; AP = accessory pathway electrogram.

Fig. 5. Surface and intracardiac

electrograms demonstrating interruption of retrograde AP conduction and complete V-A dissociation. HBE = His bundle electrogram; ABL = ablation catheter; PCS = proximal coronary sinus; MCS = mid coronary sinus; DCS = distal coronary sinus.

Catheter Ablation for Incessant Tachycardia

waveform was delivered from a standard defibrillator (Lifepack 6, Physio Control). Repeat coronary angiography following the ablation procedure again demonstrated normal coronary artery anatomy. With resumption of sinus rhythm, hemodynamic status normalized and there was no immediate hypotension related to DC energy delivery. Cardiac monitoring following ablation revealed a gradually resolving intraventricular conduction delay suggestive of flecainide effect. Manifest ventricular preexcitation occurred 48 hours after the ablation, but the patient remained free of dysrhythmias. Repeat electrophysiologic assessment revealed recovery of bidirectional accessory pathway conduction that was permanently interrupted with repeat endocardial ablation to the same site of the accessory pathway atria1 insertion. During 13 months of clinical follow-up evaluation, the patient remained free of symptoms and ventricular preexcitation without any antidysrhythmic medications.

Discussion

The success of transvenous ablation of APs has been increasingly accepted, particularly with a posteroseptal location.7-9 Closed chest ablative therapy of incessant orthodromic AVRT utilizing right-sided APs has been reported by several investigators with varying degrees of success.‘“,’ ’ However, application of this technique in patients with incessant AVRT mediated by left-sided APs has not been previously described. Catheter ablation of left free-wall pathways has been attempted via the coronary sinus as well as via a transseptal approach.‘,‘* A low success rate and an unacceptably high incidence of complications occurs following delivery of direct current ablative energy within the coronary sinus.‘3*‘4 However, ablation of the endocardial aspect of left-sided AP atria1 insertion has been described as a highly successful procedure.’ Although a transseptal approach is technically more difficult, safe delivery of ablating energy is feasible even in the acute setting of incessant and hemodynamically compromising tachycardia as demonstrated in this case. This patient presented to our institution prior to the availability of radiofrequency ablation techniques. Radiofrequency ablation is a safer and more effective means of interrupting accessory pathway conduction in our experience. ’ 5 The sole intent of this report is to report the effectiveness of catheter ablation techniques applied in the setting of hemodynamically compromising AVRT.

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This case of incessant orthodromic AVRT was probably the result of aggressive flecainide therapy that resulted in anterograde conduction block within the accessory pathway and the extensive slowing of intraventricular conduction manifest by left bundle branch block and markedly prolonged HV interval noted at the time of presentation. Similar events of atria1 proarrhythmia have been postulated by Feld et a1.16 Although absolute atrioventricular conduction time was abnormally prolonged at the site of earliest retrograde atria1 activation ( 185 ms), flecainide therapy did not alter our ability to localize the atria1 insertion. The usual pattern of eccentric retrograde atria1 activation potential recordings permitted accurate ablation catheter placement and successful tract modification. Although a second ablation procedure was necessary to permanently interrupt AP conduction, the initial procedure was an extremely effective therapeutic intervention with respect to termination of AVRT and restoration of stable hemodynamic status. The recovery of AP conduction suggests the resolution of barotrauma induced by the DC energy. The site of the second ablation was fluoroscopically identical to that of the first. The second ablation procedure was performed due to well-preserved anterograde AP conduction documented on follow-up EPS. Complete elimination of anterograde AP conduction was considered necessary to eliminate risk of sudden cardiac death in this patient with recurrent spontaneous atria1 fibrillation. This case demonstrates the safety and efficacy of closed chest catheter ablation techniques in patients with hemodynamically compromising incessant APmediated tachycardia. Prolonged temporizing measures such as transvenous overdrive pacing, recurrent cardioversion, and administration of multiple medications can be avoided by early application of definitive therapy.

References

Sealy WC, Hattler BG, Blumenschein SD et al: Surgical treatment of Wolff-Parkinson-White Syndrome. Ann Thorac Surg 8:1, I969 Scheinman NM, Morady F, Hess DS et al: Catheterinduced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. JAMA 248:851, 1982 Gallagher JJ, Svenson RH, Kasell JH et al: Catheter technique for closed-chest ablation of the atrioventricular conduction system: a therapeutic alternative

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for the treatment of refractory supraventricular tachycardia. N Engl J Med 306:194, 1982 Nathan AW, Bennett DH, Ward DE et al: Catheter ablation of atrioventricular conduction. Lancet i: 1280, 1984 Brodman R, Fisher JD: Evaluation of a catheter technique for ablation of accessory pathways near the coronary sinus using a canine model. Circulation 67:923, 1983 Ward DE, Camm AJ: Treatment of tachycardia associated with the Wolff-Parkinson-White syndrome by transvenous electrical ablation of accessory pathways. Br Heart J 53:64, 1985 Morady F, Scheinman MM, Winston SA et al: Efficacy and safety of transcatheter ablation of posteroseptal accessory pathways. Circulation 72:170, 1985 Warin JF, Haissaguerre M: Fulguration of accessory pathways in any location: report of seventy cases. PACE 12(11):215, 1989 Weber H, Schmitz L: Catheter technique for closed chest ablation of an accessory atrioventricular pathway. N Engl J Med 308:653, 1983 Webb JG, Downer E, Harris L et al: Direct endocardial

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recording and catheter ablation of an accessory pathway in a patient with incessant supraventricular tachycardia. PACE II: 1533, 1988 Kunze K, Kuck K: Transvenous ablation of accessory pathways in patients with incessant atrioventricular tachycardia. Circulation 7O:II. 1984 (Abstr) Warin JF, Haissaguerre M, LeMatayer P et al: Catheter ablation of accessory pathways with a direct approach. Circulation 78:800, 1988 Fisher JD, Brodman R, Kim SG: Attempted non-surgical electrical ablation of accessory pathways via the coronary sinus in the Wolff-Parkinson- White Syndrome. J Am Co11Cardiol 4(4):685, 1984 Bardy GH, Ivey TD, Coltori F et al: Developments, complications, and limitations of catheter-mediated electrical ablation of posterior accessory atrioventricular pathways. Am J Cardiol 6 1: 309, 1988 Swartz J, Tracy C, Fletcher R et al: A comparative study of direct current and radiofrequency atria1 endocardial ablation of accessory pathways. J Am Co11 Cardiol 17(2):109A, 1991 (Abstr) Feld GK, Chen P-S, Nicod P et al: Possible atria1 proarrhythmic effects of class Ic antiarrhythmic drugs. J Am Co11Cardiol 66:378, 1990