Ann Thorac Surg 2008;85:2136-2138. doi:10.1016/j.athoracsur.2007.12.010
© 2008 The Society of Thoracic Surgeons
Case Reports
Cardiac Resynchronization Therapy for the Failing Fontan Patient
Vladimir Sojak, MDa,*,
Uros Mazic, MDb,
Maja Cesen, MDb,
Jurgen Schrader, PhDc,
Nenad Danojevic, MDd
a Department of Cardiovascular Surgery, University Medical Center, Ljubljana, Slovenia
b Pediatric Clinic, University Medical Center, Ljubljana, Slovenia
d Department of Anesthesia, University Medical Center, Ljubljana, Slovenia
c Biotronik, Erlangen, Germany
Accepted for publication December 4, 2007.
* Address correspondence to Dr Sojak, Department of Cardiovascular Surgery, Medical Center, Zaloska 7, Ljubljana, 1000, Slovenia (Email: vladimir.sojak{at}kclj.si).
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Abstract
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Myocardial dysfunction is the leading cause of death in single-ventricle patients. Heart transplantation has traditionally been reserved for Fontan patients with end-stage myocardial dysfunction. Cardiac resynchronization therapy with multisite pacing was found to improve the myocardial performance in Fontan patients in acute postoperative settings; however, its role is unclear in chronic Fontan patients with progressive myocardial dysfunction. We present a case in which cardiac resynchronization therapy improved both hemodynamics and clinical condition in a Fontan patient with advanced myocardial dysfunction.
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Introduction
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Single-ventricle (SV) patients undergoing a Fontan operation are at risk for myocardial dysfunction, which remains the leading cause of death in this population [1]. In Fontan patients with end-stage myocardial dysfunction, heart transplantation has traditionally been the only option for improved survival [2]. Cardiac resynchronization therapy (CRT) with multisite pacing was found to improve the myocardial performance in Fontan patients in the acute postoperative setting [3]. However, its role is unclear in chronic Fontan patients with progressive myocardial dysfunction.
The patient had a SV physiology, consisting of double-inlet right ventricle, double-outlet right ventricle, and L-transposition of the great arteries. First, he underwent a hemi-Fontan procedure at the age of 12 months, followed by a fenestrated Fontan procedure with a lateral polytetrafluoroethylene (PTFE) tunnel at the age of 5 years. Seven months later, reoperation was required because of abscess formation within the lateral tunnel. A new lateral PTFE tunnel was created, and the damaged tricuspid valve not amenable to repair was closed with a prosthetic patch.
A few days later, a dual-chamber (DDD) pacemaker was implanted for iatrogenic complete atrioventricular block. Permanent epicardial leads were placed on the left atrium and posterior wall of the left ventricle (lead 1) through a left thoracotomy.
The patient was hospitalized repeatedly after the procedure because of progressive heart failure. Preoperative studies showed markedly impaired myocardial contractility, with ventricular fractional area change of 15%, moderate to severe mitral regurgitation, paced QRS duration of 210 ms, and poor clinical condition, with a New York Heart Association (NYHA) functional class of III to IV.
An operation was performed through a median sternotomy at the age of 11 years. The original atrial and ventricular leads were left in place because of good functionality. Then, temporary epicardial leads were placed on the ventricular apex (lead 2), anterior ventricular wall (lead 3), and right lateral ventricular wall (close to the atrioventricular groove, lead 4). Cathodic pacing was performed in a DDD mode with atrial sensing of the patient's own sinus rhythm using a pacing system analyzer (ICS 3000 IM; Biotronik, Berlin, Germany).
Systemic blood pressure was monitored using an indwelling arterial catheter. Cardiac output was measured by continuous real-time monitoring (LiDCO, Cambridge, UK). Hemodynamic variables were assessed in various pacing patterns (single-site vs multisite pacing and their various combinations). Hemodynamic parameters and QRS duration under various pacing patterns are given in Figure 1. The best hemodynamics with single-site and multisite pacing were achieved with the apical lead stimulation (lead 2) and a combination of left posterior, apical, and anterior lead stimulation (lead 1 + lead 2 + lead 3), respectively. Compared with baseline, optimal multisite pacing produced almost a 20% increase in cardiac output.
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Fig 1. Line graph shows hemodynamic variables, including cardiac output (CO, clear triangle), systolic blood pressure (SBP, solid circle), diastolic blood pressure (DBP, solid square), and QRS duration (QRSD, clear diamond) under various pacing patterns.
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Notably, hemodynamics became worse after the fourth ventricular lead (lead 4) was added to the previous three leads. Therefore, 2 permanent epicardial leads were placed exactly to the sites of the previous temporary leads 2 and 3 (Enpath Medical 2084 T; St. Jude Medical, St. Paul, MN, and Capsure Epi EPI 4968; Medtronic, Minneapolis, MN). Then, leads 1 and 3 were connected through a Y-connector (Dr Osypka GmbH, Rheinfelden-Herten, Germany) and put in the "left" ventricular port. Lead 2 was put in the "right" ventricular port of the pacemaker (Stratos LV-T; Biotronik, Berlin, Germany).
With the pacemaker implanted, atrioventricular delay adjustment was found to have a substantial effect on hemodynamics (Fig 2A). An optimum atrioventricular delay producing the best hemodynamics was within the range of 140 to 160 ms. Furthermore, modification of ventriculoventricular delay—"left channel" (ventricular stimulation) preceding "right channel" (ventricular stimulation)—also slightly influenced hemodynamics (Fig 2B). The most favorable hemodynamics were seen in the range of 40 to 60 ms. In addition to hemodynamic improvement, intraoperative echocardiography also revealed better contractility, increased fractional area change, and significant reduction of mitral regurgitation to a mild grade. Predischarge assessment confirmed improved myocardial performance, with a fractional area change of 20% and mild mitral regurgitation.
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Fig 2. Line graph shows impact of (A) atrioventricular (A-V) delay and (B) ventriculoventricular (V-V) delay on hemodynamic variables of cardiac output (CO, triangles), diastolic blood pressure (DBP, solid squares), and systolic blood pressure (SBP, solid circles).
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Follow-up at 1 and 3 months showed clear clinical benefit. The fractional area change rose from 22% at 1 month to 25% at 3 months. Heart size reduction is shown in Figure 3, depicting the patient's chest roentgenogram before and 3 months after CRT. The patient is currently in NYHA class II and has been withdrawn from the transplant list.
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Fig 3. Chest roentgenogram (left) before and (right) 3 months after cardiac resynchronization therapy shows the reduction in heart size.
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Comment
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In theory, CRT improves myocardial performance due to improved synchrony of contraction, shorter ejection period, longer filling period, and absence of energy losses secondary to blood shifts between earlier and later contracting parts of the myocardium.
We hypothesized that ventricular stimulation from more than two sites at the same time or with a proper delay might further enhance the synchrony of ventricular contraction. Because there are no recommendations on optimal sites for CRT in single-ventricle patients, we empirically placed epicardial ventricular leads in two perpendicular planes (anterior–posterior and basal–apical [left–right]). Optimal position rather than number of pacing leads was found to improve hemodynamics. Owing to lack of time, more detailed ventricular mapping was not performed, and it might have produced superior results. An individual approach to each single-ventricle patient is warranted because of substantial anatomic heterogeneity in this group.
With this report, we present results comparing the hemodynamic effects of various stimulation sites for CRT in the failing Fontan patient.
In conclusion, CRT might be a valid therapeutic option for failing Fontan patients due to poor myocardial function. Further follow-up and larger studies are needed to prove the long-term benefits of CRT in these patients, who otherwise would be listed for heart transplantation.
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Acknowledgments
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We would like to thank Dr Jan Janou
ek, Leipzig, Germany, for valuable suggestions and comments.
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References
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- Kiaffas MG, Van Praagh R, Hanioti C, Green DW. The modified Fontan procedure: morphometry and surgical implications Ann Thorac Surg 1999;67:1746-1753.[Abstract/Free Full Text]
- Mitchell MB, Campbell DN, Boucek MM. Heart transplantation for the failing Fontan circulation Semin Thorac Cardiovasc Surg Pediatr Card Surg Ann 2004;7:56-64.
- Bacha EA, Zimmerman FJ, Mor-Avi V, et al. Ventricular resynchronization by multisite pacing improves myocardial performance in the postoperative single-ventricle patient Ann Thorac Surg 2004;78:1678-1683.[Abstract/Free Full Text]
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Abstract
Introduction
