Journal of Interventional Cardiac Electrophysiology

, Volume 25, Issue 1, pp 53–57

Ventricular arrhythmias originating from the epicardial ventricular outflow tract complicated with peripartum cardiomyopathy

Authors

    • Division of Cardiovascular DiseaseUniversity of Alabama at Birmingham
  • H. Thomas McElderry
    • Division of Cardiovascular DiseaseUniversity of Alabama at Birmingham
  • Masahiro Muto
    • Division of CardiologyAichi Prefectural Cardiovascular and Respiratory Center
  • Taro Okada
    • Division of CardiologyAichi Prefectural Cardiovascular and Respiratory Center
  • Yoshimasa Murakami
    • Division of CardiologyAichi Prefectural Cardiovascular and Respiratory Center
  • Harish Doppalapudi
    • Division of Cardiovascular DiseaseUniversity of Alabama at Birmingham
  • Andrew E. Epstein
    • Division of Cardiovascular DiseaseUniversity of Alabama at Birmingham
  • Vance J. Plumb
    • Division of Cardiovascular DiseaseUniversity of Alabama at Birmingham
  • G. Neal Kay
    • Division of Cardiovascular DiseaseUniversity of Alabama at Birmingham
CASE REPORT

DOI: 10.1007/s10840-008-9325-z

Cite this article as:
Yamada, T., McElderry, H.T., Muto, M. et al. J Interv Card Electrophysiol (2009) 25: 53. doi:10.1007/s10840-008-9325-z

Abstract

We report two cases undergoing electrophysiological studies for ventricular arrhythmias (VAs) associated with peripartum cardiomyopathy. Those two cases demonstrated that subsequent pregnancies might result in deterioration of VAs even though they exhibit no symptoms of heart failure. Those findings may clinically impact the decision making when women with a history of peripartum cardiomyopathy desire to become pregnant again. The VA foci in both cases were determined or suggested to be in the epicardium of the ventricular outflow tract from the results of the catheter ablation and electrophysiological study. Therefore, catheter ablation of those VAs may be feasible but challenging.

Keywords

Ventricular arrhythmiaEpicardialVentricular outflow tractPeripartum cardiomyopathyRadiofrequency catheter ablation

1 Introduction

Peripartum cardiomyopathy is a rare life-threatening cardiomyopathy of unknown cause that occurs in the peripartum period in previously healthy women [1, 2]. Though there have been isolated case reports describing ventricular arrhythmias (VAs) associated with this cardiomyopathy, [3, 4] the details about those arrhythmias remain unknown. We report two cases with those VAs that underwent an electrophysiologic study.

2 Case 1

A 30-year-old woman was referred because of a reduced left ventricular systolic function (ejection fraction = 45%) and non-sustained ventricular tachycardia (NSVT). She had been diagnosed with peripartum cardiomyopathy and frequent multifocal PVCs (12,000 beats/day) after the delivery of her second child. Six months after the diagnosis, her left ventricular systolic function had normalized (ejection fraction = 58%). One year after the diagnosis, she had a new pregnancy and NSVT with pre-syncope was documented. Though she had no symptoms associated with heart failure, she underwent abortion. Written, informed consent was obtained, and an electrophysiologic study was performed after all antiarrhythmic drugs had been discontinued for more than at least five half-lives prior to the study.

At baseline, there were frequent PVCs, and multifocal PVCs were recognized. All the PVCs exhibited a left bundle branch block and right inferior axis QRS morphology and the precordial transition zone varied between leads V3 and V4. None of those PVCs exhibited any electrocardiographic characteristics that suggested an epicardial origin [5, 6]. The main PVCs with a precordial transition zone between leads V3 and V4 were identical to the documented NSVT (Fig. 1). Electroanatomic mapping was performed using a 7-French, 4-mm tip non-irrigated ablation catheter (Navi-Star™, Biosense Webster, Diamond Bar, CA, USA) through a long sheath (8-French, SR0™, St. Jude Medical, AF Division, Minnetonka, MN, USA) via the right femoral vein with the main PVC as the target as previously reported [7]. That revealed two separate sites with early ventricular activation preceding the QRS onset at the antero-septal aspect of the RVOT (Fig. 2). Pacing at the lower site (site 1) with the earliest ventricular activation of −18 ms relative to the QRS onset did not exhibit an excellent pace map (Fig. 1), and pacing at the upper site (site 2) with a ventricular activation of −16 ms relative to the QRS onset did not capture the myocardium even with the maximum output. The voltage map of the RVOT revealed a low voltage area in the peri-pulmonary valvular and anterior walls and those two sites with early ventricular activation were located within the low voltage area (Fig. 3). Mapping of the left ventricular outflow tract (LVOT) was then performed using the same ablation catheter via the right femoral artery, but no early ventricular activation preceding the QRS onset was found in the LVOT. Following that, mapping within the great cardiac vein (GCV) was performed using a 2-Fr octapolar electrode catheter (Pathfinder™, Cardima, Fremont, CA, USA) (Fig. 2). Though during the targeted PVCs, the ventricular activation within the GCV slightly preceded the QRS onset, it was later than that in the RVOT (Fig. 1). Finally, a couple of RF applications with a target temperature of 60°C and maximum power output of 50 W were delivered at sites 1 and 2, resulting in no interruption of the PVCs (Fig. 2). At this point, an epicardial approach by a pericardial puncture was considered. However, the patient refused the proposal of that approach and the session was ended. No complications occurred. The patient also refused the proposal to implant an implantable cardioverter defibrillator and has been followed up with the administration of amiodarone and a beta-blocker.
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Fig. 1

Twelve-lead electrocardiograms and cardiac tracings showing the ablation (ABL) site in case 1. ABL The ablation catheter, GCV the mapping catheter within the great cardiac vein, PM pace map, PVC premature ventricular contraction, SR sinus rhythm, V-QRS the local ventricular activation relative to the QRS onset; X d(m,p) the distal (mid, proximal) electrode pair of the relevant catheter

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Fig. 2

An electroanatomic map obtained during the targeted PVCs (left) and fluoroscopic images exhibiting the ablation sites (right) in case 1. LAO The left anterior oblique view, PA-CAU posteroanterior-caudal, PV pulmonary valve, RAO the right anterior oblique view. The other abbreviations are as in Fig. 1

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Fig. 3

A voltage map of the right ventricular outflow tract in case 1. The purple and red indicate the areas with a voltage of the local bipolar electrogram > = 1.5 mV and < = 0.5 mV, respectively. The abbreviations are as in Fig. 2

3 Case 2

A 43-year-old woman had three pregnancies in the past, with complications of preeclampsia and peripartum cardiomyopathy with the last pregnancy about 10 years ago. She also sometimes had short episodes of palpitations for over 7 years. After she had a new pregnancy, the palpitation attacks became worse, but she had no symptoms associated with heart failure. Because she was diagnosed with supraventricular tachycardia, frequent PVCs (right bundle branch block and a right inferior axis QRS morphology, more than 20,000 beats/day) and a reduced left ventricular systolic function (ejection fraction = 25%), she was referred for catheter ablation. Written, informed consent was obtained, and an electrophysiologic study was performed after all antiarrhythmic drugs had been discontinued for more than at least five half-lives prior to the study.

At baseline, the 12-lead electrocardiogram exhibited bigeminal PVCs with a left bundle branch block and right inferior axis QRS morphology and no pre-excitations during sinus beats (Fig. 4). In our laboratory, the transition zone during the electrophysiological study sometimes differed from that before the catheter ablation probably because the right precordial leads were positioned superior to the typical position, where a cutaneous pad for extrathoracic cardioversion was placed (Fig. 4). For mapping and pacing, multipolar electrode catheters were positioned in the coronary sinus (CS), His bundle (HB) region and right ventricular apex. Supraventricular tachycardia was induced by programmed ventricular stimulation and diagnosed as atrioventricular reciprocating tachycardia. Successful ablation of the accessory pathway could be achieved at the right posterior septum without any complications. Next, mapping of the PVCs was performed. Because ventricular activation preceding the QRS onset was never obtained in the right ventricular outflow tract, mapping of the LVOT was then performed using 7-French, 4-mm tip non-irrigated ablation catheter (Celsius™, Biosense Webster, Diamond Bar, CA, USA) via the right femoral artery. Although the earliest ventricular activation which preceded the QRS onset by 17 ms was obtained in the left coronary cusp, pacing at that site did not exhibit an excellent pace map (Figs. 4 and 5). The CS catheter was then advanced to the GCV and the earlier ventricular activation which preceded the QRS onset by 33 ms was recorded from the distal electrode pair of the CS catheter (Fig. 5). Pacing at that site exhibited an excellent pace map (Fig. 4). The CS catheter was pulled back and instead the ablation catheter was introduced into the GCV via the right jugular vein. An RF application with a target temperature of less than 55°C and power output titrated up to 30 W was then delivered at the earliest ventricular activation site in the GCV, resulting in the elimination of the PVCs. Only fluoroscopic imaging was used and no cineography images were recorded in order to reduce the X ray exposure to the pregnant patient. No complications occurred. Soon after the procedure, the patient underwent an abortion because the early interruption of the pregnancy might prevent any progression of her cardiomyopathy. During more than 3 months of follow-up, the patient has been free of any supraventricular or ventricular arrhythmic episodes. However, echocardiographic examination performed 3 months after the procedure, revealed no improvement in her left ventricular systolic function.
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Fig. 4

Twelve-lead electrocardiograms in case 2. Note that the QRS morphologies of the PVCs differed during baseline and the electrophysiological study because the right precordial leads were positioned superior to the typical position, where a cutaneous pad for extrathoracic cardioversion was placed during the study. LCC Left coronary cusp. The other abbreviations are as in Fig. 1

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Fig. 5

The successful ablation site in case 2. The white line indicates the angiographic catheter deployed in the ostium of the left coronary artery. HB His bundle, RV right ventricle. The other abbreviations are as in the previous figures

4 Discussion

The long-term outcome of peripartum cardiomyopathy mainly depends on the recovery of the left ventricular function. Approximately half of the patients recover completely [1, 2]. However, patients whose left ventricular dysfunction does not resolve within 6 months following delivery are known to have an extremely high mortality rate [1, 3, 8]. Additionally, it has been reported that in women who have had peripartum cardiomyopathy, subsequent pregnancies may be associated with deleterious fetal and maternal outcomes such as premature delivery and maternal cardiac dysfunction, including symptomatic heart failure and even death [8]. However, to the best of our knowledge, there have been no reports describing the effect of subsequent pregnancies on VAs in women with a history of peripartum cardiomyopathy. In the first case in this report, a subsequent pregnancy led to the PVCs developing into NSVT. In the second case, even in the absence of heart failure, the atrioventricular reciprocating tachycardia might have been accentuated by the triggering PVCs which became worse during the progression of the peripartum cardiomyopathy due to the subsequent pregnancy. Therefore, the present cases demonstrated that subsequent pregnancies might result in deterioration of VAs in those women. This report may clinically impact the decision making when those women desire to become pregnant again. Because the present cases exhibited no symptoms associated with heart failure, the deterioration of the VAs might not have been caused by peripartum cardiomyopathy. However, in the first case, the arrhythmogenic substrate of the VAs was suggested to be located within the damaged myocardium with a low voltage. Additionally, it has been demonstrated that in women who have had peripartum cardiomyopathy, subsequent pregnancies may cause asymptomatic reworsening of the left ventricular dysfunction [8]. Therefore, we believe that in the present cases, the deterioration of the VAs might have preceded the decompensation of the heart failure or may have occurred in the cases with asymptomatic reworsening of the left ventricular dysfunction.

In this report, all VA foci in both cases were determined or suggested to be in the ventricular outflow tract by the results of the catheter ablation and electrophysiological study. In Palma et al.’s report, a foci of NSVT associated with peripartum cardiomyopathy was found in the anterior wall of the right ventricle [3]. However, the 12-lead electrocardiogram of the VAs associated with peripartum cardiomyopathy in Gemici et al.’s report was very similar to that in the first case in this report [4]. Those findings suggested that the foci of the VAs associated with peripartum cardiomyopathy may be likely to be in the ventricular outflow tract even though peripartum cardiomyopathy is normally a diffuse myocardial disease and not region-specific like the other cardiomyopathies.

The VAs during the acute phase of peripartum cardiomyopathy may be expected to resolve as the left ventricular function recovers [4]. However, in VAs with peripartum cardiomyopathy without recovery of the left ventricular function, catheter ablation may be considered as an optional therapy to improve the prognosis as is the case with the other non-ischemic cardiomyopathies [9, 10]. In the first case of this report, an epicardial focus of the VAs with multiple endocardial breakout sites was suggested by the epicardial and endocardial mapping, and in the second case, the focus of the PVCs was determined to be epicardial by that being the successful ablation site. To the best of our knowledge, this is the first report that has demonstrated epicardial VA foci associated with peripartum cardiomyopathy from the electrophysiologic findings. In Palma et al.’s report, the results of the catheter ablation and histopathological analyses suggested an epicardial foci of the NSVT [3]. Those findings suggest that foci of the VAs associated with peripartum cardiomyopathy may likely be epicardial. Therefore, catheter ablation of VAs associated with peripartum cardiomyopathy may be feasible but challenging.

Copyright information

© Springer Science+Business Media, LLC 2008