Ventricular arrhythmias originating from the epicardial ventricular outflow tract complicated with peripartum cardiomyopathy
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- Yamada, T., McElderry, H.T., Muto, M. et al. J Interv Card Electrophysiol (2009) 25: 53. doi:10.1007/s10840-008-9325-z
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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.
KeywordsVentricular arrhythmiaEpicardialVentricular outflow tractPeripartum cardiomyopathyRadiofrequency catheter ablation
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.
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.
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 . 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 . 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 . 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 . 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 . 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 . 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.