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Peripartum Cardiomyopathy in Atrial Septal Defect and Eisenmenger Syndrome

Author : Y.S. Pratama, M.A. Nugroho
Upload Date : 19-04-2018

Introduction: Atrial Septal Defect (ASD) can present at any age and account for approximately 10% of all congenital heart lesions and left ventricular (LV) failure is an exceedingly rare presentation. Although LV strain indicated any LV functional reduction, left heart failure with severe reduce ejection fraction is uncommon features.

Case Presentation: A 23 years old pregnant women, primipara at 30 weeks’ gestation was referred because shortness of breath. She didn’t have sign and symptom of heart disease before. Physical examination denoted rales in 1/3 basal of chest, murmur in left lower sternal border, louder P2 sound, clubbing finger and edema in lower extremity with 80% saturation in room air. She had already performed echocardiography examination in another hospital and indicated ASD with bidirectional shunt with 23 mm in diameter, RA, RV dilatation, LVEF 68% (Teichz), TAPSE 27 mm, severe tricuspid regurgitation and high probability for pulmonary hypertension. She was planned to termination at 35 week’s gestation. After delivery sign of congestion developed with saturation only 70% in room air. Two days after, MSCT was performed because sign of hemiparesis and indicated non-hemorrhagic stroke. We decided to administered heparin 15.000 U/24 hours and aspirin. At fourth day after delivery we found left ventricular function depressed, hypokinetic in all segment with LVEF 30%. We start to give diuretic, ACE inhibitor and B-blocker. At day 10 after delivery, clinical condition improves and patient discharge.

Discussion: Severe LV systolic dysfunction is uncommon features in ASD. Recent studies using spackle tracking in Eisenmenger show that patients with Eisenmenger syndrome presented with reduced global LV longitudinal strain and RV free-wall longitudinal and transverse strain. Abnormal LV distensibility, passive elastic stiffness, diastolic dysfunction and volume overload in the RV probably is the causes of elevated LV filling pressure and genesis of left heart failure. In this case LV function improving with heart failure treatment. Coincidence between congenital shunt and severe LV systolic dysfunction that worsening rapidly after delivery suggest peripartum cardiomyopathy as a possible cause.

Conclusion: Severe LV systolic dysfunction with rapid worsening in ASD is uncommon and considered another factor in this phenomenon. We propose that peripartum cardiomyopathy is a possible cause in this case.

KEYWORDS : atrial septal defect, LV systolic dysfunction, Eisenmenger, peripartum cardiomyopathy


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