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Irreversible Acquired Noncompaction Cardiomyopathy in a Parturient with Corrected Atrial Septal Defect
Abstract Number: F-56
Abstract Type: Case Report/Case Series
Introduction: Left ventricular noncompaction (LVNC) is a rare cardiomyopathy characterized by hypertrabeculations in the left ventricle (LV)(1). Both congenital and acquired cases have been reported(2). Development of hypertrabeculations during pregnancy has been described, with most resolving completely after delivery. We report a case of unresolved pregnancy acquired LVNC cardiomyopathy.
Case presentation: A 33-year-old gravida 2 para 1 woman presented to our high risk obstetric anesthesia service for consultation during her second pregnancy. She was known to have an atrial septal defect (ASD) that had been repaired at the age of 10. Three years before, severe dyspnea during her first pregnancy had been investigated by echocardiography, which demonstrated hypertrabeculations and an LV ejection fraction of 45-50%. Since an echocardiogram performed 3 months prior had been normal, she was diagnosed with acquired LVNC syndrome. A vaginal delivery was attempted, but ventricular arrhythmias and congestive heart failure during labor resulted in an emergency cesarean delivery. Magnetic resonance imaging 2 months later confirmed hypertrabeculations and demonstrated a ratio of the thicker noncompacted endocardial layer (N) and thin epicardial compacted layer (C) (N/C ratio) ≥ 2.0 meeting the criteria for LVNC. Echocardiogram performed prior and during her second pregnancy demonstrated no resolution of her hypertrabeculations or improvement in her LV systolic function, even though she demonstrated only mild symptoms of congestive heart failure. It was decided to deliver this pregnancy by cesarean, which was performed uneventfully at term under epidural anesthesia using transthoracic echocardiography and FloTrac/Vigileo system.
Discussion: The pregnancy acquired hypertrabeculations of LVNC seem to develop at around 30-32 weeks gestation, coinciding with the concomitant increases in fluid volume. Gati et al(6) believe that this increased preload may be the mediator for the development of trabeculations, and report that the majority of cases resolve spontaneously. There were no findings of hypertrabeculations in our patient until dyspnea developed 30 weeks into her first pregnancy, which is consistent with this description. However in our case the hypertrabeculations persisted into a second pregnancy. Of note, her prior history of ASD may suggest that congenital defects unmasked by pregnancy could also have played a role in the development and persistence of the LVNC. Non-compaction cardiomyopathy developed in a parturient can lead to hemodynamic instability and may persist to impact future pregnancies.
1. Jenni R, Oechslin EN, van der Loo B. Isolated ventricular non-compaction of the myocardium in adults. Heart. 2007;93(1):11-5.
2. Munehisa Y, Watanabe H, Kosaka T, Kimura A, Ito H. Successful outcome in a pregnant woman with isolated noncompaction of the left ventricular myocardium. Internal medicine. 2007;46(6):285-9.