A 29‐year‐old African American woman presented to the emergency room complaining of dyspnea on exertion and orthopnea of 2 weeks' duration. Her symptoms progressed gradually over this period and worsened to include paroxysmal nocturnal dyspnea prior to admission. She also complained of chest pressure and nonproductive cough. She denied diaphoresis, night sweats, palpitations, recent infections, or sick contacts. The patient had a history of peripartum cardiomyopathy (PPCM) with similar but more severe presentation, which was diagnosed in 2004 and initially treated with carvedilol, lisinopril, furosemide, spironolactone, and digoxin. She discontinued all medications in 2005 when her symptoms resolved and had no recurrence until the present episode. Her physical exam was notable for tachycardia, pulmonary crackles, and pitting edema. Serum BNP was 271, troponin was >0.01, qualitative urine B‐hCG was negative, and chest x‐ray showed pulmonary vascular congestion and enlarged cardiac silhouette. Her ejection fraction on echocardiogram was 20%–25% (vs. 15% during her initial episode). Because her PPCM had been asymptomatic for more than 7 years, alternative etiologies for her dilated cardiomyopathy were explored. Hemoglobin A1c, fasting lipid panel, urine toxicology screen, TSH with free T4, HIV, acute hepatitis panel, coxsackie B virus antibodies, ferritin, B1, carnitine, selenium, and ANA were ordered. Results, however, did not support an ischemic, toxic, infectious, autoimmune, or nutrient deficiency–related etiology. With a diagnosis of recurrent PPCM, the patient continued to undergo diuresis with complete resolution of her presenting symptoms. She was placed on daily furosemide, carvedilol, and lisinopril for discharge, with close outpatient follow‐up.
PPCM is a type of dilated cardiomyopathy found in previously healthy women in the final month of pregnancy and up to 5 months after delivery. Some mechanisms have been proposed, including viral myocarditis, abnormal immune response to pregnancy, maladaptive hemodynamic changes, stress activated cytokines, excessive prolactin secretion, and prolonged tocolysis; genetic predisposition and nutritional factors have also been explored, but a definitive etiology has not been established. Recovery from PPCM is defined as return of left ventricular ejection fraction to >50% or improvement of >20% and usually occurs 3–6 months postpartum, but can occur as late as 48 months postpartum. Poor prognosis is associated with delayed diagnosis, low ejection fraction, black ethnicity, LV thrombus, multiparity, and comorbidities; the overall mortality is 6%–10%. There is an increased risk of recurrence of PPCM in subsequent pregnancies.
This case is meant to review current knowledge of PPCM and illustrate the need for timely diagnosis and consistent follow‐up in this condition, as highlighted by an unusual recurrence in the absence of pregnancy.
To cite this abstract:Shetty V, Hanson S. What to Expect When You're Not Expecting: Recurrence of Peripartum Cardiomyopathy in a Nonpregnant Patient. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 304. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/what-to-expect-when-youre-not-expecting-recurrence-of-peripartum-cardiomyopathy-in-a-nonpregnant-patient/. Accessed May 24, 2019.