Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 7  |  Issue : 6  |  Page : 777-779  

A rare case of peripartum cardiomyopathy


Department of Obstetrics and Gynecology, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India

Date of Web Publication18-Nov-2014

Correspondence Address:
Devika Bharat Bhikane
Ganga Skies, D1 flat no 803, Sant Tukaram Nagar, Pune - 411 018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.144880

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  Abstract 

Peripartum cardiomyopathy (PPCM) is defined as acute onset heart failure without demonstrable cause in the last month of pregnancy or within the first 5 months after delivery. All other causes of dilated cardiomyopathy with heart failure must be systematically excluded before accepting the diagnosis of PPCM. Such a case is reported where a 4th gravida undergoing lower segment caesarean section (LSCS) for pre-eclampsia with abruptio placenta and fetal distress landed up with pulmonary edema and later diagnosed as PPCM. She was diligently managed and subsequently followed up for 6 months and complete reversal of her cardiac function was confirmed.

Keywords: Cardiomyopathy, heart failure, peripartum, ventricular dysfunction


How to cite this article:
Chaudhari S, Gupta P, Bal H, Bhikane DB. A rare case of peripartum cardiomyopathy. Med J DY Patil Univ 2014;7:777-9

How to cite this URL:
Chaudhari S, Gupta P, Bal H, Bhikane DB. A rare case of peripartum cardiomyopathy. Med J DY Patil Univ [serial online] 2014 [cited 2024 Mar 29];7:777-9. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2014/7/6/777/144880


  Introduction Top


Peripartum cardiomyopathy (PPCM) is thought to be a default diagnosis after excluding other causes of heart failure in pregnancy. [1] There is little evidence to substantiate a pregnancy induced etiology. However, the National Heart, Lung, and Blood Institute and the Office of Rare Diseases in the year 2000 laid down certain criteria for its diagnosis. [2] The criteria for diagnosing PPCM are:

  1. Development of cardiac failure in the last month of pregnancy or within five months of delivery,
  2. Absence of an identifiable cause for the cardiac failure,
  3. Absence of recognizable heart disease before the last month of pregnancy, and
  4. Left ventricular (LV) dysfunction (ejection fraction of less than 45% or reduced shortening fraction). [2]


Symptoms of PPCM which include fatigue, edema, dyspnea are similar to those for normal spectrum of peripartum states and pregnancy co-morbidities such as pulmonary embolism and eclampsia. [3] Therefore, diagnosis is often delayed and under recognized with devastating consequences. In view of these a case of peripartum heart failure which was subsequently diagnosed as peripartum cardiomyopathy is reported.


  Case Report Top


A 35-year-old G 4 P 3 L 3 unbooked patient at 35.5 weeks period of gestation report our casualty with abdominal pain and bleeding per vaginam of 1 day duration. She had three full-term normal vaginal deliveries and all her children are alive and healthy without any antenatal and postnatal complication. She had no family history of preeclampsia. Her documents revealed that she was a case of pre-eclampsia and an urgent ultrasonography done showed evidence of abruptio placenta. On examination, she was found to have mild pallor, pulse of 100/min, blood pressure 160/90 mmHg. Obstetric examination revealed uterus of 34 weeks size, firm, tender with cephalic presentation, FHS 106/min, regular. Internal examination showed closed os and cervix uneffaced and fingers stained with dark altered blood. Bedside urine albumin test was found to be 2+. Cardiotocograph showed a nonreassuring fetal heart rate pattern, coagulation profile reports were still awaited. However, a bedside clot observation test was done and found to be normal. Hb was 9gms/dl, all other investigations were within normal limits. The patient was taken up for emergency LSCS in view of pre-eclampsia with fetal distress and abruptio placentae. A female baby of 2.2 kg was delivered. Intraoperatively a fist-sized retroplacental clot was detected. During abdominal closure patient's BP suddenly shot up to 200/120 mmHg and sPO 2 dropped to 84% and chest was full of crepitations, pink frothy sputum was extruding from the endotracheal tube. The patient was managed on the lines of pulmonary edema with Inj frusemide, ventilatory support and abdomen quickly closed. The patient was shifted to ICU on the ventilator. Investigations in ICU revealed radiological evidence of pulmonary edema, Hb- 8.4 gm/dl, platelet count - 80,000/c mm, PT - 15/12, INR 1.7, FDP - 6800 IU/L, raised CPK-MB and positive Trop T. ABG showed reduced PO 2 . A central line was established, 2 units of packed cells and 4 units of FFP were transfused. Fluid was restricted to maintain a CVP of 8 cm of water and Inj frusemide and mechanical ventilation was continued.

On post-op day 2 there was significant resolution of pulmonary edema and the patient was weaned off from the ventilator. The management was continued in collaboration with the physician. A 2D-Echo done on the same day showed global left ventricular hypokinesia with ejection fraction of 35%. Based on the progress of clinical events and above investigations we arrived at a diagnosis of PPCM.

She was continued on symptomatic management with diuretics, digoxin and ACE inhibitors and discharged on post-op day 10. 2D-Echo after 4 weeks showed an improved ejection fraction of 40% and it became 60% after 2 months. She was followed up to 6 months and all parameters remained normal. She was counseled for contraception/sterilization, which she declined.


  Discussion Top


PPCM is a diagnosis of exclusion. [1] Although the left ventricle may not be dilated, the ejection fraction is nearly always reduced below 45%.

The incidence is quoted to be varying from 1 in 15000 to 1 in 4000 deliveries, 75% present within the first month and 45% in the first week postpartum. [2],[4] Up to 7% may present in the last trimester of pregnancy. Risk factors include advanced maternal age, multiparity, multiple gestation, obesity, gestational hypertension, preeclampsia and black race. [4],[5] The etiology is uncertain; viral, autoimmune and idiopathic have been considered. [4],[6] The prognosis of PPCM is related to its presentation as well as to recovery of ventricular dysfunction. [1],[3] ECG is generally within normal limits. However, sinus tachycardia or atrial fibrillation may be there if cardiomyopathy is severe. CPK-MB and Trop-T levels are generally raised. The role of endomyocardial biopsy is controversial.

Outcome is dependent on the ejection fraction and left ventricular end-diastolic volume at diagnosis, response to medical therapy, and normalization of left ventricular function within 6 months of pregnancy. Therapy regimens include diuretics to reduce volume overload (preload), after load reduction with angiotensin-converting-enzyme inhibitors (postpartum only) and beta-blockers after signs and symptoms of congestion have improved. ACE inhibitors should be considered the mainstay of treatment for PPCM after delivery. [7] Digitalis, an inotropic agent, is also safe during pregnancy and may help to maximize contractility and rate control, but serum levels have to be closely monitored since excessive digoxin concentrations in serum have been associated with worse outcomes in women. [8],[9]

Second-generation beta-adrenoreceptor antagonists have beneficial effects in selected patients with dilated cardiomyopathy in the postpartum period in patients who continue to have symptoms and echocardiography evidence of left ventricular compromise despite more than 2 weeks of standard heart failure management. [2] Patients with significantly depressed left ventricular function (ejection fraction ≤35%) may benefit from anticoagulation therapy to prevent thrombosis and emboli. If this treatment is ineffective, more aggressive ventricular support such as intra-aortic balloon counter pulsation or heart transplantation may be considered.

The route of delivery should be preferably vaginal, reserving caesarean section for obstetric indication only.

Mortality rate varies from 7% to 50%. [3] Most common causes for mortality are progressive heart failure, arrhythmia and thromboembolism.

The prospects of future pregnancy should be discussed. 78% of women with fully recovered left ventricular function have a normal outcome. [10] Persistent ventricular dysfunction serves as a relative contra-indication to plan a future pregnancy. However, before planning a subsequent pregnancy, evaluation by cardiologist is recommended. Areas for future research include immune system dysfunction, the role of viruses, nonconventional treatments such as immunosuppressant, immunoadsorption, aphaeresis and antiviral treatment. [11]

Even though PPCM is rare, the aim of reporting this case is to create awareness of this entity, since survival depends upon accuracy of diagnosis and prompt and vigorous treatment of heart failure.

 
  References Top

1.
Nelson-Piercy C. Cardiac disease. In: Luesley DM, Baker PN, editors. Obstetrics and Gynaecology: An Evidence-Based text for MRCOG. 1 st ed. London: Arnold; 2004. p. 54-8.  Back to cited text no. 1
    
2.
Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy. National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendation and review. JAMA 2000;283:1183-8.  Back to cited text no. 2
    
3.
Abboud J, Murad Y, Chen-Scarabelli C, Saravolatz L, Scarabelli TM. Peripartum cardiomyopathy: A comprehensive review. Int J Cardiol 2007;118:295-303.   Back to cited text no. 3
    
4.
Cunningham GF, Gant NF, Leveno KJ, Gilstrap III LC, Hauth JC, Wenstrom KD, editors. Williams Obstetrics. 21 st ed. New York: McGraw-Hill; 2001. p. 1141-514.  Back to cited text no. 4
    
5.
Libby P, Bonow RO, Mann DL, Zipes DP, editors. Braunwald's heart disease: A textbook of cardiovascular medicine. 8 th ed. Philadelphia, PA: Saunders; 2007.  Back to cited text no. 5
    
6.
Heider AL, Kuller JA, Strauss RA, Wells SR. Peripartum cardiomyopathy: A review of the literature. Obstet Gynecol Surv 1999;54:526-31.  Back to cited text no. 6
    
7.
Schubiger G, Flury G, Nussberger J. Enalapril for pregnancy- induced hypertension: Acute renal failure in a neonate. Ann Inter Med 1998;108:215-6.  Back to cited text no. 7
    
8.
Adams KF Jr, Patterson JH, Gattis WA. Relationship of serum digoxin concentration to mortality and morbidity in women in the digitalis investigation group trial: A retrospective analysis. J Am Coll Cardiol 2005;46:497-504.  Back to cited text no. 8
    
9.
Phillips SD, Warnes CA. Peripartum cardiomyopathy: Current therapeutic perspectives. Curr Treat Options Cardiovasc Med 2004;6:481-8.   Back to cited text no. 9
    
10.
Sutton MS, Cole P, Plappert M, Saltzman D, Goldhaber S. Effects of subsequent pregnancy on left ventricular function in peripartum cardiomyopathy. Am Heart J 1991;121:1776-8.  Back to cited text no. 10
    
11.
Sliwa K, Förster O, Libhaber E, Fett JD, Sundstrom JB, Hilfiker-Kleiner D, et al. Peripartum cardiomyopathy inflammatory markers as predictors of outcome in 100 prospectively studied patients. Eur Heart J 2006;27:411-6.  Back to cited text no. 11
    




 

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