Association Of Preeclampsia And Peripartum Cardiomyopathy

Author Information

Thakare R*, Joshi A**, Gupta AS***
(* Third Year Resident, ** Senior Resident, *** Professor, Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)


Peripartum cardiomyopathy (PPCM) is a rare occurrence, preeclampsia being one of the associated high risk factors. We had a 27 year old primigravida with preeclampsia admitted at 31 weeks and 5 days of gestation for evaluation. She had an intrauterine fetal demise for which an induction of labor was done. She delivered vaginally. Immediate post delivery she went into cardiac failure with left ventricular ejection fraction of 20%. Diagnosis of peripartum cardiomyopathy was made by exclusion. She was managed in cardiac intensive care unit. She responded to the treatment well and was discharged subsequently.


Pre-eclampsia is a common complication in later months of pregnancy and has a wide spectrum of symptoms. Peripartum cardiomyopathy is a rare but dreadful complication of pregnancy. The diagnosis is by exclusion of other causes of cardiomyopathy. An association has been noted between peripartum cardiomyopathy and pre-eclampsia. Its diagnosis requires left ventricular ejection fraction (LVEF) of less than 45% diagnosed for the first time either in the later month of pregnancy or in the first 5 weeks post-partum. Unless the LV systolic function is normalized, this condition has a high recurrence rate.

Case Report

A 27 year old primigravida was admitted at 31 weeks and 5 days of gestation in view of newly diagnosed pre eclampsia with intrauterine growth restriction for evaluation. She was antenatally registered at 18 weeks of gestation, had regular antenatal visits, received 3 doses of injection tetanus toxoid, hematinics and calcium. She came to outpatient department at 31.5 weeks of gestation with a high BP reading of 150/90 mm of Hg and urine albumin of +4; detected for the first time. She was admitted for further evaluation.
On admission, she was afebrile, pulse was 80 beats per minute regular with good volume, blood pressure was 140/80 mm of Hg. Systemic examination was normal. No premonitory symptoms were reported, bilateral knee jerks were normal and urine albumin was +2. Per abdomen, uterus was relaxed, 28-30 weeks by fundal height and fetus was with a vertex presentation. Fetal heart sounds (FHS) were 140 bpm regular. On per vaginum examination cervical os was closed and uneffaced. PIH profile was sent (Hemoglobin was 13.1gm%, platelet count was 1.8 lac/cmm, BUN was 12.0 mg/dl, creatinine was 1.0 mg/dl, SGOT and SGPT were 24 U/L and 18U/L respectively) and all serological and biochemical parameters were within normal limits. She was started on T. Aspirin 75 mg OD and C. Nifedepin 5 mg QID. Blood pressure was controlled and monitoring was continued. On day 6 of admission fetal heart sounds were not heard and intrauterine fetal demise was confirmed on ultrasound. At that time, her general condition was fair, afebrile, pulse was regular and had good volume, blood pressure was 140/90 mm of Hg. Systemic examination was normal. Premonitory symptoms were present with brisk knee jerks, urine albumin was +2. Per abdomen uterus was 28 -30 weeks, vertex presentation, relaxed. FHS were absent. On vaginal examination external os admitted one finger, internal os closed. Repeat PIH profile was also normal (Hemoglobin 11.3 gm%, platelet count 1.7 lacs/, BUN 12.2 mg%, creatinine 0.9 mg%, SGOT 21U/L, SGPT 29U/L). Inj. Magnesium sulphate by Zuspan’s regimen was started and pre induction cervical ripening was done with dinoprostone gel method. She was monitored throughout the labor. Labor augmentation was done with oxytocin. On per abdominal examination, uterus was tonically contracted. In view of clinical suspicion of (concealed) abruption and to prevent further increase in abruption, artificial rupture of membranes was done and liquor was found to be clear. Symphysio-fundal height and abdominal girth monitoring was done and one unit of blood was transfused. Duration of first stage of labor was around 12 hours and that of second stage was 1 hour. She delivered vaginally. Retroplacental clot of approximately 350 cc was expelled out. Active management of third stage of labor was done but fluid overload was avoided. Immediately post delivery she had tachycardia 118/ min, saturation was 99% on oxygen (O2) by mask and in propped up position. One more unit of blood transfusion was transfused slowly. One hour later she continued to have tachycardia 120 beats/ min, tachypnea of 30 breaths/ min and she started bringing out pink frothy sputum. Magnesium sulphate administration was stopped, intravenous frusemide 40 mg was given and physician was called urgently. DIC profile was sent, D-dimer value was raised and rest of the coagulation profile was within normal limits. Fresh PIH profile was sent and total leucocyte count was found to be raised. Physician evaluated her and she was admitted in the medical ICU for suspected pulmonary edema for further management. Considering pulmonary embolus as a possible diagnosis a computed tomography pulmonary angiogram (CTPA) was done which showed no evidence of pulmonary embolism. Urgent 2D echocardiogram done showed an ejection fraction of 20%, mild MR and mild TR. Autoimmune profile was done and was found to be negative. Diagnosis of sepsis with peripartum cardiomyopathy was made and she was shifted to cardiac ICCU and kept on O2 and inotropic support. She was started on diuretics, beta blockers, ACE inhibitors and higher antibiotics. She had repeated fever spikes in post partum period (from day 5-7) which settled on intravenous antibiotics (piperacillin and tazobactum, metronidazole). Fever profile was negative. She responded to the management. Repeat 2D echo was done 10 days later and it showed EF of 30%. She was observed for any signs of decompensation. No further fever spikes were noted and patient was discharged 2 weeks later on lactation suppression. On discharge she was counselled regarding the possible consequences and need of pre-conceptional cardiology evaluation and if necessary a repeat 2D echocardiography before planning her next pregnancy. She followed up after discharge and was asymptomatic and well.


Preeclampsia is known to be a common condition associated with pregnancy which can prove fatal. PPCM is a rare but dreaded complication of pregnancy with an incidence of 1:4000 deliveries.[1] The echocardiographic criteria to diagnose PPCM consists of a left ventricular ejection fraction (LVEF) below 45%, left ventricular fractional shortening below 28% and a left ventricular end diastolic dimension greater than 5.5 cm or greater than 2.7 cm/m2.[2] It is a myocardial disorder of unknown cause, characterized by left ventricular systolic dysfunction. The heart failure usually develops towards end of the pregnancy or in the first few months postpartum in women without prior history of heart disease and in absence of an identifiable cause for heart failure.[2,3] Pregnancy induced hypertension is one of the risk factors others being inflammatory changes, viral myocarditis and immune mediated, though the etiology is not completely understood. PPCM can be considered as a part of  the spectrum of hypertensive heart failure of pregnancy which is characterized by the heart failure associated with any type of hypertension in pregnancy (either chronic hypertension, gestational hypertension, preeclampsia, eclampsia or preeclampsia superimposed on chronic hypertension) occurring in peripatum period in the absence of any identifiable cause and pre existing heart disease. Hull and Hidden first described an association between postpartum heart failure and hypertension in 1938 when > 85% of cases of “toxic’ postpartal” heart disease were associated with hypertension.[4] While describing PPCM, Demakis and Rahimtoola have reported that “toxemia,” (term for preeclampsia) was detected in 22% of the study subjects.[5] The anti-angiogenic factors which are elevated in pre-eclampsia may cause an angiogenic imbalance in susceptible patients and may trigger the development of peripartum cardiomyopathy. These patients present with symptoms of congestive cardiac failure (pulmonary edema, basal crepts, pedal edema, raised jugular venous pressure) or with pulmonary symptoms (tachypnea, dyspnea and cough). Association of PPCM with pre eclampsia can be considered responsible for the extremes of low ejection fractions resulting from the increased workload placed on an already failing ventricle. For the same reason, there is a rapid improvement in left ventricular function once pre-eclampsia starts to resolve post delivery.
The management of PPCM is same as of other types of non-ischaemic dilated cardiomyopathy, drugs safe in pregnancy and lactation should be selected. Approximately 30–50 % of the patients recover completely with normal LV systolic function at rest.[6] However, the risk of recurrence of PPCM is high.[6] If the disease persists after 6 months, it indicates irreversible cardiomyopathy with poor prognosis.[7]


When symptoms and signs of heart failure appear in a pre eclamptic woman, peripartum cardiomyopathy should be considered as a differential diagnosis. This condition requires high degree of suspicion, prompt diagnosis and multi disciplinary approach for successful outcome. Preconceptional counselling and assessment of cardiac function prior to next pregnancy is also very important.

  1. Brar SS, Khan SS, Sandhu GK, Jorgensen MB, Parikh N, Hsu JW, et al. Incidence, mortality, and racial differences in peripartum cardiomyopathy. Am J Cardiol 2007;100(2): 302–304.
  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 Recommendations and Review. JAMA 2000; 283(9): 1183–1188.
  3. Sliwa K, Hilfiker-Kleiner D, Petrie MC, Mebazaa A, Pieske B, Buchmann E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Working Group on peripartum cardiomyopathy. Eur J Heart Fail 2010; 12(8):767–778.
  4. Hull E, Hidden E. Postpartal heart failure. Southern Med J. 1938;31(3):265–70   
  5. Demakis JG, Rahimtoola SH. Peripartum cardiomyopathy. Circulation. 1971;44:964–8.
  6. Ramaraj R, Sorrell VL. Peripartum cardiomyopathy: causes, diagnosis, and treatment. Cleveland Clinic Journal of Medicine. 2009;76(5):289–296.
  7. Mehta NJ, Mehta RN, Khan IA. Peripartum Cardiomyopathy: Clinical and Therapeutic Aspects. Angiology. 2001;52(11):759–62.

Thakare R, Joshi A, Gupta AS. Association Of Preeclampsia And Peripartum Cardiomyopathy. JPGO Volume 5 No.7. Available from: