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European Journal of Heart Failure 2005 7(6):1057-1058; doi:10.1016/j.ejheart.2004.11.012
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© 2005 European Society of Cardiology

Pre-eclampsia with acute heart failure postpartum as primary manifestation of systemic lupus erythematosus

P. Hildbranda, C. Eigenmanna, M. Guggerb, H.P. Martic and R. Hullina,*

a Department of Cardiology, University Hospital CH-3010 Bern, Switzerland
b Institute of Pathology, Medical School, University Bern 3010 Bern, Switzerland
c Department of Nephrology, University Hospital 3010 Bern, Switzerland

* Corresponding author. Tel.: +41 31 632 8261; fax: +41 31 632 4560. E-mail address: roger.hullin{at}insel.ch


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Pre-eclampsia occurs in 2–5% of pregnancies of healthy women. Here, we present a rare case of pre-eclampsia with overt acute heart failure, which was the primary manifestation of systemic lupus erythematosus with cardiac and renal involvement.

Key Words: Pre-eclampsia • Overt acute heart failure • Lupus erythematosus

Received July 30, 2004; Revised October 1, 2004; Accepted November 11, 2004


Immediately after pre-term delivery of her 3rd child in the 36th week of gestation, a 34-year-old woman developed severe dyspnea from acute left heart failure associated with hypertension suggesting the differential diagnosis of severe pre-eclampsia or peripartum cardiomyopathy. Otherwise, this pregnancy was remarkable for low birth weight of the newborn (1640 g). The first pregnancy in 1988 had been normal; however, the second pregnancy in 2002 had been also remarkable for a low weight of the term newborn (2430 g). Worth mentioning were two spontaneous abortions in 1999 and 2001 (12th and 7th week of gestation, respectively).

Physical examination 1 day after delivery and following transfer to our care revealed sinus-tachycardia, hypertensive blood pressure (170/90 mm Hg), coarse bilateral pulmonary rales, and a harsh systolic and diastolic heart murmur. Chest X-rays showed massive pulmonary congestion. Blood screen demonstrated a normochrome normocytic anemia (hemoglobin of 11.8 g/L) and a thrombocytopenia of 106,000/mm3. Clinical chemistry was noteworthy for discretely elevated urea and creatinine (7.5 mmol/L, 93 µmol/L), CRP (43 mg/L), BNP (699 pg/mL) and troponin I (1.4 µg/L). Proteinuria one week after delivery was minimal (0.51 g/day) and hematuria was not found.

Transesophageal echocardiography at admission disclosed severe aortic regurgitation, thickened leaflets of the aortic valve and hemodynamically not relevant pericardial effusion. Left ventricular (LV) ejection fraction was reduced to 20%; LV enddiastolic diameter was dilated to 36 mm/m2 (adjusted normal: 26±4 mm/m2). In addition, a distinct but hemodynamically not relevant pericardial effusion was detectable.

Initially, left heart failure was treated with diuretics and intravenous afterload reduction. Subsequently, the renin–angiotensin system was blocked with enalapril and candesartan. With reversal of heart failure, CRP and BNP levels and hematologic parameters returned to normal. Control echocardiography 2 weeks after admission demonstrated normalized LV systolic function and size, and resolution of pericardial effusion. However, moderate aortic insufficiency persisted.

The clinical syndrome of pre-eclampsia consists of hypertension, pre-term delivery, low weight newborn and proteinuria. In our case, pericardial effusion, aortic regurgitation and history of spontaneous abortions suggested underlying autoimmune disease. Clinical suspicion was asserted by high serum titers of antinuclear antibodies (1:1280) and anti-DNA antibodies (817 IE/ml) were compatible with systemic lupus erythematosus (SLE) (Fig. 1a). Anti-cardiolipin antibodies were the only other positive autoantibodies (Fig. 1a) and complement (C3, C4) was normal. The kidney biopsy showed diffuse and global glomerulonephritis with mesangial proliferation and a membrano-proliferative component, compatible with a lupus nephritis of class IV (Fig. 1b). Therefore, immunosuppressive therapy with prednisone and cyclophosphamide was initiated.


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Fig. 1 (a) Table lists positive autoantibodies of the patient. (b) Two glomeruli with an almost global mesangial hypercellularity (arrowhead) and circumferentially thickened capillaries (arrow). Inset: subendothelial amorphous material and splitting of the basement membrane (arrow) (hemalaun and eosin, bar 100 µm, inset: silvermethenamin, bar 10 µm). (c) Thickened cusps of aortic valve. (d) Left ventricle with pericardial effusion.

 
Pre-eclampsia occurs in 2–5% of pregnancies in healthy women [1] but more often (9–32%) in pregnancies of SLE patients [2,3]. In SLE patients, pre-eclampsia is more likely to occur in case of pre-existing renal disease [4], when disease activity is increased at the beginning of pregnancy, or if SLE is associated with an antiphospholipid syndrome [5]. Thus, our patient had two risk factors to develop pre-eclampsia.

Most often, acute heart failure in pregnancy results from ischemia, hypertension, valvular or myocardial disease, whereas peripartum cardiomyopathy is rare and a diagnosis of exclusion [6]. SLE is frequently associated with coronary artery disease [7] or valve insufficiencies [8]. Angiography excluded coronary artery disease, suggesting that acute heart failure in our patient resulted from excessive workload of left ventricle due to valvulopathy, hypervolemia and acute hypertension.

Overall, pre-eclampsia with acute heart failure as primary manifestation of SLE is rare. However, in our patient aortic valve insufficiency, pericarditis and informations from gynecological history entailed specific tests, which not only identified the underlying disease but enabled specific treatment relevant for prognosis.


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  1. Roberts J.M., Cooper D.W. Pathogenesis and genetics of pre-eclampsia. Lancet (2001) 357:53–56.[CrossRef][Web of Science][Medline]
  2. Burkett G. Lupus nephropathy and pregnancy. Clin. Obstet. Gynecol. (1985) 28:310–323.[Web of Science][Medline]
  3. Wolfberg A.J., Lee-Parritz A., Peller A.J., Liebermann E.S. Association of rheumatologic disease with pre-eclampsia. Obstet. Gynecol. (2004) 103(6):1190–1193.[CrossRef][Web of Science][Medline]
  4. Hayslett J.P. Pregnancy complicated by renal disorders. In: Medicine of the fetus and mother—Reece E.A., Hobbins J.C., Mahoney M.J., et al, eds. (1992) Philadelphia: JB Lippincott. 1086–1096.
  5. Branch D.W., Andres R., Digre K.B., Rote N.S., Scott J.R. The association with antiphospholipid antibodies with severe pre-eclampsia. Obstet. Gynecol. (1989) 73:541–545.[Web of Science][Medline]
  6. Hibbard J.U., Lindheimer M., Lang R.M. A modified definition for peripartum cardiomyopathy and prognosis based on echocardiography. Obstet. Gynecol. (1999) 94:311–316.[CrossRef][Web of Science][Medline]
  7. Asanuma Y., Oeser A., Shintani A.K., Turner E., Olson N., Fazio S., et al. Premature coronary-artery atherosclerosis in systemic lupus erythematosus. N. Engl. J. Med. (2003) 349(25):2407–2415.[Abstract/Free Full Text]
  8. Roldan C.A., Shively B.K., Crawford M.H. An echocardiographic study of valvular heart disease associated with systemic lupus erythematosus. N. Engl. J. Med. (1996) 335:1424–1430.[Abstract/Free Full Text]

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