Peripartum cardiomyopathy

Peripartum cardiomyopathy

Peripartum cardiomyopathy is diagnosed when features of dilated cardiomyopathy develops in the last one month of pregnancy or within five months of delivery. Clinically there are features of left ventricular dysfunction of varying severity. Sometimes they present with pulmonary edema or cardiogenic shock. The risk peripartum cardiomyopathy increases with increasing maternal age. Echocardiography documents the severity of left ventricular dysfunction. Peripartum cardiomyopathy constitutes about 4% of all cardiomyopathies. The incidence varies from 1:3000-4000 pregnancies. It is a form of dilated cardiomyopathy and contributes to 9% of maternal mortality. Mortality estimates range from 25-50%. Future pregnancies are better avoided, though safe pregnancies in those who have fully recovered from the left ventricular dysfunction within six months have been reported. Residual left ventricular dysfunction is a definite risk factor for significant worsening in future pregnancies. Even those who have recovered have been shown to have a drop in ejection fraction during future pregnancies.

Role of bromocriptine in the treatment of peripartum cardiomyopathy

Use of bromocriptine for the treatment of peripartum cardiomyopathy has been there for some time. Prolactin can be cleaved into a toxic 16-kDa prolactin fragment (also called vasoinhibin) mediated by oxidative stress. This prolactin fragment has a role in driving peripartum cardiomyopathy [1]. Hence the role of bromocriptine in the treatment of peripartum cardiomyopathy. Suppression of lactation is a concern while using bromocriptine for peripartum cardiomyopathy. 

In a pilot study, 10 patients each with peripartum cardiomyopathy were randomized to open label bromocriptine with standard heart failure care or standard heart failure care alone [2]. One patient died in the bromocriptine group while four died in the control group. Significantly fewer patients in the bromocriptine group experienced the composite end point of poor outcome defined as death, NYHA functional class III/IV or left ventricular ejection fraction <35% at 6 months, compared to controls. Cardiac magnetic resonance imaging did not show any intracardiac thrombi. As the infants of bromocriptine treated mothers could not be breast fed, they were also studied. Infants in both groups showed normal growth and survival. 

German peripartum cardiomyopathy registry has also demonstrated the beneficial outcome with bromocriptine [4]. The study showed a high recovery rate of 96% in patients on a combination of beta-blocker, angiotensin converting enzyme inhibitor/angiotensin receptor blocker and bromocriptine. Positive family history was present in 16.5% of cases. They suggested the role of several biomarkers in peripartum cardiomyopathy including Cathepsin D, the enzyme that generates 16 kDa prolactin fragment.

References

1. Koenig T, Bauersachs J, Hilfiker-Kleiner D. Bromocriptine for the Treatment of Peripartum Cardiomyopathy. Card Fail Rev. 2018 May;4(1):46-49. 
2. Sliwa K, Blauwet L, Tibazarwa K, Libhaber E, Smedema JP, Becker A, McMurray J, Yamac H, Labidi S, Struman I, Hilfiker-Kleiner D. Evaluation of bromocriptine in the treatment of acute severe peripartum cardiomyopathy: a proof-of-concept pilot study. Circulation. 2010 Apr 6;121(13):1465-73. 
3. Haghikia A, Podewski E, Libhaber E, Labidi S, Fischer D, Roentgen P, Tsikas D, Jordan J, Lichtinghagen R, von Kaisenberg CS, Struman I, Bovy N, Sliwa K, Bauersachs J, Hilfiker-Kleiner D. Phenotyping and outcome on contemporary management in a German cohort of patients with peripartum cardiomyopathy. Basic Res Cardiol. 2013 Jul;108(4):366.