Pregnancy-related hypertension (eclampsia and preeclampsia) is discussed in Chapter 19.
1. CARDIOMYOPATHY OF PREGNANCY (PERIPARTUM CARDIOMYOPATHY)
In approximately 1 in 3000 to 4000 live births, dilated cardiomyopathy develops in the mother in the final month of pregnancy or within 6 months after delivery. Risk factors include preeclampsia, twin pregnancies, and African ethnicity. The cause is slowly being elucidated. The vasculo-hormonal hypothesis requires two events. One is genetic, a reduction in a STAT3 transcription factor that results in cleavage of prolactin from the pituitary by cathepsin D. This results in a 16-kd fragment that increases microRNA 146a that results in myocardial apoptosis. The second is from the placenta, soluble tyrosine kinase that blocks VEGF (vascular endothelial growth factor). It appears both components may be necessary to effectively result in peripartum cardiomyopathy. The course of the disease is variable; most cases improve or resolve completely over several months, but others progress to refractory heart failure. About 60% of patients make a complete recovery. Serum BNP levels are routinely elevated in pregnancy, but serial values may be useful in predicting who may be at increased risk for a worse outcome. Beta-blockers have been administered judiciously to these patients, with at least anecdotal success. Diuretics, hydralazine, and nitrates help treat the heart failure with minimal risk to the fetus. Sotalol is acceptable for ventricular or atrial arrhythmias if other beta-blockers are ineffective. Some experts advocate anticoagulation because of an increased risk of thrombotic events, and both warfarin and heparin have their proponents. In severe cases, transient use of extracorporeal oxygenation (ECMO) has been lifesaving. Recurrence in subsequent pregnancies is common, particularly if cardiac function has not completely recovered, and subsequent pregnancies are to be discouraged if the EF remains less than 55%. The risk of recurrent heart failure in a subsequent pregnancy has been estimated to be about 1 in 5 (21%). Delivery of the baby is important, though the peak incidence of the problem is in the first week after delivery and a few cases appear up to 5 weeks after delivery. Since the anti-angiogenic cleaved prolactin fragment is considered causal for peripartum cardiomyopathy, bromocriptine (a prolactin release inhibitor) has been reported to be beneficial. A multicenter trial in Europe found LVEF improved to a greater extent in patients with peripartum cardiomyopathy who were given bromocriptine than those who were not given bromocriptine. In addition, bromocriptine treatment was associated with high rate of full LV recovery and low morbidity and mortality in peripartum cardiomyopathy patients compared with other peripartum cardiomyopathy cohorts not treated with bromocriptine.
et al. Peripartum cardiomyopathy. Circulation. 2016 Apr 5;133(14):1397–409.
et al. Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study. Eur Heart J. 2017 Sep 14;38(35):2671–9.
et al. Peripartum cardiomyopathy. BMJ. 2019 Jan 30;364:k5287.