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Pathogenesis and Therapy

The etiology of PPCM remains unknown. Many investigators have proposed an inflammatory pathogenesis initiated by the resetting of maternal immune regulation in the early peripartum period (1,2). Recent reports have also suggested that genetic etiologies can be found in a significant subset of PPCM patients, as with other forms of non-ischemic dilated cardiomyopathy (3,4,5). Endomyocardial biopsy (EMB) is rarely performed in PPCM and is usually unremarkable. Despite the proposed inflammatory pathogenesis the frequency of lymphocytic infiltrates is low in most series (10 to 20%) and similar to the prevalence reported in other forms of "acute" cardiomyopathy.

The treatment program for PPCM generally involves standard medical therapy for heart failure (6). Investigations of more targeted therapies specifically for PPCM have focused on the immune pathogenesis (7). Clinical investigations of immune modulatory therapies have been limited to single center series and anecdotal reports and have not been validated in prospective controlled studies. Bromocriptine was recently reported to facilitate recovery of LV function in women with PPCM (8,9). Bromocriptine is a dopaminergic agonist which suppresses prolactin release, and its use in PPCM is based on the role of prolactin in modulating maternal immunity (10). This has been studied extensively in animal models, however clinical reports of recovery in small numbers of PPCM patients must be viewed with caution given the high rate of spontaneous resolution with this disorder (11, 12). Ongoing clinical trials of bromocriptine in Europe and South Africa will hopefully clarify its therapeutic role in PPCM.

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