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Peripartum cardiomyopathy: recent insights in its pathophysiology
Denise Hilfiker-Kleiner1, Karen Sliwa, Helmut Drexler
1Department of Cardiology and Angiology, Hannover Medical School, D-30625 Hannover, Germany. hilfiker.denise@mh-hannover.de
Insights
Peripartum/Postpartum cardiomyopathy (PPCM) involves inflammation and oxidative stress. Inhibiting prolactin, a hormone linked to PPCM development, shows promise for prevention and treatment.
Area of Science:
- Cardiology
- Endocrinology
- Reproductive Medicine
Background:
- Peripartum/Postpartum cardiomyopathy (PPCM) is a severe heart condition with unknown causes.
- Pathophysiology involves inflammation, autoimmunity, apoptosis, and microvascular dysfunction.
- Emerging evidence links PPCM to oxidative stress and prolactin cleavage.
Purpose of the Study:
- To review current knowledge on PPCM risk factors, pathomechanisms, and treatments.
- To highlight the role of prolactin cleavage in PPCM development.
- To discuss bromocriptine as a potential therapeutic agent.
Main Methods:
- Review of existing clinical and experimental data on PPCM.
- Analysis of the role of oxidative stress and prolactin in PPCM.
- Examination of bromocriptine's effects in PPCM models and early clinical studies.
Main Results:
- Prolactin cleavage into an antiangiogenic factor is a potential PPCM pathomechanism.
- Bromocriptine, by inhibiting prolactin, prevented PPCM in an animal model.
- Early clinical data suggest bromocriptine is a promising treatment for PPCM.
Conclusions:
- Prolactin inhibition may be a novel therapeutic strategy for PPCM.
- Further research is warranted to confirm bromocriptine's efficacy and safety.
- Understanding PPCM's specific pathomechanisms is crucial for effective treatment.
Abstract:
Peripartum/Postpartum cardiomyopathy (PPCM) is a serious, potentially life-threatening heart disease of uncertain etiology in previously healthy women. Previous clinical and experimental data have identified inflammation, autoimmune processes, apoptosis, and impaired cardiac (systemic) microvasculature as typical features in the pathophysiology of PPCM. However, recent data have shown that unbalanced peri/postpartum oxidative stress is linked to proteolytic cleavage of the nursing hormone prolactin into a potent antiangiogenic, proapoptotic, and pro-inflammatory factor. These observations strongly suggest that prolactin cleavage can operate as a specific pathomechanism for the development of PPCM. Consistent with these findings, inhibition of prolactin secretion by bromocriptine, a dopamine D2 receptor agonist, prevented the development of PPCM in an animal model of PPCM, and first clinical experience are promising in this respect. Thus, inhibition of prolactin release may represent a novel specific therapeutic approach to either prevent or treat patients with acute PPCM. In this review, we are highlighting the current knowledge on risk factors, potential pathomechanisms, and treatment options for PPCM.
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