Breastfeeding, Cellular Immune Activation, and Myocardial Recovery in Peripartum Cardiomyopathy

The etiology of peripartum cardiomyopathy remains unknown. One hypothesis is that an increase in the 16-kDa form of prolactin is pathogenic and suggests that breastfeeding may worsen peripartum cardiomyopathy by increasing prolactin, while bromocriptine, which blocks prolactin release, may be therap...

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Detalles Bibliográficos
Autores principales: Koczo, Agnes, Marino, Amy, Jeyabalan, Arun, Elkayam, Uri, Cooper, Leslie T., Fett, James, Briller, Joan, Hsich, Eileen, Blauwet, Lori, McTiernan, Charles, Morel, Penelope A., Hanley-Yanez, Karen, McNamara, Dennis M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
CLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6609998/
https://www.ncbi.nlm.nih.gov/pubmed/31312753
http://dx.doi.org/10.1016/j.jacbts.2019.01.010
Descripción
Sumario:The etiology of peripartum cardiomyopathy remains unknown. One hypothesis is that an increase in the 16-kDa form of prolactin is pathogenic and suggests that breastfeeding may worsen peripartum cardiomyopathy by increasing prolactin, while bromocriptine, which blocks prolactin release, may be therapeutic. An autoimmune etiology has also been proposed. The authors investigated the impact of breastfeeding on cellular immunity and myocardial recovery for women with peripartum cardiomyopathy in the IPAC (Investigations in Pregnancy Associated Cardiomyopathy) study. Women who breastfed had elevated prolactin, and prolactin levels correlated with elevations in CD8(+) T cells. However, despite elevated prolactin and cytotoxic T cell subsets, myocardial recovery was not impaired in breastfeeding women.

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