Key result
Elevated Fas/Apo-1 predicts ~256% higher 6-month mortality in women with peripartum cardiomyopathy.
Odds Ratio: 3.56 (95% CI 1.35–9.42)
p-value: p=0.01
Excessive generation of 16kDa prolactin may mediate PPCM, suggesting that inhibition of prolactin release could represent a novel therapeutic strategy.
Postpartum cardiomyopathy (PPCM) is a disease of unknown etiology and exposes women to high risk of mortality after delivery despite optimal medical therapy. Experimental data suggested that enhanced oxidative stress promotes the proteolytical processing of the lactation hormone prolactin into a biologically active derivative, the 16kDa prolactin, which appears to be a major cause for PPCM. We observed increased oxLDL levels in a subset of these PPCM patients, indicative of oxidative stress, enhanced Cathepsin D activity and substantial levels of the cleaved 16kDa form of prolactin. We therefore propose that the excessive generation of 16kDa prolactin mediates PPCM in humans and suggest that inhibition of prolactin release may represent a novel therapeutic strategy for PPCM.
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Förster et al. (2017) conducted a review in Peripartum cardiomyopathy (n=100). Elevated baseline Fas/Apo-1 vs. Lower baseline Fas/Apo-1 was evaluated on Death (OR 3.56, 95% CI 1.35-9.42, p=0.01). Elevated baseline plasma levels of Fas/Apo-1 independently predicted death (OR 3.56) in women with peripartum cardiomyopathy over 6 months of follow-up.
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