Circulating microparticles as indicators of peripartum cardiomyopathy.
OBJECTIVE
Peripartum cardiomyopathy (PPCM) is associated with high mortality and morbidity. Endothelial damage involving cathepsin-D to form a 16 kDa prolactin (PRL) peptide is pathogenetically relevant. Inhibiting PRL peptide with bromocriptine has yielded promising results. We investigated whether microparticles (MPs) can be quantified in serum as markers for diagnosis and treatment effects in PPCM.


RESULTS
Patients with PPCM were compared with age-matched healthy post-partum women (PPCTR), healthy pregnant women (PCTR), healthy non-pregnant women (NPCTR), patients with ischaemic cardiomyopathy (ICM), patients with stable coronary artery disease (CAD) and healthy controls (HCTR). Peripartum cardiomyopathy treated with bromocriptine (PPCM-BR) and with PPCM without bromocriptine-treatment as control (PPCM-BRCTR) were compared. Microparticles were determined by flow cytometry. Endothelial MPs (EMPs) were elevated in PPCM compared with PPCTR, PCTR, and NPCTR, each P< 0.001. They were significantly elevated compared with ICM, CAD, and HCTR (P< 0.001). Pregnancy (PCTR) exhibited only slight increases vs. ICM, CAD, NPCTR, and HCTR. The increase in PPCM was due to an increase of activated but not apoptotic EMPs. Platelet-derived microparticles were highly increased in PPCM compared with ICM (P< 0.001) but 9.3 ± 4.4-fold compared with CAD (P< 0.001). In NPCTR (P< 0.001) compared with NPCTR, the increase was 5.9 ± 1.7-fold (P< 0.001). Microparticles generated from monocytes (MMPs) were increased 2.4 ± 1.8-fold in PPCM compared with PCTR (P< 0.001) and 4.8 ± 3.6-fold compared with CAD (P< 0.001), whereas leucocyte MPs (LMPs) were not significantly elevated. Endothelial microparticles were significantly reduced in PPCM treated additionally with bromocriptine compared with PPCM treated only with heart failure therapy (P< 0.001).


CONCLUSIONS
Microparticle profiles may in long-term distinguish PPCM from normal pregnancy, heart failure, and vascular diseases and might be a diagnostic marker related to the pathomechanism of PPCM.
Klinik für Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Homburg, Saar, Germany. kwalent@hotmail.de
Katrin
K
Walenta
Viktoria
V
Schwarz
Stephan H
SH
Schirmer
Ingrid
I
Kindermann
Erik B
EB
Friedrich
Erich Franz
EF
Solomayer
Karen
K
Sliwa
Saida
S
Labidi
Denise
D
Hilfiker-Kleiner
Michael
M
Böhm
D000328:Adult; D000704:Analysis of Variance; D015415:Biomarkers; D001971:Bromocriptine / Q000627:therapeutic use*; D009202:Cardiomyopathies / Q000188:drug therapy* / Q000473:pathology; D016022:Case-Control Studies; D055252:Cell-Derived Microparticles / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006727:Hormone Antagonists / Q000627:therapeutic use*; D006801:Humans; D011247:Pregnancy; D011644:Puerperal Disorders / Q000188:drug therapy* / Q000473:pathology
D015415:Biomarkers; D006727:Hormone Antagonists; D001971:Bromocriptine