The Role of Melatonin in Peripartum Cardiomyopathy (PPCM)
Lauren Nicholson (MSc student)
Supervisor: AssocProf. Sandrine Lecour ; Co-supervisor/s: Prof. Karen Sliwa
Year projected started: 2012
Year projected ended: 2013
Introduction: Peripartum cardiomyopathy (PPCM) is a heart disease of unknown aetiology emerging in previously healthy women towards the end of pregnancy or first postpartum months1. Previous studies have suggested that oxidative stress contributes to the pathogenesis of PPCM2. Melatonin is a powerful endogenous antioxidant that can limit the damaging effect of oxidative stress3. Melatonin levels are known to be altered in sleep disruption, depression and other cardiac diseases.
Aims: The aim of this study was to determine if melatonin levels are disrupted in women with PPCM compared to healthy patients. We hypothesised that sleep disruption and depression may contribute to a disruption in their melatonin levels.
Methodology: Pregnant and postpartum healthy control (HC) , with (PPCM) or other cardiac diseases (CD) were recruited for the study. A sleep quality questionnaire and the Edinburgh postnatal depression scale (EPDS) was administered to all patients to compare their sleeping patterns and depression levels. Daytime and nocturnal salivary melatonin levels were also compared and the serum concentration of the stress hormone cortisol was measured. To evaluate stress and antioxidant capacity a thiobartubaric reactive substances (TBARS) and oxygen radical absorbance capacity (ORAC) assays were performed on the plasma of all women. Basic naturietic peptide (BNP) was measured in serum as a marker of heart failure.
Results: BNP levels were elevated in the postnatal PPCM compared to HC and CD women. The oxidative stress in the form of lipid peroxidation was also elevated in the postnatal PPCM group, there was no observable difference in the antioxidant capacity. The PPCM and CD groups both demonstrated increased EDPS scores and elevated serum cortisol compared to HC. The postnatal PPCM women also demonstrated delayed, fragmented, inefficient sleep. The PPCM women also demonstrated significantly higher (p<0.05) postpartum nocturnal melatonin (99.8±8.8) levels compared to HC (73.4±8.3) and CD (77.8±7.8).
Conclusion: The postnatal PPCM women demonstrated increased level of salivary nocturnal melatonin as well as increase EDPS scores and sleep disruption. Further studies are required to fully understand the mechanism of this increase as well as potential therapeutic targets.
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