Postpartum cardiomyopathy (PPCM) is a disease of unknown etiology and exposes women to high risk of mortality after delivery. Here, we show that female mice with a cardiomyocyte-specific deletion of stat3 develop PPCM. In these mice, cardiac cathepsin D (CD) expression and activity is enhanced and associated with the generation of a cleaved antiangiogenic and proapoptotic 16 kDa form of the nursing hormone prolactin. Treatment with bromocriptine, an inhibitor of prolactin secretion, prevents the development of PPCM, whereas forced myocardial generation of 16 kDa prolactin impairs the cardiac capillary network and function, thereby recapitulating the cardiac phenotype of PPCM. Myocardial STAT3 protein levels are reduced and serum levels of activated CD and 16 kDa prolactin are elevated in PPCM patients. Thus, a biologically active derivative of the pregnancy hormone prolactin mediates PPCM, implying that inhibition of prolactin release may represent a novel therapeutic strategy for PPCM.

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Despite the enormous progress in the treatment of atrial fibrillation, mainly with the use of invasive techniques, many questions remain unanswered regarding the pathomechanism of the arrhythmia and its prevention methods. The development of atrial fibrillation requires functional changes in the myocardium that result from disturbed ionic fluxes and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying the arrhythmia may result from a cellular energy deficit and oxidative stress, which are caused by mitochondrial dysfunction. The significance of mitochondrial dysfunction in the pathogenesis of atrial fibrillation remains not fully elucidated; however, it is emphasized by the reduction of atrial fibrillation burden after therapeutic interventions improving the mitochondrial welfare. This review summarizes the mechanisms of mitochondrial dysfunction related to atrial fibrillation and current pharmacological treatment options targeting mitochondria to prevent or improve the outcome of atrial fibrillation.

Our study shows age-related disorganization of ID, which may be responsible for slowed conduction of the depolarization wave within the heart, and supports the hypothesis of cardiac dysfunction in senescence.

Reperfusion of ischemic myocardium evokes rapid release of free radicals in experimental models. The aim of the study was to investigate the oxidative stress and antioxidative defense during first minutes after reopening of the infarct related artery in patients treated for acute myocardial infarction. The study group consisted of 15 patients with first ST elevation myocardial infarction (STEMI) due to left anterior descending artery occlusion. The control group included ten patients with stable ischemic heart disease (IHD). Blood samples from coronary sinus were drawn before, immediately after and about 15 min after angioplasty. Activity of superoxide dysmutase (SOD), concentration of glutathione as well as the concentrations of lipid peroxides, malodialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE) were measured. There was significantly higher concentration of MDA and HNE and higher SOD activity in STEMI patients before the reperfusion, as compared to the stable IHD group. After the reperfusion concentration of HNE in erythrocytes from STEMI patients was higher than in IHD group. At the same time the activity of SOD significantly decreased in patients with impaired tissue perfusion (myocardial blush grade <2). In conclusion, there is a slightly higher concentration of oxidative stress parameters in patients with STEMI. Diminished antioxidative defense after reperfusion is associated with impaired myocardial perfusion.