Selenium- and zinc-deficient cardiomyopathy in human intestinal malabsorption: preliminary results of selenium/zinc infusion.

Aims Patients with intestinal malabsorption may develop cardiac dysfunction the origin of which is often unclear. We sought to investigate the pathogenesis of dilated cardiomyopathy in human malabsorption. Methods and results Eighteen patients with intestinal bypass as treatment for severe obesity and cardiomyopathy underwent endomyocardial biopsy. Biopsies were processed by histology, electron microscopy, polymerase chain reaction (PCR) for cardiotropic viruses, instrumental neutron activation analysis (INAA) of 33 myocardial trace elements, and assessment of glutathione peroxidase (GPX) activity and LC3-II expression. Histology and electron microscopy showed hypertrophy/degeneration of cardiomyocytes with pronounced cell autophagy and high expression of LC3-II. PCR was negative for viral genomes. INAA showed severe myocardial selenium (Se) and zinc (Zn) deficiency and reduced GPX activity vs. both patients with idiopathic dilated cardiomyopathy and normal controls. Se and Zn were added to antifailing heart therapy in 10 patients (group A1) agreeing to a control biopsy, and the response was compared with that of 8 patients (group A2) on supportive therapy alone. After 6 months, myocardial normalization of Se, Zn, LC3-II, and GPX in group A1 was associated with recovery of cardiomyocyte degeneration and autophagy, and significant improvement in cardiac dimension and function, that remained unchanged in group A2. Conclusion A reversible Se-and Zn-deficient cardiomyopathy may occur in patients with intestinal malabsorption. It is characterized by decline of myocardial antioxidant reserve, oxidative damage of cell membranes, and enhanced cell autophagy.