TY - JOUR
T1 - Selenium-and zinc-deficient cardiomyopathy in human intestinal malabsorption
T2 - Preliminary results of selenium/zinc infusion
AU - Frustaci, Andrea
AU - Sabbioni, Enrico
AU - Fortaner, Salvador
AU - Farina, Massimo
AU - Del Torchio, Riccardo
AU - Tafani, Marco
AU - Morgante, Emanuela
AU - Ciriolo, Maria Rosa
AU - Russo, Matteo A.
AU - Chimenti, Cristina
PY - 2012/2
Y1 - 2012/2
N2 - 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.
AB - 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.
KW - Cardiomyopathy
KW - Malabsorption
KW - Trace elements
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U2 - 10.1093/eurjhf/hfr167
DO - 10.1093/eurjhf/hfr167
M3 - Article
C2 - 22186680
AN - SCOPUS:84856187041
VL - 14
SP - 202
EP - 210
JO - European Journal of Heart Failure
JF - European Journal of Heart Failure
SN - 1388-9842
IS - 2
ER -