In the last twenty years, new imaging techniques to assess atrial function and to predict the risk of recurrence of atrial fibrillation after treatment have been developed. The present review deals with the role of th...In the last twenty years, new imaging techniques to assess atrial function and to predict the risk of recurrence of atrial fibrillation after treatment have been developed. The present review deals with the role of these techniques in the detection of structural and functional changes of the atrium and diagnosis of atrial remodeling, particularly atrial fibrosis. Echocardiography allows the detection of anatomical, functional changes and deformation of the atrial wall during the phases of the cardiac cycle. For this, adequate acquisition of atrial images is necessary using speckle tracking imaging and interpretation of the resulting strain and strain rate curves. This allows to predict new-onset atrial fibrillation and recurrences. Its main limitations are inter-observer variability, the existence of different software manufacturers, and the fact that the software used were originally developed for the evaluation of the ventricular function and are now applied to the atria. Cardiac magnetic resonance, using contrast enhancement with gadolinium, plays a key role in the visualization and quantification of atrial fibrosis. This is the established method for in vivo visualization of myocardial fibrotic tissue. The non-invasive evaluation of atrial fibrosis is associ- ated with the risk of recurrence of atrial fibrillation and with electro-anatomical endocardial mapping. We discuss the limitations of these techniques, derived from the difficulty of demonstrating the correlation between fibrosis imaging and histology, and poor intra- and inter- observer reproducibility. The sources of discordance are described, mainly due to image acquisition and processing, and the challenges ahead in an attempt to eliminate differences between operators.展开更多
In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investi...In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure.展开更多
文摘In the last twenty years, new imaging techniques to assess atrial function and to predict the risk of recurrence of atrial fibrillation after treatment have been developed. The present review deals with the role of these techniques in the detection of structural and functional changes of the atrium and diagnosis of atrial remodeling, particularly atrial fibrosis. Echocardiography allows the detection of anatomical, functional changes and deformation of the atrial wall during the phases of the cardiac cycle. For this, adequate acquisition of atrial images is necessary using speckle tracking imaging and interpretation of the resulting strain and strain rate curves. This allows to predict new-onset atrial fibrillation and recurrences. Its main limitations are inter-observer variability, the existence of different software manufacturers, and the fact that the software used were originally developed for the evaluation of the ventricular function and are now applied to the atria. Cardiac magnetic resonance, using contrast enhancement with gadolinium, plays a key role in the visualization and quantification of atrial fibrosis. This is the established method for in vivo visualization of myocardial fibrotic tissue. The non-invasive evaluation of atrial fibrosis is associ- ated with the risk of recurrence of atrial fibrillation and with electro-anatomical endocardial mapping. We discuss the limitations of these techniques, derived from the difficulty of demonstrating the correlation between fibrosis imaging and histology, and poor intra- and inter- observer reproducibility. The sources of discordance are described, mainly due to image acquisition and processing, and the challenges ahead in an attempt to eliminate differences between operators.
基金supported by the State Key Program of National Natural Science of China(81230007)
文摘In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure.
