Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is characterized by fibro-fatty replacement of the right ventricle.However,the feasibility and significance of myocardial fibrosis detec-ted by delaye...Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is characterized by fibro-fatty replacement of the right ventricle.However,the feasibility and significance of myocardial fibrosis detec-ted by delayed enhancement (DE) using 3.0T magnetic resonance imaging (MRI) in.ARVD /C is seldomly studied.Methods Twenty-seven consecutive patients were prospectively evaluated for ARVD /C.Magnetic reso-nance imaging was performed on a 3.0T scanner.Ten minutes after intravenous administration of 0.2 mmol /kg of gadodiamide,DE-MRI was obtained.Diagnosis of ARVD /C was based upon the Task Force criteria and in-cluded MRI findings.Results Seventeen(59% ) of 27 patients met the Task Force criteria for ARVD /C.Right ven-tricle DE was found in all (100% ) ARVD /C patients compared with none (0%) of the 10 patients without ARVD /C (P <0.001) .Additional left ventricular DE was found in 8/17 ARVD/C patients while without left ventricular mor-phological and functional abnormalities detected by echocardiography or MRI.Conclusions DE using 3.0T MRI could effectively detect myocardial fibrosis in the right and left ventricular myocardium in ARVD /C patients.Detection of myocardial fibrosis may have an important clinical significance in ARVD/C diagnosis.Histological left ventricle in-volvement may be easily missed by echocardiography.展开更多
Objective To investigate the efficacy of venetoclax combined with hypomethylating agents(Ven-HMA),in patients with core binding factor acute myeloid leukemia(CBF-AML)intolerant to intensive induction therapy.Methods T...Objective To investigate the efficacy of venetoclax combined with hypomethylating agents(Ven-HMA),in patients with core binding factor acute myeloid leukemia(CBF-AML)intolerant to intensive induction therapy.Methods This study retrospectively analyzed patients newly diagnosed with CBF-AML who were aged<60 years and who received Ven-HMA as induction therapy at the Department of Hematology,the First Affiliated Hospital of Soochow University,between January 2020 and June 2023.展开更多
文摘Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is characterized by fibro-fatty replacement of the right ventricle.However,the feasibility and significance of myocardial fibrosis detec-ted by delayed enhancement (DE) using 3.0T magnetic resonance imaging (MRI) in.ARVD /C is seldomly studied.Methods Twenty-seven consecutive patients were prospectively evaluated for ARVD /C.Magnetic reso-nance imaging was performed on a 3.0T scanner.Ten minutes after intravenous administration of 0.2 mmol /kg of gadodiamide,DE-MRI was obtained.Diagnosis of ARVD /C was based upon the Task Force criteria and in-cluded MRI findings.Results Seventeen(59% ) of 27 patients met the Task Force criteria for ARVD /C.Right ven-tricle DE was found in all (100% ) ARVD /C patients compared with none (0%) of the 10 patients without ARVD /C (P <0.001) .Additional left ventricular DE was found in 8/17 ARVD/C patients while without left ventricular mor-phological and functional abnormalities detected by echocardiography or MRI.Conclusions DE using 3.0T MRI could effectively detect myocardial fibrosis in the right and left ventricular myocardium in ARVD /C patients.Detection of myocardial fibrosis may have an important clinical significance in ARVD/C diagnosis.Histological left ventricle in-volvement may be easily missed by echocardiography.
文摘Objective To investigate the efficacy of venetoclax combined with hypomethylating agents(Ven-HMA),in patients with core binding factor acute myeloid leukemia(CBF-AML)intolerant to intensive induction therapy.Methods This study retrospectively analyzed patients newly diagnosed with CBF-AML who were aged<60 years and who received Ven-HMA as induction therapy at the Department of Hematology,the First Affiliated Hospital of Soochow University,between January 2020 and June 2023.