Non-compaction of the ventricular myocardium （NVM） is a rare congenital genetic heart defect that was initially reported 17 years ago by means of autopsy; few cases have been published since then. It has been classi...Non-compaction of the ventricular myocardium （NVM） is a rare congenital genetic heart defect that was initially reported 17 years ago by means of autopsy; few cases have been published since then. It has been classified as the primary inherited cardiomyopathy by the American Heart Association Scientific Statement in 2006 under contemporary definitions and classification of cardiomyopathies. It is caused by an arrested development of muscle fiber compaction, a process that normally takes place dunng early embryogenesls, which is characterized by numerous sinusoids or trabeculae that are excessive in number and abnormal in prominence and by deep intratrabecular recesses covered by endothelium that exhibits continuity with ventricular endocardium. It usually involves one and/or more segments of the left ventricle, while the clinical manifestations are highly variable,展开更多
文摘目的探讨双能CT(dual-energy CT,DECT)在定量评估老年男性COPD肺功能分级与胸椎钙(水)密度关系的应用价值。方法选取老年男性COPD患者124例,按肺功能分级结果进行分组,比较不同肺功能分级组间胸椎钙(水)密度值差异性,并分析胸椎钙(水)密度值与肺功能检查及CT肺气肿指数(percentage of attenuation areas voxels,LAV%)结果相关性。结果COPD 1级和2级组间胸椎钙(水)密度值无统计学差异(P>0.05),COPD 1、2级分别与COPD 3级和4级组间胸椎钙(水)密度值有统计学差异(P均<0.05),COPD 3级和4级组间胸椎钙(水)密度值有统计学差异(P<0.05);胸椎钙(水)密度值与FEV_(1)/FVC%及FEV_(1)%pred存在线性关系,分别呈中度和较高度正性相关(r值分别为0.679和0.745,F值分别为111.68和187.07,P均<0.05);胸椎钙(水)密度值与LAV%存在线性关系,呈较高度负性相关(r值为-7.23,F值为117.52,P<0.05)。结论老年男性COPD患者胸椎钙(水)密度值随肺功能分级进展而减少,利用DECT可定量反应老年男性COPD患者胸椎钙(水)密度变化,对预防此类患者胸椎骨质疏松有重要临床意义。
文摘Non-compaction of the ventricular myocardium （NVM） is a rare congenital genetic heart defect that was initially reported 17 years ago by means of autopsy; few cases have been published since then. It has been classified as the primary inherited cardiomyopathy by the American Heart Association Scientific Statement in 2006 under contemporary definitions and classification of cardiomyopathies. It is caused by an arrested development of muscle fiber compaction, a process that normally takes place dunng early embryogenesls, which is characterized by numerous sinusoids or trabeculae that are excessive in number and abnormal in prominence and by deep intratrabecular recesses covered by endothelium that exhibits continuity with ventricular endocardium. It usually involves one and/or more segments of the left ventricle, while the clinical manifestations are highly variable,
