ABSTRACT
Objective To explore the value of coronary CT angiography (CCTA) in prediction of major adverse cardiac events (MACE) in patients with coronary plaques.Methods Totally 256 coronary atherosclerotic plaque patients underwent CCTA.The degree of coronary stenosis was assessed quantitatively,and the plaque components were analyzed and classified.The occurrence of MACE was followed up.Three models were established for predicting MACE,including model 1 (classification of CCTA stenosis),model 2 (classification of CCTA stenosis combined with plaque typing) and model 3 (CCTA combined with plaque typing and clinical risk factors).The ability of the three models to predict MACE was evaluated.Results Follow-up was completed in 209 patients.Forty-six patients had experienced MACE.Classification of CCTA stenosis and plaque typing were used to assess the risk of MACE,and the hazard ratio (HR) was 4.47 and 3.43,respectively,both higher than those of clinical risk factors.The predictive ability of MACE by model 2 and model 3 was significantly superior to that of model 1 (P＜0.05),and there was no significant difference between model 2 and model 3 (P=0.076).Conclusion CCTA can assess the risk of MACE from both coronary stenosis and plaque typing.The new modality of CCTA stenosis classification combined with plaque typing could promote the ability of CCTA to predict the risk of MACE.
ABSTRACT
Objective To explore the value of coronary CT angiography (CCTA) in prediction of major adverse cardiac events (MACE) in patients with coronary plaques.Methods Totally 256 coronary atherosclerotic plaque patients underwent CCTA.The degree of coronary stenosis was assessed quantitatively,and the plaque components were analyzed and classified.The occurrence of MACE was followed up.Three models were established for predicting MACE,including model 1 (classification of CCTA stenosis),model 2 (classification of CCTA stenosis combined with plaque typing) and model 3 (CCTA combined with plaque typing and clinical risk factors).The ability of the three models to predict MACE was evaluated.Results Follow-up was completed in 209 patients.Forty-six patients had experienced MACE.Classification of CCTA stenosis and plaque typing were used to assess the risk of MACE,and the hazard ratio (HR) was 4.47 and 3.43,respectively,both higher than those of clinical risk factors.The predictive ability of MACE by model 2 and model 3 was significantly superior to that of model 1 (P＜0.05),and there was no significant difference between model 2 and model 3 (P=0.076).Conclusion CCTA can assess the risk of MACE from both coronary stenosis and plaque typing.The new modality of CCTA stenosis classification combined with plaque typing could promote the ability of CCTA to predict the risk of MACE.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the clinical feature of a family with hereditary hemorrhagic telangiectasia (HHT), and to study the mutation of its related genes.</p><p><b>METHODS</b>Medical histories of the family were analyzed to detect HHT patients according to the diagnostic criteria. ENG and ALK-1 genes of the proband and her two daughters were analyzed. DNA from the three patients' peripheral blood was extracted. The exons 2-10 and their intron-exon boundaries of ALK1 were amplified with PCR, and then the PCR products were sequenced and analyzed to identify the mutation.</p><p><b>RESULTS</b>There were 11 people in 41 family members of 4 generations were diagnosed as HHT. The proband and her two daughters suffered from multiple organ damage, the younger daughter appeared only imaging features instead of corresponding clinical symptoms. A missense mutation at the 1321 bp of cDNA (c.1321G>A) was detected in the exon 9 of ALK1, which resulted in valine 441 to methionine replacement in ALK-1 protein (p.Val441Met).</p><p><b>CONCLUSION</b>A Chinese family with HHT was studied and a missense mutation (c.1321G>A, p.Val441Met) of ALK-1 was discovered. This mutation is the genetic basis of the family with HHT and is reported for the first time in China. This research will not only help to further investigate molecular mechanism of pathogenesis of HTT, but also provide evidences and references for the following gene screening and genetic counseling on HTT family members.</p>