中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
16期
2976-2980
,共5页
磁共振成像%心肌病,肥厚性%心内膜心肌纤维化症%心肌损伤标志物
磁共振成像%心肌病,肥厚性%心內膜心肌纖維化癥%心肌損傷標誌物
자공진성상%심기병,비후성%심내막심기섬유화증%심기손상표지물
Magnetic resonance imaging%Cardiomyopathy,hypertrophic%Endomyocardial fibrosis%Myocardial damage markers
目的：运用3.0 T心脏磁共振（CMR）延迟强化（LGE）技术对肥厚性心肌病（HCM）心肌纤维化进行定量检测，并获得LGE与心肌标志物即心肌代谢酶的关系，从而探究HCM患者心肌标志物升高是否与心肌纤维化造成的心肌细胞损伤有关。方法纳入34例HCM患者（HCM组）与20例健康志愿者（正常对照组）。两组均行3.0 T CMR扫描，包括短轴位心脏电影及LGE序列。心脏功能用短轴为心脏电影序列测定；运用LGE序列测定HCM与正常对照组的LGE参数，包括总LGE率、LGE体积及LGE质量；测定与心肌损伤程度有关的血清心肌标志物含量，包括肌酸激酶同工酶、肌钙蛋白。采用独立样本t检验及Pearson积矩相关对心肌标志物及LGE参数进行统计分析。结果 HCM组肌酸激酶同工酶、肌钙蛋白均大于临床正常范围。通过LGE检测，HCM 组的LGE参数，包括总LGE率、LGE体积及LGE质量均大于正常对照组[分别为（18.95±9.87）%vs.（50.82±14.18）%、（8.50±4.50）ml vs.（86.26±41.99）ml及（9.00±4.80）g vs.（90.58±44.11）g，均P＜0.05]。Pearson积矩相关证明，HCM组肌酸激酶同工酶与总LGE率、LGE体积呈正相关（r值分别为0.759、0.448，P值分别为0.000、0.008）。肌钙蛋白与总LGE率、LGE体积呈正相关（r值分别为0.647、0.578，P值均为0.000）。结论3.0 T CMR LGE技术可用于肥厚性心肌病心肌纤维化的定量检测，HCM患者心肌标志物与心肌的LGE率呈正相关，表明心肌纤维化造成的心肌细胞损伤可能导致心肌细胞内的代谢酶类即心肌标志物释放，从而影响心肌的代谢功能，最终造成心脏功能损伤。
目的：運用3.0 T心髒磁共振（CMR）延遲彊化（LGE）技術對肥厚性心肌病（HCM）心肌纖維化進行定量檢測，併穫得LGE與心肌標誌物即心肌代謝酶的關繫，從而探究HCM患者心肌標誌物升高是否與心肌纖維化造成的心肌細胞損傷有關。方法納入34例HCM患者（HCM組）與20例健康誌願者（正常對照組）。兩組均行3.0 T CMR掃描，包括短軸位心髒電影及LGE序列。心髒功能用短軸為心髒電影序列測定；運用LGE序列測定HCM與正常對照組的LGE參數，包括總LGE率、LGE體積及LGE質量；測定與心肌損傷程度有關的血清心肌標誌物含量，包括肌痠激酶同工酶、肌鈣蛋白。採用獨立樣本t檢驗及Pearson積矩相關對心肌標誌物及LGE參數進行統計分析。結果 HCM組肌痠激酶同工酶、肌鈣蛋白均大于臨床正常範圍。通過LGE檢測，HCM 組的LGE參數，包括總LGE率、LGE體積及LGE質量均大于正常對照組[分彆為（18.95±9.87）%vs.（50.82±14.18）%、（8.50±4.50）ml vs.（86.26±41.99）ml及（9.00±4.80）g vs.（90.58±44.11）g，均P＜0.05]。Pearson積矩相關證明，HCM組肌痠激酶同工酶與總LGE率、LGE體積呈正相關（r值分彆為0.759、0.448，P值分彆為0.000、0.008）。肌鈣蛋白與總LGE率、LGE體積呈正相關（r值分彆為0.647、0.578，P值均為0.000）。結論3.0 T CMR LGE技術可用于肥厚性心肌病心肌纖維化的定量檢測，HCM患者心肌標誌物與心肌的LGE率呈正相關，錶明心肌纖維化造成的心肌細胞損傷可能導緻心肌細胞內的代謝酶類即心肌標誌物釋放，從而影響心肌的代謝功能，最終造成心髒功能損傷。
목적：운용3.0 T심장자공진（CMR）연지강화（LGE）기술대비후성심기병（HCM）심기섬유화진행정량검측，병획득LGE여심기표지물즉심기대사매적관계，종이탐구HCM환자심기표지물승고시부여심기섬유화조성적심기세포손상유관。방법납입34례HCM환자（HCM조）여20례건강지원자（정상대조조）。량조균행3.0 T CMR소묘，포괄단축위심장전영급LGE서렬。심장공능용단축위심장전영서렬측정；운용LGE서렬측정HCM여정상대조조적LGE삼수，포괄총LGE솔、LGE체적급LGE질량；측정여심기손상정도유관적혈청심기표지물함량，포괄기산격매동공매、기개단백。채용독립양본t검험급Pearson적구상관대심기표지물급LGE삼수진행통계분석。결과 HCM조기산격매동공매、기개단백균대우림상정상범위。통과LGE검측，HCM 조적LGE삼수，포괄총LGE솔、LGE체적급LGE질량균대우정상대조조[분별위（18.95±9.87）%vs.（50.82±14.18）%、（8.50±4.50）ml vs.（86.26±41.99）ml급（9.00±4.80）g vs.（90.58±44.11）g，균P＜0.05]。Pearson적구상관증명，HCM조기산격매동공매여총LGE솔、LGE체적정정상관（r치분별위0.759、0.448，P치분별위0.000、0.008）。기개단백여총LGE솔、LGE체적정정상관（r치분별위0.647、0.578，P치균위0.000）。결론3.0 T CMR LGE기술가용우비후성심기병심기섬유화적정량검측，HCM환자심기표지물여심기적LGE솔정정상관，표명심기섬유화조성적심기세포손상가능도치심기세포내적대사매류즉심기표지물석방，종이영향심기적대사공능，최종조성심장공능손상。
ObjectiveTo quantitatively detect myocardial fibrosis of hypertrophic cardiomyopathy (HCM) by 3.0 T cardiac magnetic resonance(CMR) Late gadolinium enhancement (LGE) technology, and get the relationship of LGE and myocardial markers, to investigate whether HCM patients' elevated myocardial markers are associated with myocardial fibrosis.Methods34 HCM patients and 20 healthy volunteers were enrolled in this research. HCM patients and 20 healthy volunteers were underwent 3.0 T Cardiac Magnetic Resonance scanning, including short axis cine sequences and LGE sequences. Left ventricular function was obtained on short axis cine sequence. LGE parameters, including total LGE rate, total LGE volume and total LGE mass were detected on LGE sequences. Myocardial marker, including creatine kinase isoenzyme and troponin were detected. Independent samplet-test and Pearson correlation were used.Results All myocardial markers of HCM patients were greater than clinical normal range. By LGE detection, LGE parameters of HCM group, including total LGE rate, total LGE volume and total LGE mass, were greater than normal control group (18.95±9.87vs.50.82±14.18; 8.50±4.50vs. 4.50±41.99; 9.00±4.80vs. 90.58±44.11, allP<0.05). Pearson correlation has been proved that creatine kinase isoenzyme of HCM patients were positively correlated to LGE rate and LGE volume (r=0.759,P=0.000;r=0.448, P=0.008). Troponin of HCM patients were also positively correlated to LGE rate and LGE volume (r=0.647,P=0.000;r=0.578,P=0.000).Conclusions Myocardial fibrosis of Hypertrophic Cardiomyopathy was quantitatively accessed by 3.0 T cardiac magnetic resonance late gadolinium enhancement technologies. Creatine kinase isoenzyme and troponin of HCM patients were positively correlated to LGE. Myocardial fibrosis may induce myocardial markers in the myocardial cells releasing, which affect the myocardial metabolic function further and induced heart function damage eventually.
