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。
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.