Choi Hong-Mi, Kim Kyung-Hee, Lee Joo Myung, Yoon Yeonyee E, Lee Seung-Pyo, Park Eun-Ah, Lee Whal, Kim Yong-Jin, Cho Goo-Yeong, Sohn Dae-Won, Kim Hyung-Kwan
Department of Internal Medicine, Cardiovascular Center, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea.
Department of Internal Medicine, Division of Cardiology, Sejong General Hospital.
Heart. 2015 Jun;101(11):870-6. doi: 10.1136/heartjnl-2014-306555. Epub 2015 Apr 20.
We hypothesised that, in hypertrophic cardiomyopathy (HCM), late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is progressive and can be predicted by baseline CMR findings and HCM phenotype.
In this single-centre cohort study, 71 patients with HCM (59±13 years; 48 men) were prospectively enrolled with clinical, echocardiographic and CMR data. Two consecutive CMR scans were performed with a time interval of 582±174 days. The LGE extent was quantified as a proportion of total LV myocardium (%LGE).
LGE was present in 65 patients (91.5%) at the first CMR (CMR-1). In all, LGE extent was significantly increased (p<0.001). A difference in %LGE between the two CMR scans was correlated with the initial %LGE (r=0.44, p<0.001). LGE progression, defined as >4% increase in LGE at the second CMR, was present in 19 patients with non-apical HCM (36.5%), but in only one apical HCM (5.3%). Also, LGE progression rate was significantly higher in non-apical (0.15%/month) versus apical HCM (0.025%/month) (p=0.001). On the multivariate model #1 including only clinical variables (age, history of paroxysmal atrial fibrillation, LV outflow tract obstruction on echocardiography, beta-blocker use, family history of sudden death, family history of HCM, syncope, non-sustained ventricular tachycardia, rate pressure product, and HCM phenotype), only apical HCM phenotype was associated with less LGE progression (p=0.038). On the multivariate model #2 including CMR variables additional to the model #1, %LGE at CMR-1 was the only determinant for LGE progression (p=0.007). When the analysis was limited to patients with preserved EF, results remained unchanged.
Myocardial fibrosis in HCM is a progressive phenomenon. Non-apical phenotype and a higher LGE extent at CMR-1 are both associated with greater LGE progression.
我们假设，在肥厚型心肌病（HCM）中，心脏磁共振成像（CMR）上的延迟钆增强（LGE）是进行性的，并且可以通过基线CMR检查结果和HCM表型进行预测。
在这项单中心队列研究中，前瞻性纳入了71例HCM患者（年龄59±13岁；男性48例），收集其临床、超声心动图和CMR数据。连续进行两次CMR扫描，时间间隔为582±174天。LGE范围被量化为左心室心肌总量的比例（%LGE）。
在首次CMR检查（CMR-1）时，65例患者（91.5%）存在LGE。总体而言，LGE范围显著增加（p<0.001）。两次CMR扫描之间的%LGE差异与初始%LGE相关（r=0.44，p<0.001）。LGE进展定义为第二次CMR时LGE增加>4%，在19例非心尖部HCM患者中出现（36.5%），但在心尖部HCM患者中仅1例出现（5.3%）。此外，非心尖部HCM的LGE进展率（0.15%/月）显著高于心尖部HCM（0.025%/月）（p=0.001）。在仅包含临床变量（年龄、阵发性心房颤动病史、超声心动图显示的左心室流出道梗阻、β受体阻滞剂使用情况、猝死家族史、HCM家族史、晕厥、非持续性室性心动过速、心率血压乘积和HCM表型）的多变量模型#1中，仅心尖部HCM表型与较少的LGE进展相关（p=0.038）。在包含模型#1之外的CMR变量的多变量模型#2中，CMR-1时的%LGE是LGE进展的唯一决定因素（p=0.007）。当分析仅限于射血分数保留的患者时，结果保持不变。
HCM中的心肌纤维化是一种进行性现象。非心尖部表型和CMR-1时较高的LGE范围均与更大的LGE进展相关。
