Kauer Floris, van Dalen Bas M, Michels Michelle, Schinkel Arend F L, Vletter Wim B, van Slegtenhorst Marjon, Soliman Osama I I, Geleijnse Marcel L
Department of Cardiology, The Thoraxcenter, Erasmus University Medical Center, Rotterdam, The Netherlands.
Department of Genetics, The Thoraxcenter, Erasmus University Medical Center, Rotterdam, The Netherlands.
Eur Heart J Cardiovasc Imaging. 2017 Apr 1;18(4):383-389. doi: 10.1093/ehjci/jew213.
The echocardiographic focus to detect abnormalities in genetically hypertrophic cardiomyopathy (HCM) affected subjects without left ventricular (LV) hypertrophy (G+/LVH-) has been on diastolic abnormalities in transmitral flow and longitudinal myocardial function with tissue Doppler imaging. The aim of this study was to assess diastolic LV unstrain and untwist.
Forty-one consecutive genotyped family members of HCM patients (mean age 37 ± 11 years, 16 men) and 41 age- and gender-matched healthy volunteers underwent speckle-tracking echocardiography to measure untwist and unstrain. No significant differences between G+/LVH- and control subjects were seen in maximal systolic twist and global longitudinal strain. In diastole, the early peak untwist rate was significantly lower in G+/LVH- subjects compared with control subjects (62 ± 19°s - 1 vs. 76 ± 30°s - 1, P <0.05), whereas the late peak untwist rate tended to be higher. Untwist from maximal twist until the first 20% of diastole was delayed in G+/LVH- subjects (39.3 ± 12.9% vs. 51.3 ± 15.6%, P <0.005). Late diastolic unstrain rate was significantly higher in G+/LVH- subjects in the inferoseptal wall (111 ± 33 s - 1 vs. 94 ± 32 s - 1, P = 0.024), the inferolateral wall (105 ± 42 vs. 75 ± 35 s - 1, P = 0.007) and the anteroseptal wall (97 ± 26 vs. 80 ± 23 s - 1, P = 0.010). Unstrain from maximal twist until the first 20% of diastole was delayed in G+/LVH- subjects in the inferoseptal (18.9 ± 14.0% vs. 30.1 ± 17.7%, P = 0.005), inferolateral (27.1 ± 16.3% vs. 39.2 ± 18.0%, P = 0.015) and anteroseptal (19.1 ± 14.7% vs. 35.8 ± 18.5%, P = 0.0003) segments.
In mutation carriers, for HCM LV, untwist and unstrain are delayed and untwist rate and unstrain rate are decreased.
在无左心室肥厚（G+/LVH-）的遗传性肥厚型心肌病（HCM）患者中，超声心动图检测异常的重点一直是二尖瓣血流舒张期异常以及组织多普勒成像评估的纵向心肌功能。本研究的目的是评估左心室舒张期无应变和无扭转情况。
41例连续的HCM患者的基因分型家庭成员（平均年龄37±11岁，16例男性）和41例年龄及性别匹配的健康志愿者接受斑点追踪超声心动图检查以测量无扭转和无应变情况。G+/LVH-组与对照组在最大收缩期扭转和整体纵向应变方面未见显著差异。在舒张期，G+/LVH-组患者的早期峰值无扭转率显著低于对照组（62±19°s-1 vs. 76±30°s-1，P<0.05），而晚期峰值无扭转率则有升高趋势。G+/LVH-组患者从最大扭转到舒张期前20%的无扭转延迟（39.3±12.9% vs. 51.3±15.6%，P<0.005）。G+/LVH-组患者下间隔壁（111±33 s-1 vs. 94±32 s-1，P=0.024）、下侧壁（105±42 vs. 75±35 s-1，P=0.007）和前间隔壁（97±26 vs. 80±23 s-1，P=0.010）的舒张期末期无应变率显著更高。G+/LVH-组患者下间隔（18.9±14.0% vs. 30.1±17.7%，P=0.005）、下侧壁（27.1±16.3% vs. 39.2±18.0%，P=0.015）和前间隔（19.1±14.7% vs. 35.8±18.5%，P=0.0003）节段从最大扭转到舒张期前20%的无应变延迟。
在突变携带者中，对于HCM患者的左心室，无扭转和无应变延迟，无扭转率和无应变率降低。
