Speckle tracking echocardiography to assess regional ventricular function in patients with apical hypertrophic cardiomyopathy.
Speckle tracking echocardiography to assess regional ventricular function in patients with apical hypertrophic cardiomyopathy.
复制标题
DOI：
10.4330/wjc.v9.i4.363
复制
发表时间：
2017-04-26
影响因子：
1.9
通讯作者：
Lax JA
中科院分区：
文献类型：
--
作者：
Saccheri MC;Cianciulli TF;Morita LA;Méndez RJ;Beck MA;Guerra JE;Cozzarin A;Puente LJ;Balletti LR;Lax JA
目的：应用斑点跟踪超声心动图探讨根尖肥厚性心肌病（HCM）患者中心壁和心内膜段的局部收缩应变。我们前瞻性评估了20例根尖HCM患者（平均年龄53±16岁，范围：18-81岁，男性10例）。我们测量了左心室中壁和心内膜的整体纵向峰值收缩应变（GLPSS）。4根根尖段舒张期厚度为16.25±2.75 mm。所有患者整体收缩功能正常，分数缩短50%±8%。尽管左室（LV）收缩功能异常，但所有患者中壁GLPSS均下降，其中心尖节段GLPSS（-7.3%±-8.8%）高于基底节段GLPSS(-15.5%±-6.93%)，而心内膜GLPSS明显升高并达到正常值（心尖节段：-22.8%±-7.8%，基底节段：-17.9%±-7.5%）。本研究表明，二维应变的减少主要局限于心内膜，而心内膜心肌变形在HCM中得以保留，可用于鉴别亚临床左室功能障碍。这种收缩应变的跨壁异质性在HCM中从未被描述过，可以用心肌深部肌纤维紊乱的分布来解释。这一新发现的临床应用可能有助于进一步了解HCM的病理生理。
To explore regional systolic strain of midwall and endocardial segments using speckle tracking echocardiography in patients with apical hypertrophic cardiomyopathy (HCM). We prospectively assessed 20 patients (mean age 53 ± 16 years, range: 18-81 years, 10 were male), with apical HCM. We measured global longitudinal peak systolic strain (GLPSS) in the midwall and endocardium of the left ventricle. The diastolic thickness of the 4 apical segments was 16.25 ± 2.75 mm. All patients had a normal global systolic function with a fractional shortening of 50% ± 8%. In spite of supernormal left ventricular (LV) systolic function, midwall GLPSS was decreased in all patients, more in the apical (-7.3% ± -8.8%) than in basal segments (-15.5% ± -6.93%), while endocardial GLPPS was significantly greater and reached normal values (apical: -22.8% ± -7.8%, basal: -17.9% ± -7.5%). This study shows that two-dimensional strain was decreased mainly confined to the mesocardium, while endocardium myocardial deformation was preserved in HCM and allowed to identify subclinical LV dysfunction. This transmural heterogeneity in systolic strain had not been previously described in HCM and could be explained by the distribution of myofibrillar disarray in deep myocardial areas. The clinical application of this novel finding may help further understanding of the pathophysiology of HCM.