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肥厚型心肌病中的主动脉生物力学

Aortic biomechanics in hypertrophic cardiomyopathy.

作者信息

Badran Hala Mahfouz, Soltan Ghada, Faheem Nagla, Elnoamany Mohamed Fahmy, Tawfik Mohamed, Yacoub Magdi

机构信息

Cardiology Department, Menoufiya University, Egypt.

Cardiology Department, Menoufiya University, Egypt ; The BAHCM National Program, Egypt.

出版信息

Glob Cardiol Sci Pract. 2015 Jul 3;2015(2):27. doi: 10.5339/gcsp.2015.27. eCollection 2015.

DOI:10.5339/gcsp.2015.27
PMID:26566526
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4625403/
Abstract

BACKGROUND

Ventricular-vascular coupling is an important phenomenon in many cardiovascular diseases. The association between aortic mechanical dysfunction and left ventricular (LV) dysfunction is well characterized in many disease entities, but no data are available on how these changes are related in hypertrophic cardiomyopathy (HCM).

AIM OF THE WORK

This study examined whether HCM alone is associated with an impaired aortic mechanical function in patients without cardiovascular risk factors and the relation of these changes, if any, to LV deformation and cardiac phenotype.

METHODS

141 patients with HCM were recruited and compared to 66 age- and sex-matched healthy subjects as control group. Pulse pressure, aortic strain, stiffness and distensibility were calculated from the aortic diameters measured by M-mode echocardiography and blood pressure obtained by sphygmomanometer. Aortic wall systolic and diastolic velocities were measured using pulsed wave Doppler tissue imaging (DTI). Cardiac assessment included geometric parameters and myocardial deformation (strain and strain rate) and mechanical dyssynchrony.

RESULTS

The pulsatile change in the aortic diameter, distensibility and aortic wall systolic velocity (AWS') were significantly decreased and aortic stiffness index was increased in HCM compared to control (P < .001) In HCM AWS' was inversely correlated to age(r = - .32, P < .0001), MWT (r = - .22, P < .008), LVMI (r = - .20, P < .02), E/Ea (r = - .16, P < .03) LVOT gradient (r = - 19, P < .02) and severity of mitral regurg (r = - .18, P < .03) but not to the concealed LV deformation abnormalities or mechanical dyssynchrony. On multivariate analysis, the key determinant of aortic stiffness was LV mass index and LVOT obstruction while the role LV dysfunction in aortic stiffness is not evident in this population.

CONCLUSION

HCM is associated with abnormal aortic mechanical properties. The severity of cardiac phenotype, not LV deformation, is interrelated to aortic stiffness in patients with HCM. The increased aortic stiffness seems to be promising module that can be added as clinical risk parameter in HCM.

摘要

背景

心室-血管耦合是许多心血管疾病中的一个重要现象。在许多疾病实体中,主动脉机械功能障碍与左心室(LV)功能障碍之间的关联已得到充分表征,但关于肥厚型心肌病(HCM)中这些变化如何相关的数据尚不可得。

研究目的

本研究调查了在无心血管危险因素的患者中,单纯HCM是否与主动脉机械功能受损相关,以及这些变化(如果存在)与左心室变形和心脏表型的关系。

方法

招募了141例HCM患者,并与66例年龄和性别匹配的健康受试者作为对照组进行比较。通过M型超声心动图测量的主动脉直径和血压计测得的血压计算脉压、主动脉应变、僵硬度和扩张性。使用脉冲波多普勒组织成像(DTI)测量主动脉壁的收缩期和舒张期速度。心脏评估包括几何参数、心肌变形(应变和应变率)以及机械不同步。

结果

与对照组相比,HCM患者主动脉直径的搏动变化、扩张性和主动脉壁收缩期速度(AWS')显著降低,主动脉僵硬度指数增加(P <.001)。在HCM中,AWS'与年龄(r = -.32,P <.0001)、心肌壁厚度(MWT)(r = -.22,P <.008)、左心室质量指数(LVMI)(r = -.20,P <.02)、E/Ea(r = -.16,P <.03)、左心室流出道梯度(r = -19,P <.02)和二尖瓣反流严重程度(r = -.18,P <.03)呈负相关,但与隐匿性左心室变形异常或机械不同步无关。多因素分析显示,主动脉僵硬度的关键决定因素是左心室质量指数和左心室流出道梗阻,而左心室功能障碍在该人群中对主动脉僵硬度的作用不明显。

结论

HCM与主动脉机械特性异常有关。在HCM患者中,心脏表型的严重程度而非左心室变形与主动脉僵硬度相关。主动脉僵硬度增加似乎是一个有前景的指标,可作为HCM的临床风险参数。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/a8b1bab4ec55/gcsp-2015-02-027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/df367f30537f/gcsp-2015-02-027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/a6ddfaed8fec/gcsp-2015-02-027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/75b1378c830c/gcsp-2015-02-027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/374b74797834/gcsp-2015-02-027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/4771783540d0/gcsp-2015-02-027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/a8b1bab4ec55/gcsp-2015-02-027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/df367f30537f/gcsp-2015-02-027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/a6ddfaed8fec/gcsp-2015-02-027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/75b1378c830c/gcsp-2015-02-027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/374b74797834/gcsp-2015-02-027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/4771783540d0/gcsp-2015-02-027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c27/4625403/a8b1bab4ec55/gcsp-2015-02-027-g006.jpg

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