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同一致病突变的肥厚型心肌病患者的血浆金属蛋白酶水平与左心室重构。

Plasma metalloproteinase levels and left ventricular remodeling in hypertrophic cardiomyopathy in patients with an identical mutation.

机构信息

Department of Medicine and Geriatrics, Kochi Medical School, Oko-cho, Nankoku-shi, Kochi 783-8505, Japan.

出版信息

J Cardiol. 2011 Nov;58(3):261-5. doi: 10.1016/j.jjcc.2011.07.011. Epub 2011 Sep 3.

DOI:10.1016/j.jjcc.2011.07.011
PMID:21890325
Abstract

BACKGROUND AND PURPOSE

Although it has been reported that matrix metalloproteinases (MMPs) are associated with left ventricular (LV) remodeling in patients with hypertrophic cardiomyopathy (HCM), the impact of plasma MMP levels in patients with HCM is somewhat vague.

METHODS AND SUBJECTS

Plasma levels of MMP-2, MMP-9, and clinical/echocardiographic findings were evaluated in 16 HCM patients with preserved LV ejection fraction (defined as LV ejection fraction more than 50%) caused by an identical frameshift mutation (S593fs: a one-base deletion of a thymidine at nucleotide 11,645) in the cardiac myosin-binding protein C gene.

RESULTS

MMP-2 levels were inversely related to LV ejection fraction (r(2)=-37, p=0.01). MMP-9 levels were inversely related to LV end-diastolic dimension (r(2)=-0.24, p=0.06) and positively related to the maximum LV wall thickness (r(2)=0.25, p=0.04). During follow-up period of 4.1 ± 1.2 years, LV ejection fraction decreased from 68.5 ± 7.4% to 64.9 ± 9% (p=0.03). Among clinical, echocardiographic findings at baseline and levels of biomarkers, high MMP-9 levels were only related to the decrease of LV ejection fraction from baseline to follow-up (r(2)=0.39, p=0.009).

CONCLUSIONS

MMP-2 levels are related to reduced LV systolic function in HCM patients with preserved LV ejection fraction caused by an identical cardiac myosin-binding protein C gene abnormality. On the other hand, MMP-9 levels are associated with small LV size and the degree of LV hypertrophy and related to the deterioration in LV systolic function during follow-up. These results suggest that MMPs are important in the process of LV remodeling in HCM.

摘要

背景与目的

尽管已有研究报道基质金属蛋白酶(MMPs)与肥厚型心肌病(HCM)患者的左心室(LV)重构有关,但 MMP 血浆水平对 HCM 患者的影响尚不清楚。

方法与对象

评估了 16 例因心肌肌球蛋白结合蛋白 C 基因相同移码突变(S593fs:核苷酸 11645 处胸腺嘧啶碱基缺失一个碱基)导致左心室射血分数(定义为左心室射血分数大于 50%)保留的 HCM 患者的 MMP-2、MMP-9 血浆水平和临床/超声心动图表现。

结果

MMP-2 水平与左心室射血分数呈负相关(r²=-37,p=0.01)。MMP-9 水平与 LV 舒张末期内径呈负相关(r²=-0.24,p=0.06),与最大 LV 壁厚度呈正相关(r²=0.25,p=0.04)。在 4.1±1.2 年的随访期间,左心室射血分数从 68.5±7.4%降至 64.9±9%(p=0.03)。在临床、基线超声心动图表现和生物标志物水平中,只有 MMP-9 水平与从基线到随访的左心室射血分数降低相关(r²=0.39,p=0.009)。

结论

MMP-2 水平与由相同心肌肌球蛋白结合蛋白 C 基因突变引起的保留左心室射血分数的 HCM 患者左心室收缩功能降低有关。另一方面,MMP-9 水平与 LV 体积小和 LV 肥厚程度有关,并与随访期间左心室收缩功能恶化有关。这些结果表明 MMPs 在 HCM 的 LV 重构过程中很重要。

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