Impact of Metalloproteinases on Left Ventricular Remodeling and Heart Failure Events in Patients With Hypertrophic Cardiomyopathy

Impact of Metalloproteinases on Left Ventricular Remodeling and Heart Failure Events in Patients With Hypertrophic Cardiomyopathy
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DOI:
10.1253/circj.cj-09-1013
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发表时间:
2010-06-01
影响因子:
3.3
通讯作者:
Doi, Yoshinori L.
Doi, Yoshinori L.
中科院分区:
医学3区
文献类型:
--
作者:
Kitaoka, Hiroaki;Kubo, Toru;Doi, Yoshinori L.

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背景:肥厚型心肌病(HCM)患者血浆基质金属蛋白酶(MMP2、MMP9、TIMP-1)水平与临床表现及心力衰竭事件的关系尚不明确。同时测定血浆B型利钠肽(BNP)水平。有重度症状的患者血清MMP2水平高于无症状或轻度症状的患者。血清MMP2、TIMP 1水平与左心房收缩末期内径、左心房内径呈正相关,与左心室射血分数呈负相关。MMP2水平与脑钠素水平呈正相关(r=0.52P=0.0009)。然而,MMP9水平与超声心动图参数和血浆BNP水平无关。6例患者在3.2+/-0.7年的随访期内发生了复杂的心力衰竭事件。血浆MMP2水平高(<1170 ng/ml)者预后较低者差。结论:血浆MMP2水平升高与肥厚性心肌梗死患者的左心室重构及预后不良有关。提示细胞外胶原基质的调节可能是肥厚性心肌病治疗的靶点之一。(保监会J 2010;74:1191-1196)
Background: The impact of matrix metalloproteinase (MMP) on left ventricular (LV) remodeling and heart failure events is unresolved in patients with hypertrophic cardiomyopathy (HCM).Methods and Results: Plasma levels of MMP-2, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1 and clinical findings and heart failure events were evaluated in 41 HCM patients, including 8 with LV systolic impairment. Plasma B-type natriuretic peptide (BNP) levels were also measured. MMP-2 levels in patients with severe symptoms were higher than that in those with no or mild symptoms. The levels of MMP-2 and TIMP-1 were positively related to LV end-systolic and left atrial dimensions, and inversely related to LV ejection fraction. MMP-2 levels were positively related to BNP levels (r=0.52, P=0.0009). However, MMP-9 levels were not related to echocardiographic parameters and plasma BNP levels. Six patients had complicated heart failure events during the follow-up period of 3.2+/-0.7 years. Patients with high plasma MMP-2 levels (>1,170 ng/ml) revealed a poorer prognosis than those with low MMP-2 levels.Conclusions: Elevated levels of MMP-2 were related to LV remodeling and poor prognosis in patients with HCM. These results suggest that regulation of the extracellular collagen matrix might be one of the therapeutic targets in patients with HCM. (Circ J 2010; 74: 1191-1196)