Changes in plasma profiles of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in stress-induced cardiomyopathy.

Changes in plasma profiles of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in stress-induced cardiomyopathy.
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DOI:
10.1016/j.cardfail.2012.04.002
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发表时间:
2012-06
影响因子:
6
通讯作者:
Spinale, Francis G.
Spinale, Francis G.
中科院分区:
医学2区
文献类型:
--
作者:
Essa, Essa M.;Zile, Michael R.;Stroud, Robert E.;Rice, Allison;Gumina, Richard J.;Leier, Carl V.;Spinale, Francis G.

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心肌细胞外基质组成的短暂变化可能导致应激性心肌病(SIC)中的心室收缩功能障碍。我们检查了 SIC 临床表现后早期发生的血浆基质金属蛋白酶 (MMP) 和金属蛋白酶组织抑制剂 (TIMP) 的变化。 10 名 SIC 患者入组。分析了六种主要 MMP(MMP-1、-2、-3、-7、-8、-9)和所有 4 种 MMP 组织抑制剂(TIMP-1、-2、-3、-4)的血浆浓度,并与 15 名对照受试者的数据进行比较。临床表现后 24 小时内,SIC 患者的 MMP-1 水平较低(0.41±0.13 vs 0.70±0.13 pg/mL,p = 0.048)和 MMP-8 水平(1.61±0.34 vs 4.84±1.38 pg/mL,p = 0.001),而 TIMP-4 水平较高(3.06±0.40 vs 2.16±0.18 pg/mL,p = 0.05)与对照相比。 9 名 SIC 患者中有 7 名左室舒张末压升高,但所有左室舒张末期尺寸和容积均正常。患有 SIC 的患者的 MMP 和 TIMP 谱与高血压心脏病和舒张性心力衰竭中描述的谱相似,但与心肌梗塞后的谱不同。我们的研究结果在报告的前 24 小时内揭示了 SIC 中独特的生物分子特征。
Transient changes in the composition of the myocardial extracellular matrix may contribute to the ventricular systolic dysfunction in Stress-induced cardiomyopathy (SIC). We examined the changes in plasma matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) that occur early after the clinical presentation of SIC. Ten patients with SIC were enrolled. Plasma concentrations of the six major MMPs (MMP-1,-2,-3,-7,-8,-9) and all 4 tissue inhibitors of MMPs (TIMP-1,-2,-3,-4) were analyzed and compared with data from fifteen control subjects. Within 24 hours of the clinical presentation, SIC patients had lower MMP-1 levels (0.41±0.13 vs 0.70±0.13 pg/mL, p = 0.048) and MMP-8 levels (1.61±0.34 vs 4.84±1.38 pg/mL, p = 0.001) and higher TIMP-4 levels (3.06±0.40 vs 2.16±0.18 pg/mL, p =0.05) compared to control. Seven of nine SIC patients had elevated LV end-diastolic pressures, and all had normal LV end-diastolic dimensions and volumes. Patients afflicted with SIC had MMPs and TIMPs profiles similar to those described in hypertensive heart disease and diastolic heart failure and different than the profiles following myocardial infarction. Our findings uncovered a unique biomolecular profile in SIC during the first 24 hours of presentation.
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