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退伍耐力运动员心肌纤维化的生化证据。

Biochemical evidence of myocardial fibrosis in veteran endurance athletes.

作者信息

Lindsay M Mitchell, Dunn Francis G

机构信息

Department of Cardiology, Western Infirmary, Glasgow, UK.

出版信息

Br J Sports Med. 2007 Jul;41(7):447-52. doi: 10.1136/bjsm.2006.031534. Epub 2007 Feb 20.

Abstract

BACKGROUND

Studies on exercise-induced left ventricular hypertrophy (LVH) in veteran athletes suggest the presence of abnormal diastolic filling and incomplete regression of LVH on cessation of exercise.

HYPOTHESIS

Myocardial fibrosis occurs in exercise induced LVH in veteran athletes.

AIM

To document non-invasively the presence of fibrosis in veteran athletes

DESIGN

Prospective case-control study.

SETTING

City centre district general hospital.

PARTICIPANTS

45 normotensive elite veteran athletes and 45 normal sedentary subjects.

INTERVENTIONS

Echocardiographic assessment was made of LV mass, LV systolic and LV diastolic function. Plasma carboxyterminal propeptide of collagen type I (PICP), carboxyterminal telopeptide of collagen type I (CITP) and tissue inhibitor of matrix metalloproteinase type I (TIMP-1) were measured as markers of collagen synthesis, degradation and inhibition of degradation, respectively.

RESULTS

Veteran athletes had significant elevation in LV dimensions and calculated LV mass index (LVMI). Diastolic and systolic function was normal. Plasma PICP (259 vs 166 microg/l, p<0.001), CITP (5.4 vs 2.9 microg/l, p<0.001) and TIMP-1 (350 vs 253 ng/ml, p = 0.01) were elevated in the cohort of athletes. There was a further elevation of TIMP-1 in athletes with echocardiographic LVH, defined as an LVMI >130 g/m(2) (417 vs 266 ng/ml, p = 0.02).

CONCLUSION

There is biochemical evidence of disruption of the collagen equilibrium favouring fibrosis in veteran athletes with LVH. This may suggest that fibrosis occurs as part of the hypertrophic process in veteran athletes.

摘要

背景

对资深运动员运动诱导的左心室肥厚(LVH)的研究表明,存在舒张期充盈异常以及运动停止后左心室肥厚不完全消退的情况。

假设

资深运动员运动诱导的左心室肥厚中会发生心肌纤维化。

目的

以非侵入性方式记录资深运动员中纤维化的存在情况。

设计

前瞻性病例对照研究。

地点

市中心区综合医院。

参与者

45名血压正常的精英资深运动员和45名正常久坐不动的受试者。

干预措施

对左心室质量、左心室收缩功能和左心室舒张功能进行超声心动图评估。分别测量血浆I型胶原羧基末端前肽(PICP)、I型胶原羧基末端端肽(CITP)和I型基质金属蛋白酶组织抑制剂(TIMP-1)作为胶原合成、降解和降解抑制的标志物。

结果

资深运动员的左心室尺寸和计算得出的左心室质量指数(LVMI)显著升高。舒张和收缩功能正常。运动员队列中的血浆PICP(259对166微克/升,p<0.001)、CITP(5.4对2.9微克/升,p<0.001)和TIMP-1(350对253纳克/毫升,p = 0.01)升高。在超声心动图显示左心室肥厚(定义为LVMI>130克/平方米)的运动员中,TIMP-1进一步升高(417对266纳克/毫升,p = 0.02)。

结论

有生化证据表明,左心室肥厚的资深运动员中胶原平衡受到破坏,有利于纤维化。这可能表明纤维化是资深运动员肥厚过程的一部分。

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