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扩张型心肌病患者心脏中交感神经支配改变、氧化代谢与收缩功能之间的关系;一项使用正电子发射断层扫描的非侵入性研究

Relationship between altered sympathetic innervation, oxidative metabolism and contractile function in the cardiomyopathic human heart; a non-invasive study using positron emission tomography.

作者信息

Bengel F M, Permanetter B, Ungerer M, Nekolla S G, Schwaiger M

机构信息

Nuklearmedizinische Klinik und Poliklinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Str, 22, 81675 Munich, Germany.

出版信息

Eur Heart J. 2001 Sep;22(17):1594-600. doi: 10.1053/euhj.2000.2556.

DOI:10.1053/euhj.2000.2556
PMID:11492989
Abstract

AIMS

To identify functional and metabolic correlates of impaired presynaptic sympathetic innervation in the cardiomyopathic human heart using non-invasive correlative imaging.

METHODS AND RESULTS

In 10 patients with idiopathic dilated cardiomyopathy, presynaptic catecholamine uptake sites were quantified by positron emission tomography with C-11 hydroxyephedrine. Oxidative metabolism was measured using C-11 acetate. Global and regional function was assessed by tomographic radionuclide angiography. Left ventricular ejection fraction in patients was 19%+/-10%. Myocardial hydroxyephedrine retention was abnormally low in 58%+/-38% of the left ventricles. Globally and regionally, hydroxyephedrine retention was significantly correlated with ventricular function (r=0.67, P=0.03 with left ventricular ejection fraction; r=0.31, P<0.01 with regional endocardial shortening). Multivariate analysis confirmed hydroxyephedrine retention as the closest independent determinant of left ventricular ejection fraction. Oxidative metabolism was determined by rate pressure product as a measure of workload (r=0.78, P<0.01) and peripheral vascular resistance as a measure of afterload (r=-0.61, P=0.06), but did not correlate with hydroxyephedrine retention (r=0.08 for global, r=0.04 for regional parameters).

CONCLUSION

Alterations of presynaptic sympathetic innervation in dilated cardiomyopathy are associated with impaired contractile function, suggesting a common pathogenetic pathway. Overall oxidative metabolism, however, was not directly correlated with these findings. Normal regulatory mechanisms for oxidative metabolism were operational.

摘要

目的

运用非侵入性相关成像技术,确定心肌病患者心脏中突触前交感神经支配受损的功能和代谢相关性。

方法与结果

对10例特发性扩张型心肌病患者,采用C-11羟基麻黄碱正电子发射断层扫描定量突触前儿茶酚胺摄取位点。用C-11乙酸盐测量氧化代谢。通过断层放射性核素血管造影评估整体和局部功能。患者左心室射血分数为19%±10%。58%±38%的左心室心肌羟基麻黄碱摄取异常低。在整体和局部,羟基麻黄碱摄取与心室功能显著相关(与左心室射血分数r = 0.67,P = 0.03;与局部心内膜缩短r = 0.31,P < 0.01)。多变量分析证实羟基麻黄碱摄取是左心室射血分数最密切的独立决定因素。氧化代谢由心率血压乘积作为工作量指标(r = 0.78,P < 0.01)和外周血管阻力作为后负荷指标(r = -0.61,P = 0.06)决定,但与羟基麻黄碱摄取无关(整体r = 0.08,局部参数r = 0.04)。

结论

扩张型心肌病中突触前交感神经支配的改变与收缩功能受损有关,提示存在共同的致病途径。然而,整体氧化代谢与这些发现无直接关联。氧化代谢的正常调节机制仍在起作用。

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