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人类免疫缺陷病毒的病毒载量可能是内皮功能障碍的一个独立危险因素。

Viral load of the human immunodeficiency virus could be an independent risk factor for endothelial dysfunction.

作者信息

Blum Arnon, Hadas Vered, Burke Michael, Yust Israel, Kessler Ada

机构信息

Department of Internal Medicine A, Poria Medical Center, Lower Galilee, Israel.

出版信息

Clin Cardiol. 2005 Mar;28(3):149-53. doi: 10.1002/clc.4960280311.

Abstract

BACKGROUND

Recent reports of myocardial infarction in young persons infected with human immunodeficiency virus (HIV) who are receiving protease inhibitor therapy have raised concerns about premature coronary artery disease in this population. However, endothelial dysfunction, hypercoagulability, hypertriglyceridemia, and abnormal coronary artery pathology have been observed in association with HIV infection prior to the availability of protease inhibitor therapy.

HYPOTHESIS

The study was undertaken to determine the association between endothelial function, viral load, CD4+ count, and other well-established risk factors for atherosclerosis.

METHODS

This prospective, case-controlled study compared viral (HIV) load and the CD4+ T-lymphocyte count and endothelial function in 24 HIV-positive carriers. Brachial artery diameter, HIV viral load, and CD4 count were measured.

RESULTS

We found that viral load correlated inversely with endothelial function; the higher the viral load, the worse the endothelial dysfunction (p < 0.005).

CONCLUSION

High viral load appears to be associated with endothelial dysfunction in patients with HIV. This preliminary observation supports the infectious theory that viruses may play an important role in the pathogenesis of atherosclerosis.

摘要

背景

近期有报道称,接受蛋白酶抑制剂治疗的感染人类免疫缺陷病毒(HIV)的年轻人发生心肌梗死,这引发了对该人群过早出现冠状动脉疾病的担忧。然而,在蛋白酶抑制剂治疗出现之前,就已观察到与HIV感染相关的内皮功能障碍、高凝状态、高甘油三酯血症和冠状动脉病理异常。

假说

本研究旨在确定内皮功能、病毒载量、CD4 + 细胞计数与其他已明确的动脉粥样硬化危险因素之间的关联。

方法

这项前瞻性病例对照研究比较了24名HIV阳性携带者的病毒(HIV)载量、CD4 + T淋巴细胞计数和内皮功能。测量肱动脉直径、HIV病毒载量和CD4计数。

结果

我们发现病毒载量与内皮功能呈负相关;病毒载量越高,内皮功能障碍越严重(p < 0.005)。

结论

高病毒载量似乎与HIV患者的内皮功能障碍有关。这一初步观察结果支持了病毒可能在动脉粥样硬化发病机制中起重要作用的感染理论。

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