肿瘤坏死因子样凋亡微弱诱导物（TWEAK）在晚期缺血性和非缺血性心力衰竭中的预测价值的差异。
Differences in the predictive value of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in advanced ischemic and non-ischemic heart failure.
机构信息
Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
出版信息
Atherosclerosis. 2010 Dec;213(2):545-8. doi: 10.1016/j.atherosclerosis.2010.08.061. Epub 2010 Aug 19.
OBJECTIVE
To assess the prognostic value of the pro-apoptotic, but also cell growth-inducing molecule soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) in heart failure (HF).
METHODS
We assayed sTWEAK levels in 351 patients with advanced HF (non-ischemic: 130, ischemic: 221). During a median follow-up of 4.9 years, 195 patients (56%) died.
RESULTS
sTWEAK concentrations were associated with extended survival in patients with non-ischemic (P=0.022), but not with ischemic HF (P=0.82). The inverse association in non-ischemic HF remained significant in a multivariable Cox regression model (P=0.025) with a hazard ratio of 0.40 (95% confidence interval: 0.21-0.77) comparing the third to the first tertile (P=0.007).
CONCLUSION
Low sTWEAK levels independently predict mortality in advanced non-ischemic HF. sTWEAK-induced proliferation of cardiomyocytes may explain its impact on suvival. The different prognostic value of sTWEAK in ischemic and non-ischemic HF may point towards distinct pathogenic pathways determining the course of disease.
目的
评估促凋亡但也能诱导细胞生长的分子可溶性肿瘤坏死因子样凋亡弱诱导剂（sTWEAK）在心力衰竭（HF）中的预后价值。
方法
我们检测了 351 例晚期 HF 患者（非缺血性：130 例，缺血性：221 例）的 sTWEAK 水平。在中位随访 4.9 年期间，195 例患者（56%）死亡。
结果
sTWEAK 浓度与非缺血性 HF 患者的延长生存相关（P=0.022），但与缺血性 HF 无关（P=0.82）。在多变量 Cox 回归模型中，非缺血性 HF 中的这种反向关联仍然具有统计学意义（P=0.025），与第三个三分位相比，第一个三分位的危险比为 0.40（95%置信区间：0.21-0.77）（P=0.007）。
结论
低 sTWEAK 水平独立预测晚期非缺血性 HF 患者的死亡率。sTWEAK 诱导的心肌细胞增殖可能解释了其对生存率的影响。sTWEAK 在缺血性和非缺血性 HF 中的不同预后价值可能表明决定疾病进程的不同致病途径。
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