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EDTA螯合劑或降伴糖尿病心梗患者的心血管事件

2013-11-28 10:21 閱讀:1070 來源:愛愛醫(yī) 作者:孫福慶 責(zé)任編輯:云霄飄逸
[導(dǎo)讀] 于AHA2013科學(xué)年會公布的美國一項(xiàng)研究表明,在年齡大于50歲且伴有糖尿病的心肌梗死后患者中,EDTA螯合劑治療可顯著減少心血管事件。但該研究并未充分證明對所有的伴糖尿病心梗后患者常規(guī)用螯合療法。

    結(jié)果顯示,在633例(37%)糖尿病患者中,EDTA組的5年主要終點(diǎn)發(fā)生率顯著降低(25%對38%;危險比[HR] 0.59)。對多亞組實(shí)施Bonferroni校正之后上述結(jié)果依然具有顯著性(校正P=0.002)。EDTA組的全因死昂率和次要終點(diǎn)發(fā)生率均顯著降低,但對多亞組進(jìn)行校正之后顯著性消失。減少1項(xiàng)主要終點(diǎn)的需治療數(shù)為6.5。在1075例非糖尿病患者中相關(guān)事件則無減少。

    于AHA2013科學(xué)年會公布的美國一項(xiàng)研究表明,在年齡大于50歲且伴有糖尿病的心肌梗死后患者中,EDTA螯合劑治療可顯著減少心血管事件。但該研究并未充分證明對所有的伴糖尿病心梗后患者常規(guī)用螯合療法。論文11月19日在線發(fā)表于《循環(huán)》。

    此項(xiàng)TACT研究以年齡≥50歲且既往伴有心肌梗死的患者為受試者,共633例糖尿病患者,被隨機(jī)分為EDTA螯合劑組(322例)或安慰劑組(311例)。主要終點(diǎn)為死亡、心梗再發(fā)、卒中、冠脈血運(yùn)重建或心絞痛住院;次要終點(diǎn)為心血管死亡、心梗再發(fā)或卒中。

    結(jié)果顯示,在633例(37%)糖尿病患者中,EDTA組的5年主要終點(diǎn)發(fā)生率顯著降低(25%對38%;危險比[HR]0.59)。對多亞組實(shí)施Bonferroni校正之后上述結(jié)果依然具有顯著性(校正P=0.002)。EDTA組的全因死昂率和次要終點(diǎn)發(fā)生率均顯著降低,但對多亞組進(jìn)行校正之后顯著性消失。減少1項(xiàng)主要終點(diǎn)的需治療數(shù)為6.5.在1075例非糖尿病患者中相關(guān)事件則無減少。

    原文閱讀:

    Abstract

    Background—The Trial to Assess Chelation Therapy (TACT) showed clinical benefit of an EDTA-based infusion regimen in patients aged ≥50 years with prior myocardial infarction. Diabetes mellitus before enrollment was a prespecified subgroup.

    Methods and Results—Patients received 40 infusions of EDTA chelation or placebo. A total of 633 (37%) patients had diabetes mellitus (322 EDTA and 311 placebo)。 EDTA reduced the primary end point (death, reinfarction, stroke, coronary revascularization, or hospitalization for angina; 25% versus 38%; hazard ratio, 0.59; 95% confidence interval [CI], 0.44–0.79; P<0.001) for over 5 years. The result remained significant after Bonferroni adjustment for multiple subgroups (99.4% CI, 0.39–0.88; adjusted P=0.002)。 All-cause mortality was reduced by EDTA chelation (10% versus 16%; hazard ratio, 0.57; 95% CI, 0.36–0.88; P=0.011), as was the secondary end point (cardiovascular death, reinfarction, or stroke; 11% versus 17%; hazard ratio, 0.60; 95% CI, 0.39–0.91; P=0.017)。 However, after adjusting for multiple subgroups, those results were no longer significant. The number needed to treat to reduce 1 primary end point over 5 years was 6.5 (95% CI, 4.4–12.7)。There was no reduction in events in non–diabetes mellitus (n=1075; P=0.877), resulting in a treatment by diabetes mellitus interaction (P=0.004)。

    Conclusions—Post–myocardial infarction patients with diabetes mellitus aged ≥50 demonstrated a marked reduction in cardiovascular events with EDTA chelation. These findings support efforts to replicate these findings and define the mechanisms of benefit. However, they do not constitute sufficient evidence to indicate the routine use of chelation therapy for all post–myocardial infarction patients with diabetes mellitus.


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