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首页> 外文期刊>Journal of cardiac failure >The role of a common adenosine monophosphate deaminase (AMPD)-1 polymorphism in outcomes of ischemic and nonischemic heart failure.
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The role of a common adenosine monophosphate deaminase (AMPD)-1 polymorphism in outcomes of ischemic and nonischemic heart failure.

机译:常见的单磷酸腺苷脱氨酶(AMPD)-1多态性在缺血性和非缺血性心力衰竭结果中的作用。

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BACKGROUND: A common variant of the adenosine monophosphate deaminase (AMPD)-1 gene (C34T) results in enzymatic inactivity and may increase adenosine in cardiac muscle and confer cardioprotection through ischemic preconditioning. METHODS AND RESULTS: We hypothesized that AMPD1 carriers with ischemic heart failure (HF) in the Beta-Blocker Evaluation of Survival Trial (BEST) might have a relative survival advantage. Patients (n = 1038, 20% black) with ischemic (58%) and nonischemic (42%) HF were followed for an average of 2.0 years for cardiovascular mortality. DNA was purified from blood using phenol/chloroform. Genotyping was performed by polymerase chain reaction with 5' exonuclease chemistry. Differences in survival were assessed by comparing Kaplan-Meier curves with the log-rank test. Genotype frequencies differed by ethnicity (P < .001) but not by disease etiology. AMPD1 genotype did not significantly modify survival in the entire study population (hazard ratio [HR] = 0.91, 95% CI = 0.61-1.37), among ischemics (HR = 0.73, CI = 0.44-1.22, P = .23), or ischemic non-blacks (HR = 0.74, CI = 0.44-1.24, P = .25). Genotype did not modify the effect of bucindolol on mortality. CONCLUSIONS: Results of this study failed to confirm a reported survival benefit among HF patients carrying the AMPD1 T-allele. However, further studies in larger, more homogeneous populations should explore the possibility of a modest survival advantage for patients with ischemic HF.
机译:背景:单磷酸腺苷脱氨酶(AMPD)-1基因(C34T)的常见变体导致酶活性降低,并可能增加心肌中的腺苷并通过缺血预处理来保护心脏。方法和结果:我们假设在试验性Beta-Blocker评估生存试验(BEST)中,患有缺血性心力衰竭(HF)的AMPD1携带者可能具有相对生存优势。患有缺血性(58%)和非缺血性(42%)HF的患者(n = 1038,黑色占20%),平均心血管死亡时间为2。0年。使用苯酚/氯仿从血液中纯化DNA。通过具有5'核酸外切酶化学的聚合酶链反应进行基因分型。通过比较Kaplan-Meier曲线与对数秩检验来评估生存差异。基因型频率因种族而异(P <.001),但因疾病病因而异。 AMPD1基因型没有显着改变整个研究人群的生存率(危险比[HR] = 0.91,95%CI = 0.61-1.37),缺血性(HR = 0.73,CI = 0.44-1.22,P = .23),或缺血性非黑人(HR = 0.74,CI = 0.44-1.24,P = .25)。基因型没有改变丁三醇对死亡率的影响。结论:本研究结果未能证实报道的携带AMPD1 T等位基因的HF患者的生存获益。然而,在更大,更同质的人群中进行进一步的研究应探讨缺血性HF患者适度生存优势的可能性。

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