Role and mechanism of thrombospondin in response to beta blocker therapy in patients with congestive heart failure

我们检测了非缺血性充血性心力衰竭患者应用β受体阻滞剂治疗前、治疗后6个月和12个月的血浆Ala523Thr基因多态性(G/A)和凝血酶敏感蛋白-1水平，并与正常健康志愿者进行比较。在正常健康志愿者中，GG组和非GG组的血浆凝血酶原蛋白-1水平无显著差异。在非缺血性充血性心力衰竭患者中，GG组与非GG组的血浆凝血酶敏感蛋白-1水平差异无统计学意义。β受体阻滞剂治疗前至治疗后12个月BNP水平的变化与血浆凝血酶原蛋白-1水平的变化显著相关。凝血酶敏感蛋白-1可能在非缺血性充血性心力衰竭慢性期的血流动力学优化中发挥作用。

We evaluated Ala523Thr polymorphism(G/A) and thrombospondin-1 plasma levels in nonischemic congestive heart failure patients before, 6, and 12 months after administration of beta blocker therapy and in normal healthy volunteers. There were no significant differences of thrombospondin-1 plasma levels between GG group and non GG group in normal healthy volunteers. No significant differences of thrombospondin-1 plasma levels were found between GG group and non GG group in nonischemic congestive heart failure patients. There were significant correlations between changes in BNP levels from before to 12 months after administration of beta blocker therapy and those in plasma thrombospondin-1 levels. Thrombospondin-1 may play a role in hemodynamic optimization at the chronic stage of nonischemic congestive heart failure.