Center of Excellence on Aging, G D'Annunzio University Foundation, Chieti, Italy.
J Thromb Haemost. 2010 May;8(5):914-22. doi: 10.1111/j.1538-7836.2010.03820.x. Epub 2010 Jan 24.
Thromboembolism is a relatively common complication of chronic heart failure (HF) and the place of antiplatelet therapy is uncertain.
We characterized the rate of thromboxane and prostacyclin biosynthesis in chronic HF of ischemic origin, with the aim of separating the influence of HF on platelet activation from that of the underlying ischemic heart disease (IHD).
We compared urinary 11-dehydro-thromboxane (TX)B(2), 2,3 dinor 6-keto-PGF(1alpha,) 8-iso-prostaglandin (PG)F(2alpha), and plasma N-terminal pro-brain natriuretic peptide (NT-pro-BNP), asymmetric dimethylarginine (ADMA), and soluble CD40 ligand (sCD40L), in 84 patients with HF secondary to IHD, 61 patients with IHD without HF and 42 healthy subjects.
HF patients not on aspirin had significantly higher urinary 11-dehydro-TXB(2) as compared with healthy subjects (P < 0.0001) and IHD patients not on aspirin (P = 0.028). They also showed significantly higher 8-iso-PGF(2alpha) (P = 0.018), NT-pro-BNP (P = 0.021) and ADMA (P < 0.0001) than IHD patients not on aspirin. HF patients on low-dose aspirin had significantly lower 11-dehydro-TXB(2) (P < 0.0001), sCD40L (P = 0.007) and 2,3-dinor-6-keto-PGF(1alpha) (P = 0.005) than HF patients not treated with aspirin. HF patients in NYHA classes III and IV had significantly higher urinary 11-dehydro-TXB(2) than patients in classes I and II, independently of aspirin treatment (P < 0.05). On multiple linear regression analysis, higher NT-pro-BNP levels, lack of aspirin therapy and sCD40L, predicted 11-dehydro-TXB(2) excretion rate in HF patients (R(2) = 0.771).
Persistent platelet activation characterizes HF patients. This phenomenon is related to disease severity and is largely suppressable by low-dose aspirin. The homeostatic increase in prostacyclin biosynthesis is impaired, possibly contributing to enhanced thrombotic risk in this setting.
摘要 背景：血栓栓塞是慢性心力衰竭（HF）的一种相对常见的并发症，抗血小板治疗的地位尚不确定。
我们描述了缺血性起源的慢性 HF 中血栓烷和前列环素生物合成的速率，目的是将 HF 对血小板激活的影响与潜在的缺血性心脏病（IHD）的影响分开。
我们比较了尿 11-脱氢血栓烷（TX）B（2），2,3-二去甲 6-酮-PGF（1α），8-异前列腺素（PG）F（2α），血浆 N-末端脑钠肽前体（NT-pro-BNP），不对称二甲基精氨酸（ADMA）和可溶性 CD40 配体（sCD40L）在 84 例 HF 继发于 IHD 的患者，61 例 IHD 无 HF 的患者和 42 例健康受试者。
未服用阿司匹林的 HF 患者的尿 11-脱氢-TXB（2）水平明显高于健康受试者（P <0.0001）和未服用阿司匹林的 IHD 患者（P = 0.028）。与未服用阿司匹林的 IHD 患者相比，他们还显示出明显更高的 8-异前列腺素（PG）F（2α）（P = 0.018），NT-pro-BNP（P = 0.021）和 ADMA（P <0.0001）。低剂量阿司匹林治疗的 HF 患者的 11-脱氢-TXB（2）（P <0.0001），sCD40L（P = 0.007）和 2,3-二去甲-6-酮-PGF（1α）（P = 0.005）明显低于未服用阿司匹林的 HF 患者。NYHA 分级 III 和 IV 的 HF 患者的尿 11-脱氢-TXB（2）明显高于 I 级和 II 级患者，与阿司匹林治疗无关（P <0.05）。多元线性回归分析显示，较高的 NT-pro-BNP 水平，缺乏阿司匹林治疗和 sCD40L 可预测 HF 患者的 11-脱氢-TXB（2）排泄率（R（2）= 0.771）。
持续性血小板激活是 HF 患者的特征。这种现象与疾病的严重程度有关，并且可以通过低剂量阿司匹林来很大程度上抑制。前列腺素生物合成的稳态增加受到损害，这可能导致在这种情况下血栓形成风险增加。
