Keith M, Geranmayegan A, Sole M J, Kurian R, Robinson A, Omran A S, Jeejeebhoy K N
Toronto Hospital, Centre for Cardiovascular Research, Ontario, Canada.
J Am Coll Cardiol. 1998 May;31(6):1352-6. doi: 10.1016/s0735-1097(98)00101-6.
We sought to study the markers of lipid peroxidation and defenses against oxidative stress in patients with varying degrees of heart failure.
Despite advances in other areas of cardiovascular disease, the morbidity and mortality from congestive heart failure (CHF) are increasing. Data mainly from animal models suggest that free radical injury may promote myocardial decompensation. However, there are no studies in humans correlating the severity of heart failure with increased free radical injury and antioxidants.
Fifty-eight patients with CHF and 19 control subjects were studied. In addition to complete clinical and echocardiographic evaluations, the prognosis of these patients was established by measuring the levels of soluble tumor necrosis factor-alpha receptors 1 and 2 (sTNF-R1 and sTNF-R2). Oxidative stress was evaluated by measuring plasma lipid peroxides (LPO), malondialdehyde (MDA), glutathione peroxidase (GSHPx) and vitamin E and C levels.
The patients' age range, cause of heart failure and drug intake were comparable across the different classes of heart failure. Heart failure resulted in a significant increase in LPO (p < 0.005), MDA (p < 0.005), sTNF-R1 (p < 0.005) and sTNF-R2 (p < 0.005). There was a significant positive correlation between the clinical class of heart failure and LPO, MDA, sTNF-R1 and sTNF-R2 levels. There was an inverse correlation between GSHPx and LPO. With increased lipid peroxidation in patients with CHF, the levels of vitamin C decreased, but vitamin E levels were maintained.
These data demonstrate a progressive increase in free radical injury and encroachment on antioxidant reserves with the evolution of heart failure; they also suggest that oxidative stress may be an important determinant of prognosis. The therapeutic benefit of administering antioxidant supplements to patients with CHF should be evaluated.
我们试图研究不同程度心力衰竭患者脂质过氧化的标志物以及抗氧化应激的防御机制。
尽管心血管疾病的其他领域取得了进展,但充血性心力衰竭(CHF)的发病率和死亡率仍在上升。主要来自动物模型的数据表明,自由基损伤可能促进心肌失代偿。然而,尚无人类研究将心力衰竭的严重程度与自由基损伤增加及抗氧化剂相关联。
对58例CHF患者和19例对照者进行研究。除了完整的临床和超声心动图评估外,通过测量可溶性肿瘤坏死因子-α受体1和2(sTNF-R1和sTNF-R2)水平来确定这些患者的预后。通过测量血浆脂质过氧化物(LPO)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSHPx)以及维生素E和C水平来评估氧化应激。
不同心力衰竭分级的患者年龄范围、心力衰竭病因和药物摄入情况具有可比性。心力衰竭导致LPO(p < 0.005)、MDA(p < 0.005)、sTNF-R1(p < 0.005)和sTNF-R2(p < 0.005)显著增加。心力衰竭临床分级与LPO、MDA、sTNF-R1和sTNF-R2水平之间存在显著正相关。GSHPx与LPO呈负相关。随着CHF患者脂质过氧化增加,维生素C水平降低,但维生素E水平保持稳定。
这些数据表明,随着心力衰竭的进展,自由基损伤逐渐增加,抗氧化储备受到侵蚀;它们还表明氧化应激可能是预后的重要决定因素。应评估给CHF患者补充抗氧化剂的治疗益处。