Yesilbursa Dilek, Serdar Akin, Senturk Tunay, Serdar Zehra, Sağ Saim, Cordan Jale
Cardiology Department, Uludag University Medical School, Kardiyoloji Anabilim Dali, Gorukle, Bursa, Turkey.
Heart Vessels. 2006 Jan;21(1):33-7. doi: 10.1007/s00380-005-0854-4.
Recent evidence suggests that postischemic myocardial dysfunction ("stunning") may be mediated by oxygen free radicals. Various studies have reported the beneficial effects of antioxidants in ischemia-reperfusion injury. The aim of this study was to assess the effect of N-acetylcysteine (NAC) treatment on oxidative stress, infarct size, and left ventricular (LV) function, as adjunct therapy in myocardial infarction (MI). Patients with acute MI received either 15 g NAC infused over 24 h (n = 15) or no NAC (n = 15), combined with streptokinase. Peripheral venous blood was serially sampled to measure creatine kinase (CK)-MB levels. Plasma malondialdehyde (MDA) level was measured at admission and after 4 and 24 h. Echocardiography was performed within 3 days of MI and after 3 months. At admission, plasma MDA levels were not different between the groups. In the NAC-treated patients plasma MDA levels decreased, whereas in the nontreated NAC patients MDA levels increased at 4 and 24 h (P < 0.01 and P < 0.001, respectively). Left ventricular ejection fraction was higher (P < 0.05) and LV end-systolic and end-diastolic diameters were lower (P < 0.001 and P < 0.001) in patients receiving NAC on day 3. Left ventricular wall motion score index was significantly lower in patients treated with NAC on day 3 (P < 0.05). Left ventricular diastolic parameters were not different whether patients were treated with NAC or not. No difference in reduction of infarct size was detected between the groups according to CK-MB levels. It was thus demonstrated that administration of NAC in combination with streptokinase significantly diminished oxidative stress and improved LV function in patients with acute MI. These encouraging results would justify the performance of a larger controlled study.
最近的证据表明，缺血后心肌功能障碍（“心肌顿抑”）可能由氧自由基介导。多项研究报道了抗氧化剂在缺血再灌注损伤中的有益作用。本研究的目的是评估N-乙酰半胱氨酸（NAC）治疗作为心肌梗死（MI）辅助治疗对氧化应激、梗死面积和左心室（LV）功能的影响。急性MI患者接受24小时内静脉输注15克NAC（n = 15）或不接受NAC（n = 15），并联合链激酶治疗。连续采集外周静脉血以测量肌酸激酶（CK）-MB水平。在入院时、4小时和24小时后测量血浆丙二醛（MDA）水平。在MI后3天内和3个月后进行超声心动图检查。入院时，两组间血浆MDA水平无差异。在接受NAC治疗的患者中，血浆MDA水平下降，而在未接受NAC治疗的患者中，MDA水平在4小时和24小时时升高（分别为P < 0.01和P < 0.001）。在第3天，接受NAC治疗的患者左心室射血分数较高（P < 0.05），左心室收缩末期和舒张末期直径较低（分别为P < 0.001和P < 0.001）。在第3天，接受NAC治疗的患者左心室壁运动评分指数显著较低（P < 0.05）。无论患者是否接受NAC治疗，左心室舒张参数均无差异。根据CK-MB水平，两组间梗死面积缩小无差异。因此证明，NAC与链激酶联合应用可显著减轻急性MI患者的氧化应激并改善左心室功能。这些令人鼓舞的结果为开展更大规模的对照研究提供了依据。
