Mazurek Walentyna, Salomon Piotr
Katedra i Klinika Kardiologii, Wrocławiu.
Pol Merkur Lekarski. 2002 Jan;12(67):15-9.
Natriuretic peptides ANP, BNP and CNP with their receptors A, B, and C play an important role in maintaining the homeostasis. They have vasodilating, diuretic and natriuretic actions and regulate the systemic resistance. These peptides have been proved to contribute in pathogenesis of many diseases, for example heart failure, hypertension, acute coronary events or hepatic and renal insufficiency. The aim of our study was the estimation whether ANP or BNP could be markers of postinfarct heart failure in patients after thrombolytic therapy. The survey was made in 96 patients with acute myocardial infarction (AMI), who were treated in Department of Cardiology of University School of Medicine in Wrocław. Patients were divided into 2 groups. The first group consisted of 56 patients with reperfusion after thrombolytic therapy and the second group created 40 patients without reperfusion. All patients were administered acethylsalicylic acid, 100 mg r-tPA (recombined tissue plasminogen activator) i.v. within 90 min and heparin in typical doses for the first 3-5 days. Venous blood samples for ANP and BNP estimation were taken before thrombolysis and then in 1st, 3rd, 5th and 30th day after treatment. We also measured the ejection fraction and activity of CPK and CK-MB in all the patients. Patients stayed under clinical observation for 12 months. Our study showed that the levels of ANP and BNP increase in 1st day after treatment in all patients with AMI. The normalization of ANP and BNP occurs in 3rd day after treatment in patients with reperfusion and in patients without reperfusion there are increased levels of these peptides even in 30th day. The increased level of BNP (> 160 pg/ml) is a significant risk factor of left ventricle systolic dysfunction, renewed AMI and sudden death in all patients with AMI after thrombolytic therapy whereas the increased level of ANP (> 100 pg/ml)--only in patients without reperfusion. Taking BNP as a marker of postinfarct heart failure it is possible to asses the risk of this complication in first day after thrombolytic therapy and choose the most proper treatment.
利钠肽(心房钠尿肽、脑钠肽和C型钠尿肽)及其受体A、B和C在维持体内平衡中发挥着重要作用。它们具有血管舒张、利尿和利钠作用,并调节全身阻力。这些肽已被证明在许多疾病的发病机制中起作用,例如心力衰竭、高血压、急性冠脉事件或肝肾功能不全。我们研究的目的是评估心房钠尿肽或脑钠肽是否可以作为溶栓治疗后心肌梗死后心力衰竭的标志物。这项调查针对96例急性心肌梗死(AMI)患者进行,这些患者在弗罗茨瓦夫大学医学院心脏病学系接受治疗。患者被分为两组。第一组由56例溶栓治疗后再灌注的患者组成,第二组由40例未再灌注的患者组成。所有患者均接受100mg乙酰水杨酸、静脉注射重组组织型纤溶酶原激活剂(r-tPA),在90分钟内完成,前3至5天给予常规剂量的肝素。在溶栓前以及治疗后的第1天、第3天、第5天和第30天采集静脉血样本用于评估心房钠尿肽和脑钠肽。我们还测量了所有患者的射血分数以及肌酸磷酸激酶(CPK)和肌酸激酶同工酶(CK-MB)的活性。患者接受了12个月的临床观察。我们的研究表明,所有急性心肌梗死患者治疗后第1天心房钠尿肽和脑钠肽水平升高。再灌注患者治疗后第3天心房钠尿肽和脑钠肽恢复正常,而未再灌注患者即使在第30天这些肽的水平仍升高。脑钠肽水平升高(>160pg/ml)是所有溶栓治疗后的急性心肌梗死患者左心室收缩功能障碍、再次发生急性心肌梗死和猝死的重要危险因素,而心房钠尿肽水平升高(>100pg/ml)——仅在未再灌注患者中出现。将脑钠肽作为心肌梗死后心力衰竭的标志物,可以在溶栓治疗后的第一天评估这种并发症的风险,并选择最恰当的治疗方法。