Plebani M, Zaninotto M
Department of Laboratory Medicine, University Hospital of Padua, Via Giustiniani, 2, I-35128 Padua, Italy.
Int J Clin Lab Res. 1999;29(2):56-63. doi: 10.1007/s005990050064.
In the early twentieth century, acute myocardial infarction secondary to acute thrombotic coronary occlusion was considered a rare, fatal condition. Acute myocardial infarction is now one of the most-commmon serious illnesses in the industrialized world. Laboratory medicine now plays a crucial role in identifying risk factors, early events, and conditions triggering plaque rupture in coronary ischemic disease. However, the greatest progress in laboratory research has resulted from the discovery of new and more-promising biochemical markers of myocardial damage. The discovery of cardiac troponins, in particular, has heralded a new age in the diagnosis and treatment or management of a broad spectrum of diseases, grouped together under the heading of acute coronary syndrome, and including stable and unstable angina, and non-Q wave infarction to Q-wave infarction. Cardiac troponins, which are selectively released by damaged myocardiocytes, have a specificity that has not only allowed an improvement in the diagnosis of acute cardiac ischemic disorders, but has also enabled us to make a more-reliable stratification of risk and prediction of outcome. It is generally agreed that two biochemical markers should be used: an early marker (and we recommed myoglobin for this) and a definitive marker, which is cardiac troponin (I or T). Future research is likely to include the standardization of methods for measuring current markers, troponin I in particular, the assessment of rapid bedside tests, and the investigation of the relationship between cardiac markers and emerging immunological and coagulation parameters. Thrombogenesis is now recognized as important in the final process of coronary atherosclerosis, and new markers of thrombogenesis should be used to evaluate the risk of plaque rupture and to monitor the outcome of thrombolytic therapy. Moreover, recent vascular biology studies have provided information on the developmental stages of atherosclerosis and emphasized the importance of the endothelium as a modulator of vascular reactivity, atherogenesis, and plaque stability. The different types of laboratory test (biochemical, immunological, and coagulative) now available, should soon allow improvement in the diagnosis and therapy of ischemic coronary diseases.
在二十世纪初，急性血栓性冠状动脉闭塞继发的急性心肌梗死被认为是一种罕见的致命疾病。如今，急性心肌梗死是工业化国家最常见的严重疾病之一。检验医学在识别冠状动脉缺血性疾病的危险因素、早期事件以及引发斑块破裂的情况方面发挥着关键作用。然而，实验室研究取得的最大进展源于发现了更新且更具前景的心肌损伤生化标志物。尤其是心肌肌钙蛋白的发现，开创了一个新时代，用于诊断和治疗或管理一系列归为急性冠状动脉综合征的疾病，包括稳定型和不稳定型心绞痛，以及非Q波梗死至Q波梗死。受损心肌细胞选择性释放的心肌肌钙蛋白具有特异性，这不仅改善了急性心脏缺血性疾病的诊断，还使我们能够更可靠地进行风险分层和预后预测。人们普遍认为应使用两种生化标志物：一种早期标志物（我们推荐使用肌红蛋白）和一种确诊标志物，即心肌肌钙蛋白（I或T）。未来的研究可能包括测量现有标志物（特别是肌钙蛋白I）方法的标准化、床边快速检测的评估，以及心脏标志物与新兴免疫和凝血参数之间关系的研究。血栓形成现在被认为在冠状动脉粥样硬化的最终过程中很重要，新的血栓形成标志物应被用于评估斑块破裂的风险并监测溶栓治疗的结果。此外，最近的血管生物学研究提供了有关动脉粥样硬化发展阶段的信息，并强调了内皮作为血管反应性、动脉粥样硬化形成和斑块稳定性调节因子的重要性。现有的不同类型实验室检测（生化、免疫和凝血检测），应该很快就能改善缺血性冠状动脉疾病的诊断和治疗。
