Deicher R, Nikfardjam M, Woisetschläger C, Gottsauner-Wolf M, Huber K
Klinischen Abteilung für Kardiologie der Universitätsklinik für Innere Medizin II, Wien.
Acta Med Austriaca. 1999;26(2):70-82.
This article discusses recent developments in the field of acute coronary syndromes including pathophysiological mechanisms as well as therapeutic strategies. A plaque disruption is caused by different stimuli in a plaque prone to rupture, i.e. a plaque with a lipid-rich core and high local concentration of inflammatory cells (T-cells, monocytes/macrophages, mast cells). These cells are capable of producing matrix degradation products and can reduce stability of a plaque. Thrombus formation, based on platelet activation and aggregation as well as fibrin formation, is the main consequence of plaque disruption. Depending on the degree of thrombus formation occlusion is followed clinically by unstable angina (subtotal occlusion) or by acute myocardial infarction (total occlusion). Accompanying vasoconstriction may further aggravate the situation. Principles of therapy are thrombus dissolution as well as prevention of new thrombus formation: main goals of thrombolytic therapy in acute myocardial infarction are a prompt (less than 3 hours), complete, and sustained (prevention of early thrombotic reocclusion) reperfusion.
本文讨论了急性冠状动脉综合征领域的最新进展，包括病理生理机制以及治疗策略。斑块破裂是由易破裂斑块中的不同刺激因素引起的，即具有富含脂质核心和高局部炎症细胞浓度（T细胞、单核细胞/巨噬细胞、肥大细胞）的斑块。这些细胞能够产生基质降解产物并降低斑块的稳定性。基于血小板活化、聚集以及纤维蛋白形成的血栓形成是斑块破裂的主要后果。根据血栓形成的程度，临床上随后会出现不稳定型心绞痛（次全闭塞）或急性心肌梗死（完全闭塞）。伴随的血管收缩可能会使情况进一步恶化。治疗原则是溶解血栓以及预防新血栓形成：急性心肌梗死溶栓治疗的主要目标是迅速（少于3小时）、完全且持续（预防早期血栓再闭塞）的再灌注。
