Hellstern P, Bach J, Haubelt H, Preiss A, Winkelmann B R, Senges J
Institut für Hämostaseologie und Transfusionsmedizin, Ludwigshafen.
Med Klin (Munich). 2001 Apr 15;96(4):217-27. doi: 10.1007/pl00002197.
Hemostatic disorders are substantially involved in the pathogenesis of coronary heart disease and acute coronary syndromes. In addition to biochemical markers, gene polymorphisms of hemostasis have been intensively studied in terms of their association with coronary risk. These include polymorphisms of the genes of platelet glycoproteins, fibrinogen, prothrombin, factors V, VIII and XIII, plasminogen activator inhibitor-1 and tissue-type plasminogen activator. An association of a certain gene polymorphism with an increased coronary risk has usually been demonstrated in retrospective case-control studies. However, numerous clinical studies have not yet been able to identify any of these polymorphisms as unequivocal risk factors of coronary heart disease or acute coronary syndromes. These inconsistencies are mainly due to the complexity of the pathogenesis of coronary heart disease and the minor contribution of a single polymorphism to total coronary risk. This review reports on essential requirements of future studies as a prerequisite to improve our understanding of the genetic basis of coronary heart disease.
止血障碍在冠心病和急性冠脉综合征的发病机制中起着重要作用。除了生化标志物外，止血相关基因多态性与冠心病风险的关联也得到了深入研究。这些基因包括血小板糖蛋白、纤维蛋白原、凝血酶原、因子V、VIII和XIII、纤溶酶原激活物抑制剂-1和组织型纤溶酶原激活物的基因多态性。在回顾性病例对照研究中，通常已证明某种基因多态性与冠心病风险增加有关。然而，众多临床研究尚未能够将这些多态性中的任何一种确定为冠心病或急性冠脉综合征的确切危险因素。这些不一致主要归因于冠心病发病机制的复杂性以及单个多态性对总冠心病风险的微小贡献。本综述报告了未来研究的基本要求，作为提高我们对冠心病遗传基础理解的先决条件。
