New Theory on Thrombus Formation in Atherosclerosis, January 31, 2005

New Theory on Thrombus Formation in Atherosclerosis, January 31, 2005

When atherosclerosis occurs, thrombus formation in arteries is the fundamental cause of patient death. Whether it’s unstable coronary heart disease or myocardial infarction, the ultimate cause of death is thrombus formation, which is essentially atherosclerotic plaque. This plaque can rupture or detach, leading to blockage of coronary vessels and subsequent myocardial infarction. It has now been revealed that atherosclerotic plaques are rich in fibrin and fibrin peptides, interconnected by a dense network of capillaries. Given these characteristics of thrombi, thrombi themselves can cause internal bleeding, and the aforementioned rupture or detachment further increase the risk factors and mortality rate of coronary heart disease. Causes of thrombus formation: ① Lipid deposition; ② Platelet aggregation; ③ Endothelial adhesion.

Based on these reasons, it is believed that the primary cause of CAD (coronary heart disease) evolving into ACS (acute coronary syndrome), TIA (transient ischemic attack), and PAD (peripheral arterial disease) is thrombus formation.

Thrombus formation in atherosclerosis: ① C-reactive protein; ② Fibrinogen; ③ Fibrin peptide A; ④ CD40ligand; ⑤ Amyloid substance A; ⑥ Adhesion factors for blood vessels and cells; ⑦ Prothrombin fragments. Among these factors, testing for C-reactive protein, prothrombin, fibrinogen, and fibrin peptide A is the most critical measure, especially C-reactive protein—if its level is high, the likelihood of thrombus formation is greater.