title: Thrombus aspiration therapy and coronary thrombus components in patients with acute ST-elevation myocardial infarction.
abstract: Inflammation and oxidative stress play key roles in atherosclerotic plaque instability, and plaque rupture/erosion and subsequent thrombus formation constitute the principal mechanisms of total vessel occlusion and acute ST-elevation myocardial infarction (STEMI). Plaque disruption triggers the formation of initial platelet aggregates that grow in association with an increase in fibrin formation, leading to persistent coronary flow obstruction and blood coagulation. The fibrin network may trap large numbers of erythrocytes and inflammatory cells to form an erythrocyte-rich thrombus. In fact, previous clinical studies have shown that not only platelet-rich white thrombi, but also erythrocyte-rich red thrombi can be visualized using angioscopy in patients with acute coronary syndrome. Recently, the development of thrombus aspiration and distal protection devices has significantly improved the clinical outcomes of percutaneous intervention in STEMI patients and has enabled the evaluation of antemortem coronary artery thrombi. This is important because previous autopsy studies were unable to differentiate coronary thrombi responsible for myocardial ischemia from postmortem clots. Using frozen samples of aspirated thrombi and specific monoclonal antibodies, we investigated the cellular components of thrombi (platelets, erythrocytes, fibrin and inflammatory cells, such as myeloperoxidase-positive cells) and pathologically evaluated the relationships between erythrocyte-rich thrombi and inflammation, oxidative stress and clinical outcomes in STEMI patients. Therefore, this review article focuses on the efficacy of thrombus aspiration therapy and the components of aspirated intracoronary thrombi in STEMI patients and presents the results of recent studies regarding the relationship between the composition of aspirated intracoronary thrombi and clinical outcomes.
authors: Department of Cardiology, Osaka City General Hospital, Osaka 534-0021, Japan. kei.yunoki@gmail.com
authors: Kei
authors: K
authors: Yunoki
authors: Takahiko
authors: T
authors: Naruko
authors: Kenichi
authors: K
authors: Sugioka
authors: Mayumi
authors: M
authors: Inaba
authors: Akira
authors: A
authors: Itoh
authors: Kazuo
authors: K
authors: Haze
authors: Minoru
authors: M
authors: Yoshiyama
authors: Makiko
authors: M
authors: Ueda
mesh_terms: D055252:Cell-Derived Microparticles / Q000473:pathology; D003328:Coronary Thrombosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D004912:Erythrocytes / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D018384:Oxidative Stress; D058226:Plaque, Atherosclerotic / Q000473:pathology; D013396:Suction; D017131:Thrombectomy; D013925:Thromboplastin / Q000502:physiology
chemical_list: D013925:Thromboplastin