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 erythrocyterich 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.

Coronary thrombus composition: Links with inflammation, platelet and endothelial markers

“…In STEMI patients presenting later that 6 h from symptom onset, insignificantly shorter clotting time, stiffer clot and longer clot lysis time were noted [8]. Similar results on coronary thrombus composition were obtained using histochemical techniques [9,10] or magnetic resonance imaging [11]. It has also been reported that the ruptured plaque is more prone to initiate the fibrin-rich thrombus formation as opposed to the eroded plaque [12].…”

“…It has also been reported that the ruptured plaque is more prone to initiate the fibrin-rich thrombus formation as opposed to the eroded plaque [12]. Moreover, serum myeloperoxidase (MPO) derived from activated neutrophils and monocytes is elevated in ACS and MPO-positive neutrophils represent a larger component of intracoronary thrombi in the ACS patients with eroded plaques [9,13,14].…”

Comparison between the Outcomes of Intracoronary and Intravenous Administration of Eptifibatide during Primary Percutaneous Coronary Intervention in Patients with Acute ST-Elevation Myocardial Infarction

“…These results can be explained by the high local concentrations of eptifibatide achieved in IC administration in comparison to the IV route. Similar to abciximab and tirofiban, eptifibatide is a GPI that blocks the final common pathway of platelet aggregation by binding to platelet GP b/ a receptors, which bind to fibrinogen and other adhesive proteins that crosslink adjacent platelets 4,[33][34][35] . It also has dose-dependent antiplatelet, dethrombotic, and anti-inflammatory features [6][7][8][34][35][36] .…”

“…Similar to abciximab and tirofiban, eptifibatide is a GPI that blocks the final common pathway of platelet aggregation by binding to platelet GP b/ a receptors, which bind to fibrinogen and other adhesive proteins that crosslink adjacent platelets 4,[33][34][35] . It also has dose-dependent antiplatelet, dethrombotic, and anti-inflammatory features [6][7][8][34][35][36] . Because they compete with fibrinogen in binding to the platelet GP b/ a receptor, high localized concentrations of the drug may enable the dissociation of bound fibrinogen and dissolve the formed thrombus 6,[36][37][38] .…”

Case Report: INTRAPROCEDURAL STENT THROMBOSIS IN PERCUTANEOUS CORONARY ANGIOPLASTY

“…The use of intracoronary imaging modalities such as Intra Vascular Ultra Sound (IVUS) and Optical Coherence Tomography (OCT) is very helpful as guiding the expansion and apposition of the stent to be more adequate (Buchanan et al 2012). Also look for mechanical predisposing factors underlying ST (Yunoki et al 2012).…”