Thrombus Aspirated from Patients with ST-Elevation Myocardial Infarction: Association between 3-Nitrotyrosine and Inflammatory Markers - Insights from ARTERIA Study.

Recent studies have demonstrated that inflammatory cells are a component that plays a role in thrombus formation in ST-elevation myocardial infarction (STEMI). 3-nitrotyrosine (3-NO2-Tyr), a specific marker for protein modification by nitric oxide-derived oxidants, is increased in human atherosclerotic lesions. The purpose of this study was to determine the possible association of inflammatory markers of coronary thrombi with nitroxidative stress. Intracoronary thrombus (n=51) and blood from the systemic circulation were obtained by thromboaspiration in 138 consecutive STEMI patients presenting for primary percutaneous coronary intervention (PCI). Each blood and intracoronary thrombus were measured simultaneously the following biomarkers: C-reactive protein (CRP), 3-NO2-Tyr, soluble CD 40 ligand (sCD40L), vascular cellular adhesion molecule-1 (VCAM-1) and haemoglobin content (only in coronary thrombus). Time delay in minutes from symptom onset to PCI was 244 ± 324. Serum CRP was positively correlated to CRP content in the thrombus (r= 0.395; p = 0.02) and serum sCD40L was negatively correlated to sCD40L in the thrombus (r= -0.394; p = 0.02). Patients were divided into tertiles according to thrombi 3-NO2-Tyr concentration: 1(st)tertile (<0.146ng/mg), 2(nd)tertile (0.146-0.485ng/mg) and 3(rd)tertile (>0.485ng/mg). Thus, thrombus in the highest tertile had significantly higher levels of CRP (p=0.002), VCAM-1 (p=0.003) and haemoglobin (p=0.002). In conclusion, the present study demonstrated that coronary thrombi with higher levels of 3-NO2-Tyr content often contain more inflammatory markers which could have a direct impact on the efficacy of drugs or devices used for coronary reperfusion.

Inflammatory markers in blood and thrombus aspirated from patients with acute myocardial infarction with st-segment elevation: ARTERIA trial study design and rationale.

The mechanism of coronary thrombus formation is a complex phenomenon that involves different cellular components. ARTERIA is a prospective, multicenter study that will include patients presenting with a diagnosis of ST-elevation acute coronary syndrome undergoing thrombus aspiration during an emergency primary percutaneous coronary revascularization. The purpose of the ARTERIA study is to try to clarify whether there is an association between inflammatory markers measured in blood and in intracoronary thrombi and, if any, what set of molecules provides better prognostic information in these patients. Our study will help to elucidate the complex relationship between thrombus and circulating blood.

Recurrent intraventricular thrombus six months after ST-elevation myocardial infarction in a diabetic man: a case report.

BACKGROUND: Percutaneous coronary intervention with placement of a drug-eluting stent in a diabetic patient with ST-elevation myocardial infarction is a relatively common procedure, and always requires subsequent treatment with dual antiplatelet therapy. It is sometimes necessary to add oral anticoagulation therapy because of individual clinical circumstances, which further increases the risk of bleeding. CASE PRESENTATION: A 66-year-old hypertensive diabetic man with a history of gastrointestinal bleeding was admitted with an ST-elevation inferior myocardial infarction that had been evolving over 72 h. Electrocardiography showed ST segment elevation in the inferior leads and Q waves in the inferior and anterior leads. He reported a similar episode of chest pain 1 month previously, for which he had not sought medical treatment. Coronary angiography showed chronic occlusion of the mid-left anterior descending coronary artery, and acute occlusion of the mid-right coronary artery. He was treated by percutaneous coronary intervention, with placement of a drug-eluting stent in the right coronary artery. Soon after admission, transthoracic echocardiography showed abnormal left ventricular contractility and a large left intraventricular thrombus. Three weeks after admission, the patient was discharged on dual antiplatelet therapy (clopidogrel and aspirin) and oral anticoagulation therapy (acenocoumarol). Four months after discharge, transthoracic echocardiography showed absence of left ventricular thrombus and resolution of the abnormal contractility in the area supplied by the revascularized right coronary artery. Given the high risk of bleeding, oral anticoagulation therapy was stopped. Six months later, transthoracic echocardiography showed recurrent left ventricular apical thrombus, and an underlying hypercoagulable state was ruled out. Oral anticoagulation therapy was restarted on an indefinite basis, and dual antiplatelet therapy was continued. CONCLUSIONS: The present case illustrates the need for repeat transthoracic echocardiography following the withdrawal of oral anticoagulation therapy in patients with ST-elevation myocardial infarction, both to monitor thrombus status and to assess left ventricular segmental contraction. In patients who require anticoagulation, avoidance of a drug-eluting stent is strongly preferred and second-generation stents are recommended. The alternative regimen of oral anticoagulation and clopidogrel may be considered in this scenario. In patients with recurrent intraventricular thrombus an underlying hypercoagulable state should be ruled out.