Thrombosis and Acute coronary syndrome

Abbate, Rosanna; Cioni, Gabriele; Ricci, I.; Miranda, Marco; Gori, Anna Maria

doi:10.1016/j.thromres.2011.12.026

Cited by 86 publications

(61 citation statements)

References 30 publications

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“…Acute coronary syndrome (ACS) arises from the formation of thrombus at damaged atherosclerotic plaques in coronary arteries [1][2][3][4][5][6][7][8][9][10][11]. Acute coronary syndrome is a complex disease determined by both genetic and environmental issues.…”

Section: Introductionmentioning

confidence: 99%

Identification of gene variants related to the nitric oxide pathway in patients with acute coronary syndrome

Umman

Çakmakoğlu

Çinçin

et al. 2015

Gene

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Section: Introductionmentioning

confidence: 99%

Identification of gene variants related to the nitric oxide pathway in patients with acute coronary syndrome

Umman

Çakmakoğlu

Çinçin

et al. 2015

Gene

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“…Thrombin, in the final step of coagulation, interacting with fibrinogen, forms fibrin and activates factors V, VIII and XII. In addition, thrombin formation during the initial phases of the coagulative process is further significantly increased by a positive feedback loop and platelet activation [2]. During AMI, as well as afterwards, a ‘hypercoagulable state' is detectable using methods assessing ongoing thrombin and fibrin formation and cleavage in plasma [3].…”

Section: Introductionmentioning

confidence: 99%

Thrombin Generation and Platelet Reactivity at Hospital Discharge and 6-Month Outcome after the Acute Coronary Syndrome in Diabetic and Nondiabetic Patients

et al. 2014

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Objectives: Increased plasma thrombogenesis and blood platelet reactivity are associated with a worse outcome in patients with the acute coronary syndrome (ACS). The aim of this study was to test the clinical utility of combining a thrombin generation test and platelet aggregation in predicting future ischemic events after ACS. Methods: The study included patients hospitalized due to ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention with stent implantation. Blood for platelet aggregation and thrombin generation was collected at hospital discharge. We performed whole-blood platelet aggregation with arachidonic acid (AA), collagen, adenosine diphosphate and thrombin receptor-activating peptide (TRAP) as agonists and the thrombin generation test using a fluorescence method. Patients were followed for up to 6 months. The combined end point of the study consisted of death, stroke, myocardial infarction or repeated target vessel revascularization. Results: The study enrolled 161 patients. The end point occurred in 30 patients (18.6%). Thrombin generation showed a significantly prolonged lag time, time to thrombogram peak and start of the tail of the thrombogram in diabetic patients who reached the study end point but not in nondiabetics. End point occurrence was not connected with platelet reactivity at hospital discharge in the whole group. In the diabetic subgroup, increased platelet aggregation induced with AA and TRAP at hospital discharge was connected with a more frequent occurrence of the study end point. Conclusions: In diabetic patients after STEMI, thrombin generation measures as well as TRAP- and AA-induced platelet aggregation at hospital discharge are associated with an ensuing ischemic event during the 6-month follow-up.

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“…The pathophysiology of atherosclerotic plaque is essential to understand the criticality of these diseases and the correct functioning of pharmacological strategies [2].…”

mentioning

confidence: 99%

Thrombosis and Acute coronary syndrome

Cited by 86 publications

References 30 publications

Identification of gene variants related to the nitric oxide pathway in patients with acute coronary syndrome

Identification of gene variants related to the nitric oxide pathway in patients with acute coronary syndrome

Thrombin Generation and Platelet Reactivity at Hospital Discharge and 6-Month Outcome after the Acute Coronary Syndrome in Diabetic and Nondiabetic Patients

New Insights on Long-Term Aspirin Therapy in Primary Prevention for Cardiovascular Disease

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