The effect of heparin administration time on thrombolysis in myocardial infarction flow grade in patients with acute ST-elevation myocardial infarction treated with primary percutaneous coronary intervention

Keywords: Angioplasty; Heparin; Myocardial Infarction; ST-Elevation Myocardial Infarction; Thrombolysis Date of submission: 06 Nov. 2021, Date of acceptance: 20 Dec. 2021 Introduction Myocardial infarction (MI) is a cardiac emergency in which the patient may die or suffer from the complications of the disease if emergency medical care is not provided in the golden time.1 ST-segment elevation MI (STEMI) resulting from thrombotic occlusion of a coronary artery overlaid on a ruptured atherosclerotic plaque is one of the leading causes of mortality and morbidity worldwide.2,3 The primary goal of the initial treatment in MI is early coronary reperfusion.4 The ideal reperfusion strategy in patients with STEMI is primary percutaneous coronary intervention (PPCI), mainly when performed in the first 2 hours following diagnosis.5,6 Primary angioplasty may result in a more inclusive and steady patency rate of the infarct-related artery (IRA) compared with thrombolytic therapy.7 In angiography, blood flow in IRA is evaluated by a simple qualitative system called the thrombolysis in myocardial infarction (TIMI) risk score. Reperfusion may be induced by adjunctive therapy and limit myocardial injury.10 Intravenous (IV) unfractionated heparin (UFH) (a heterogeneous mixture of polysaccharide molecules) has been found to be efficient in early thrombin activity and occlusion reduction, and improves the culprit artery patency.11,12 In addition, it is a well-known procedure for anticoagulant therapy at the time of percutaneous coronary intervention (PCI) in patients with STEMI.13 Heparin is an anticoagulant agent that inactivates thrombin and factor Xa through activating the antithrombin III in body, and eventually inhibits clot formation.14 Heparin is mainly useful to prevent and treat venous thromboembolism (VTE) and pulmonary embolism (PE), reduce the risk of molar thrombosis after MI, and treat patients presenting with unstable angina and MI.15 UFH binds strongly to plasma proteins which results in unpredictable levels of free heparin in the blood circulation. [...]UFH presents significant alterations in antithrombotic results and needs close monitoring.12 However, in the clinical setting of patients with acute STEMI, there are some controversies about the role of early heparin administration time on the patients' outcome and the culprit vessel patency. [...]we tried to evaluate the findings of previous papers in a randomized clinical trial by investigating the effect of