Active clinical trials for "Myocardial Infarction"

Reducing NOX-2, MMP-9, and TGF-β1 Expression in Preventing Ventricular Remodelling Post Acute ST-Segment Elevation Myocardial Infarction using Colchicine (Post Late Reperfusion Percutaneous Coronary Intervention and Non-Reperfusion and In Vitro Study on Ischemic Rat Cardiomyocyte Culture Model). Coronary heart disease (CHD) is the most common cause of mortality and disability worldwide. The handling of reperfusion in Indonesia is still far below the required standard. Most STEMI patients in Indonesia arrive late to a health facility with symptoms that have been present for more than 12 hours (late-onset). Heart failure following a myocardial infarction is one of the long-term complications of STEMI. Patients with STEMU who do not receive reperfusion were more likely to develop this consequence. According to several studies, microtubules in cardiomyocytes have been identified as an essential regulator of cardiomyocytes' ability to respond to shear stress, which offers compression resistance and facilitates mitochondrial energy production. Microtubule densification, which occurs due to remodelling in heart failure, disrupts the microtubule network. The role of reactive oxygen species (ROS) produced by ischemic myocardium in this remodelling is thus inextricably linked. NADPH oxidase is one of the enzymes involved (NOX). NOX-2 levels have been reported to be higher in myocardial infarction and cardiac remodelling, and it has a close interaction with microtubule network, with damage of microtubule tissue increasing NOX-2 generation of reactive oxygen species. By eroding the ECM and triggering cytokines and chemokines to recruit inflammatory cells to eliminate necrotic cardiomyocytes, matrix metalloproteinase 9 (MMP-9) aids tissue rebuilding. Induction and activation of endogenous TGF-signaling pathways after myocardial infarction have also been discovered to play a function. TGF-β may play a role in the resolution of the inflammatory response in the early stages of infarct repair by inactivating macrophages and decreasing endothelial cell chemokine and cytokine production. TGF-β stimulates the fibrogenic pathway by causing extracellular matrix deposition and fibrosis later. Colchicine is a commonly prescribed anti-inflammatory medication with a low cost. the mechanism of colchicine is tubulin binding, which prevents microtubule assembly and polymerization. Colchicine inhibits microtubule development at low concentrations and promotes microtubule depolymerization at higher concentrations. Several studies have demonstrated that low-dose colchicine can help reduce severe cardiac outcomes such as cardiovascular mortality, stroke, and cardiac arrest following myocardial infarction. Colchicine is known to cause partial restoration of microtubule tissue in the perinuclear region. Colchicine has also been shown in earlier research to reduce the expression of MMP-9, NOX2, and TGF-β This study aims to evaluate whether colchicine could prevent ventricular remodelling in STEMI patients with delayed reperfusion and non reperfusion. The minor hypothesis of this study was colchicine can lower NOX-2, MMP-9, and TGF-β expression in the clinical situation of patients with delayed and non-reperfusion STEMI following PCI. Randomization with 1:1 allocation were used to classify the patients, each group include 41 patients with one group receiving colchicine therapy and standard therapy and the other receiving standard therapy only. Colchicine administration was the independent variable. STEMI patients with delayed and non-reperfusion IKP who met the inclusion criteria are included in this randomized clinical trial. Left ventricular end-diastolic volume (LVEDV) was the dependent variable while serum MMP-9, NOX-2, and TGF-β were the intermediate variables. In the treatment group, colchicine 1 mg is administered before PCI or admission to the ICCU, and colchicine is continued at 0.5 mg/day for a month. Within 24 to 36 hours of treatment initiation, the patient had echocardiography, NOX-2, MMP-9, and TGF-β levels evaluated. On days 4-5, a second NOX-2, MMP-9, and TGF-β screening were performed. The follow up two months after treatment initiation includes an assessment of drug compliance, symptoms, and echocardiography. Depending on the normality of the data distribution, the difference between groups is performed using the unpaired T-test or the Mann-Whitney test. The significant difference between the treatment groups is indicated by a p-value of 0.05.

Introduction: The prevalence of left ventricular(LV) thrombus after acute myocardial infarction has decreased with thrombolysis and primary angioplasty intervention worldwide. However, most of the patients in our country present late after the onset of ischemia resulting in a comparable increase proportion of late presentation MI compared to developed countries. This delayed presentation is associated with the increased incidence of LV thrombus, associated with increased cerebrovascular and cardiovascular events resulting in increased morbidity and mortality. The Vitamin K Antagonist Warfarin is indicated in recent guidelines for the duration of 3-6 months. The use of Warfarin is less in our part of the world due to the requirement of frequent International Normalized Ration (INR) monitoring and dietary restrictions. Novel oral anticoagulants (NOACs) are an alternate option for such hindrance to the treatment of LV thrombus. This research will help assess the safety and efficacy of Rivaroxaban, one of the NOACs compared to warfarin. Objectives: Our aim will be to compare the efficacy of rivaroxaban compared to warfarin in the complete resolution of post-MI LV thrombus. The primary efficacy endpoint of our study will be a resolution of LV thrombus as assessed by cardiac MRI at the end of 3 months of the study period. The secondary endpoint will be the comparison of the safety of both drugs measured by the incidence of major bleeding and embolic events. Methods: The patients who present late after acute MI in our center with LV thrombus will be enrolled in our study. The diagnosis of LV thrombus will be diagnosed by cardiac MRI, which is considered the gold standard for the diagnosis. The patients then will be randomized in a 1:1 ratio to either warfarin or rivaroxaban within 24 hours of diagnosis of LV thrombus. The warfarin group will be prescribed the warfarin in the dose of 5mg daily and the dose titrated according to the INR value to maintain the INR range of 2 to 3. Rivaroxaban group will be prescribed 15 to 20mg according to the indication. The research group consisting of the principal investigator and coinvestigators will be responsible for the recruitment and overall study procedures.

Contemporary data are lacking regarding the management of left ventricular thrombus (LVT) developed after ST segment elevation myocardial infarction

Ticagrelor-based De-escalation of Dual Antiplatelet Therapy After Coronary Artery Bypass Grafting trial (TOP-CABG trial) is a multicenter, randomized, double-blind, non-inferiority, parallel controlled trial. The aim of TOP-CABG is to investigate whether de-escalated dual antiplatelet therapy (De-DAPT) is non-inferior to dual antiplatelet therapy (DAPT) in efficacy on inhibiting great saphenous vein (SVG) graft occlusion and is superior in reducing bleeding events in patients accepting coronary artery bypassing grafting.

Glucose monitoring after Acute Myocardial infarct in people with diabetes is a Dexcom funded study that is investigating whether the use of continuous glucose monitors (Dexcom ONE model) in people with type 2 diabetes facilitates time in glycaemic range in the 6 months after an acute myocardial infarction. As an exploratory outcome it will investigate whether time in glycaemic range is associated with changes in mortality and major adverse cardiac events in the 6 months after acute myocardial infarct.

In the present study, we aim to investigate the effects of dobutamine infusion and/or a single intravenous (IV) dose of the IL-6 antagonist Tocilizumab administered after percutaneous coronary intervention (PCI) to patients with acute myocardial infarction (AMI) presenting < 24 hours from onset of chest pain and an intermediate to high risk of cardiogenic shock (CS) by assessment with the ORBI risk score (≥10 - not in overt shock at hospital admission). Plasma concentrations of N-terminal pro-B-type natriuretic peptide (NTproBNP) as a proxy for development of cardiogenic shock (CS) and hemodynamic instability will be sampled for primary endpoint analysis. Effects on clinical parameters, mortality, morbidity as well as specific indicators of inflammation, cardiac function, and infarct size will secondarily be assessed noninvasively. The rationale behind the current study is that inflammatory and neurohormonal responses are associated with subclinical hemodynamic instability in patients with AMI with high risk of CS have worse outcomes. The potentially unstable condition may be targeted pharmacologically as an add-on to existing therapy. This is investigated in patients at elevated risk of CS by sampling biomarkers reflecting the inflammatory and neurohormonal responses, as well as determining effects on patient outcomes and infarct size.

Although recommended therapy for patients with ST-segment elevation myocardial infarction is primary PCI, it remains unestablished whether patients with a symptom duration of more 12 hours benefit from acute revascularisation. This study aims to investigate whether acute intervention is superior to subacute intervention in these patients.

REDUCING INFLAMMATION IN ISCHEMIC STROKE WITH COLCHICINE, AND TICAGRELOR IN HIGH-RISK PATIENTS-EXTENDED TREATMENT IN ISCHEMIC STROKE.

In a single-center, open-label, prospective, controlled, clinical study, it is planned to include 300 patients hospitalized in the cardiology department of SBHI Penza regional clinical hospital n.a. N.N. Burdenko. Recruitment of patients will be carried out at the Department of Therapy of the Medical Institute of the Penza State University. Patients meeting the inclusion criteria and not meeting the exclusion criteria will be included in the study. Initially, lipid-lowering treatment with atorvastatin is prescribed at a dose of 80 mg / day from the first 24-96 hours of AMI in addition to the standard therapy. If there is no achievement of the target level of LDL-C, ≤1.5 mmol / L after 5-6 weeks from the AMI onset, patients additionally receive ezetimibe at a dose of 10 mg 1 time / day. Standard AMI treatment includes dual antiplatelet therapy, ACE inhibitors, beta-blockers (if indicated). Prescription of proton pump inhibitors and nitrates is possible (if indicated). The total follow-up is 96 weeks. Prescreening - 600 people; screening and randomization - 300 people. Parameters of electrical myocardial heterogeneity, myocardial deformation characteristics, vascular rigidity, and quality of life will be assessed according to the study plan.

Myocardial infarction (MI), as one of the many complications of COVID-19, is one of the contributing patients of patients' death. This study attempts on developing an intervention of MI by regenerating damaged cardiomyocytes due to insufficiency of oxygen in cardiac muscles, triggered by an occlusion of coronary artery (MI). Heart patch developed from amnion bilayer seeded with amnion epithelial stem cells and patient's autologous cardiomyocytes is used as a therapy. Patients who undergo bypass (CABG) surgery are given heart patch, and then patients condition are observed by ECG, Echo, blood test, and radiology (technetium-99m)