View clinical trials related to Acute Myocardial Infarction.
Filter by:Background: Acute myocardial infarction (AMI) is the second cause of death worldwide. After AMI, the heart failure (HF) is a main cause of patient rehospitalization and death. Despite the total ischemic time of AMI is decreasing in general at present, the incidence of HF after AMI remains high. The incidence of HF in Switzerland and the United States are 25% and 14-16%, respectively, and the epidemiological statistic of AMI in the past 10 years was lacking in China, but the rate has been exceeded 22% by conservative estimation. Early cardiac rehabilitation quality improvement system has been shown to reduce incidence of post-infarction HF and improve cardiovascular function. However, early cardiac rehabilitation has low proportion and poor quality, which lacks of standard. Objective: The purposes of this quality improvement study are to evaluate a pointed, two-phase intervention system to improve the proportion and quality of cardiac rehabilitation; to standardize the early cardiac rehabilitation procedure to improve the prognosis among patients with post-infarction HF. Methods: Including the period I of cardiac rehabilitation, pre-discharge (baseline) assessment and the period II of cardiac rehabilitation. Statistical analysis: Data analyses are performed using the software package SAS version 9.2 and all tests are 2-sided with P<0.05 denoting statistical significance. Quantitative data changes between groups which are compared with using the paired Student's t test and Wilcoxon rank sum test according to the data distribution, and categorical data is analyzed by chi-square test and ranked data is analyzed by Wilcoxon rank sum test. The investigator compare the incidence of heart failure in early rehabilitation patients between two phases according to the chi-square test of the rate of two groups, to explore the role of early cardiac rehabilitation after AMI in reducing the incidence of HF after AMI.
The goal of this study is to find out how fast a drug called selatogrel (ACT-246475) can prevent platelets from binding together. This study will also help to find out more about the safety of this new drug. The drug selatogrel (ACT-246475) will be used in 2 different doses (8 mg or 16 mg) and will be administered in the thigh.
A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Safety and Efficacy Study of Dutogliptin in Combination with Filgrastim in Early Recovery Post-Myocardial Infarction
A total of 50 participants diagnosed with ACS (group A ticagrelor 180mg/d, n=25), group B (clopidogrel 75mg + rivaroxaban 5mg/ d, n=25)) were consecutively enrolled and treated with study drugs on top of aspirin (100mg/d) for 1 month. VerifyNow® and Global thrombosis test were performed at day 2 and 1 month after administration of study drugs. The investigators compared aspirin reaction unit (ARU) and P2Y12 reaction unit (PRU), occlusion time (OT) which reflects shear stress-induced thrombotic activity, and lysis time (LT) which showed endogenous lytic activity between the two strategies at both time points.
The purpose of this study is to evaluate the safety, efficacy, and pharmacokinetics (PK) of three dose levels of FDY-5301 compared to placebo in STEMI patients undergoing PCI.
The aim of this study is to compare circadian variability of antiplatelet effect of prasugrel and ticagrelor maintenance doses during the initial days after acute myocardial infarction.
The aim is to examine the expression of αvβ3 integrin using a novel selective radiotracer in patients with myocardial infarction and investigate if it is a suitable tool for predicting myocardial recovery and thus prognosis.
Approx. 65% of resuscitated patients at the intensive care unit for internal medicine are due to myocardial infarction. Almost all patients are initially diagnosed and treated in the cath lab. Therapy usually consists of one or more stent implantations. After implantation of a coronary stent, dual platelet inhibition is necessary for 12 months. Insufficient platelet inhibition causes an pronounced increase in risk of stent thrombosis. Therefore, secured inhibition and knowledge of the individual platelet function is valuable.
Thoracic pain can be caused by a life threatening disease as for instance a heart attack. Fast diagnosis and treatment is necessary for an advantageous clinical outcome. When a patient enters the emergency unit, an electrocardiogram (ECG) can diagnose a heart attack by recording the electrical activity of the patients' heart. However, an increasing number of patients with an acute myocardial infarction (AMI) are presenting without significant abnormalities on ECG In the latter group, diagnosis is dependent of elevated biochemical markers of myocardiocyte necrosis in the blood such as troponin. Generally, troponins are determined in blood and are analyzed by radiometry or at the hospital's laboratory. Time loss in the acquisition of troponin levels can occur during the workflow due to blood sampling difficulties, transport of the blood samples, processing in the laboratory, and processes inherent to the measuring assays. Roche developed a portable point-of-care (POC) device that determines troponin-T in a few minutes by using small volumes of the patient's blood with the added value that this device can be used in a pre-hospital setting which might save a significant amount of time in determining troponin levels.In this way, a faster diagnosis of AMI can be made improving patients' outcome.
Recent studies have shown that the systemic inflammation caused by periodontal disease (PD) can determine important changes in the coronary arteries, favoring atherosclerosis progression and development of acute coronary syndromes (ACS). The aim of ATHERODENT study is to assess the interrelation between PD, inflammation and progression of coronary atherosclerosis in patients with ACS. Material and methods: This case-control observational study will enroll 100 patients (group 1 - ACS and associated PD, and group 2 -ACS and no PD), in whom the following data will be collected: (1) demographic and clinical data, (2) cardiovascular risk factors, (3) full characterization of PD markers, (4) systemic inflammatory biomarkers, (5) imaging biomarkers derived from transthoracic echocardiography, computed tomography, coronary angiography, optical coherence tomography and intravascular ultrasound, and (6) assessment of the presence of specific oral bacteria in samples of coronary plaques collected by coronary atherectomy, which will be performed during percutaneous revascularization interventions, when indicated in selected cases, in the atherectomy sub-study. The follow-up will be performed at 1, 3, 6, 12, 15, 18 and 24 months. The primary endpoint of the study will be represented by the rate of major adverse cardiovascular events (MACE rates) in PD vs non-PD patients and in correlation with: (1) the level of systemic inflammation triggered by PD and/or by ACS at baseline; (2) the vulnerability degree of atheromatous plaques in the coronary tree (culprit and non-culprit lesions); and (3) the presence and burden of oral bacteria in atheromatous plaques. Secondary endpoints will be represented by: (1) the rate of progression of vulnerability degree of non-culprit coronary plaques; (2) the rate of progression of atheromatous burden and calcium scoring of the coronary tree; and (3) the rate of occurrence of left ventricular remodeling and postinfarction heart failure.