Active clinical trials for "Myocardial Infarction"

Of the patients diagnosed with ST-segment elevation myocardial infarction (STEMI) who underwent reperfusion therapy and have thrombolysis in myocardial infarction (TIMI) 3 flow, about 40% have flow alterations in the coronary microcirculation, which leads to worse remodeling of the left ventricle with a consequent increase in the mortality of this population. Clopidogrel is the only known antiplatelet medication that brings benefits to the coronary microcirculation. Ticagrelor is significantly superior to clopidogrel in terms of decreasing mortality. The main objective of this study is to compare the effect of ticagrelor versus clopidogrel on the coronary microcirculation by the Myocardial Perfusion Score Index (MPSI) obtained using Microbubble Contrasted Echocardiography (MCE) in patients who have STEMI and treated with thrombolysis.

Researchers are looking for a better way to prevent the formation of blood clots in people who have or have had: an irregular and often rapid heartbeat a blocked blood flow to the heart a blocked or reduced blood flow to a part of the brain. When a blood clot forms in the body in patients with the above conditions, it may block vessels of the heart, the brain and/or other parts of the body. This may lead to heart attack, stroke and other serious complications. Blood clots are formed in a process known as coagulation. This is a complex series of steps that must occur in a specific sequence. Medications are already available to prevent the formation of blood clots. They work by interrupting one or more of the coagulation steps and are therefore known as anticoagulants. They decrease the risk of the above-mentioned complications. The study treatment asundexian works by blocking a very specific step in the blood clotting process, the activation of a protein called Factor XIa. Due to its very specific action that is not thought to be involved in the main blood clotting steps needed to stop bleeding (e.g. like from a cut finger), asundexian is expected to reduce the risk of bleeding that is still seen with existing anticoagulants. Since people who need an anticoagulant may also have liver problems, information on asundexian use in this group is needed. The main purpose of this study is to learn how asundexian moves into, through and out of the body in participants with a mild or moderate reduction in liver function compared to participants with normal liver function who are similar in age, weight, and gender. To answer this question, researchers will measure the average highest level of asundexian in the blood (also referred to as Cmax) the average total level of asundexian in the blood (also referred to as AUC). that were reached after intake of a single tablet of asundexian. The researchers will compare these data between participants with reduced liver function and matched participants with normal liver function to look for differences. Each participant will be in the study for up to 4 weeks. Participants will stay in-house for 6 days, starting the day before taking asundexian. In addition, two visits to the study site are planned. During the study, the doctors and their study team will: do physical examinations check vital signs take blood and urine samples examine heart health using an electrocardiogram (ECG) ask the participants questions about how they are feeling and what adverse events they are having. An adverse event is any medical problem that a participant has during a study. Doctors keep track of all adverse events that happen in studies, even if they do not think the adverse events might be related to the study treatments.

Platelet activation and aggregation leads to myocardial infarction. Platelet P2Y12 receptors are essential for platelet activation. Antagonists against the P2Y12 receptor, which are established in secondary prevention of myocardial infarction, have unexplained anti-inflammatory effects. A novel P2Y12 receptor antagonist ticagrelor reduced infection-related mortality compared to clopidogrel, previous standard treatment for patients with myocardial infarction. Activated platelets release pro-inflammatory and procoagulant platelet extracellular vesicles. The investigators assume that decrease in infection-related mortality in patients treated with ticagrelor may be explained by greater inhibition of the release of platelet vesicles by ticagrelor, compared to clopidogrel. This study is expected to identify an additional mechanism of action of ticagrelor, which might contribute to the observed clinical benefits in patients treated with ticagrelor.

During acute coronary syndrome, the American College of Cardiology and the American Heart Association recommend oxygen delivery to patients with less than 90% oxygen saturation. Oxygen therapy in these patients for a duration of at least 6 hours, but also stipulates that it is reasonable to administer oxygen to all acute coronary syndrome patients during the first six hours following the presentation. Hyperoxia also has well-established risks. Our research hypotheses are: (I) that current practices tend to use high oxygen flows resulting in high SpO2 levels during acute coronary syndrome. (II) there is a high rate of desaturation in patients with acute coronary syndrome and an automatic adaptation of oxygen flows may reduce this frequency. (III) that excessive oxygenation targets have no advantage. Our hypothesis is that maintaining a SpO2 of 90 to 94% is at least equivalent when compared to higher saturation objectives (SpO2 of 94 to 100%) with regard to the occurrence of complications in the patient in acute coronary syndrome . We will use two SpO2 targets with the FreeO2 system, 92 and 97%.

The purpose of this investigation is to evaluate when genetic variation in the carboxylesterase 1 (CES1) gene influences antiplatelet therapy response, as assessed by ex vivo platelet aggregometry, in healthy participants treated with clopidogrel and ticagrelor. We hypothesize that genetic variation in CES1 will significantly impact on-clopidogrel platelet aggregation while having a minimal effect in ticagrelor-treated subjects. Specific Aim: To conduct a prospective randomized crossover study of clopidogrel and ticagrelor in healthy individuals stratified by CES1 genotype. Participants will be recruited by CES1 genotype into a randomized crossover study of clopidogrel (75 mg daily for 7d) and ticagrelor (90 mg twice daily for 7d) with extensive phenotyping including ex vivo platelet aggregometry performed pre- and post-drug administration in order to assess the interaction of genotype and drug choice on on-treatment platelet function.

Evaluative pilot study for safety and feasibility with administration of autologous bone bone marrow derived mononuclear cells by endoventricular catheter into the normal border zone fo the ischemic lesion.

The overall objectives of this study are to improve medication adherence of patients and subsequent health outcomes. This study is designed to examine the existence of strong associations between social networks and health behavior. This study intends to demonstrate that social forces are particularly effective at building enduring habits for healthy behavior, specifically adherence to statin medication for this study. The investigators believe the improved medication adherence will result in fewer additional vascular events, following the most recent of these events, and will result in fewer patient hospitalizations. The investigators will leverage insights from the fields of social comparison (being provided with information about the actions of others prompts social comparison that can significantly influence behavior), social pressures (encouragement or discouragement from others is a powerful social force that can influence individual behavior), and social triggers (cues in the environment can motivate people to take certain actions and have powerful effects on purchasing behavior). The results of this study and experience gained from the implementation of these interventions will be used to inform new versions of a larger trial intervention to be tested in new patient cohorts in a rapid cycle framework.

Study objective is the evaluation of safety and efficacy at 9 months of combination treatment of bare metal Stent plus Paclitaxel Eluting Balloon vs bare metal stent (conventional treatment) in patients with acute myocardial infarction with systolic time elevation of less than 12 hours of evolution.

The objective of this study was to evaluate the effectiveness of a FCEM-focused hybrid CR program for survivors of myocardial infarction (MI). The study sought to compare the long-term impact of FCEM-based intervention with a standard CR program in terms of mortality rates and different aspects of health related quality of life (HRQoL), which includes soft outcomes such as levels of stress, anxiety, psychological distress, quality of life (QoL), and hard outcomes such as the percentage of ejection fraction (EF), independent functioning, and functional exercise capacity status.

The prevalence of type 2 diabetes is growing steadily. Patients with diabetes, cardiovascular complications (such as myocardial infarction (MI)) are more frequent and severe than in non-diabetic subjects. The anti-diabetic therapies available have little or no effect on the incidence of cardiovascular events. It is therefore urgent in diabetics develop new therapeutic strategies to reduce the occurrence of MI or limit the consequences. In the two weeks following MI, monocytes / macrophages are the most represented in the ischemic heart tissue cells. The infiltration by monocytes / macrophages after infarction MI is a two-phase process. In the first phase, monocytes / macrophages M1 promote digestion injured areas, and monocytes / macrophages M2 intervene to promote angiogenesis, collagen deposition and contribute to tissue repair. The optimal repair after myocardial infarction depends on effective recruitment of monocytes and macrophages M1 transition needed to digest the damaged tissue and M2 macrophages necessary for tissue repair. The balance between these two phenotypes M1 and M2 is controlled by different modulators, such as transcription factors, cellular miRNA and miRNA extracellular contained in the microvesicles (MVs). Interestingly, plasma MVs circulating essentially derived monocytes and platelets contain miRNA and are impaired by inflammation or during various pathological situations (such as IDM). Furthermore, metabolic disorders such as hypercholesterolemia (often associated with diabetes) affect the transition from M1 to M2 response and response delay cardiac repair. To date, the mechanisms that control the M1 / M2 transition at heart level are not elucidated. Moreover, the impact of diabetes, which leads to chronic low-grade inflammation, is not explored. Targeting the immune response by promoting the transition M1 / M2 after MI could be an innovative therapeutic approach. However, better characterization of the response of M1 and M2 macrophages after MI and the mechanisms by which they contribute to tissue remodeling and the effect of diabetes are needed. The goal is to study how the phenotypes / macrophage functions after MI are changed by diabetes and to determine the potential role of miRNAs contained in secreted MVs in the transition M1 / M2 after MI. Monocytes / macrophages from subjects with normal blood sugar or diabetes who underwent an IDM (10 per group) will be characterized phenotypically. Their ability to produce MVs will be analyzed. These MVs will be tested functionally for their ability to orient the polarization of healthy recipients monocytes. The content of these MVs in terms of miRNAs will be analyzed in detail. By bioinformatics analysis, some miRNAs of interest (based on their abundance and target genes) will be selected. These miRNAs are over-expressed in macrophages and MVs produced by these cells will be analyzed for their ability to modulate differentiation of monocytes recipients. Finally, the circulating levels of these miRNAs of interest will be measured after 1 year of IDM and will be correlated to the clinical phenotype of patients (recurrence, arrhythmias, heart failure). Ultimately, the goal is to identify VMs that can promote the differentiation of monocytes to an alternative phenotype and identify miRNAs responsible for this effect. This could help in the future, in a subject with impaired ability of monocytes to differentiate alternatively, can change by introducing the miRNA of interest to re-inject or inject MVs macrophage containing the miRNA of interest and thus correct the defect of differentiation.