View clinical trials related to Infarction.
Filter by:The STOP-HF study is a prospective, randomized, controlled trial recruiting asymptomatic individuals with risk factors for left ventricular dysfunction from 50 primary care clinics in Dublin and south east Ireland. It is designed to determine whether using natriuretic peptide measurement as a screening tool following a general cardiovascular risk factor screen will reduce the prevalence and severity of ventricular dysfunction in conjunction with specialist follow-up at St. Vincent's University Hospital.
Percutaneous coronary intervention (PCI) with stent implantation is the preferred reperfusion strategy for treatment of acute myocardial infarction (AMI). Despite advances in both devices and pharmacological support for AMI patients undergoing PCI, the risk of recurrent ischemic events has been higher than that of elective PCI. Among therapeutic options for surmounting clopidogrel hyporesponsiveness, higher loading doses and maintenance doses of clopidogrel achieved significant enhancements in the speed of onset and intensity of inhibition and these approaches have been widely adapted in clinical practice. Interestingly, recent studies found that carriers of the loss-of-function hepatic cytochrome (CYP) 2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events than did non-carriers, in the setting of PCI and acute coronary syndrome (ACS). These findings raise the need of solutions to overcome enhanced post-clopidogrel platelet reactivity by the influence of the loss-of-function CYP2C19 allele. Increasing the dose of clopidogrel, new potent P2Y12 antagonists (such as prasugrel), or other antiplatelet drugs such as cilostazol may be alternative antiplatelet regimens in patients with the loss-of-function CYP variant. A recent study demonstrated that adjunctive cilostazol to dual antiplatelet therapy (triple antiplatelet therapy) intensified platelet inhibition as compared with a high maintenance-dose (MD) of 150 mg/day. Therefore, triple antiplatelet therapy could also be an alternative antiplatelet therapy to improve platelet inhibition and clinical outcomes in carriers of CYP2C19 mutant allele. The purpose of this study was to determine the impact of adjunctive cilostazol on platelet inhibition in carriers and non-carriers of the loss-of-function CYP2C19 allele. The investigators compared the enhanced inhibition of platelet aggregation by adjunctive cilostazol 100 mg twice daily versus high-MD clopidogrel 150 mg/day in AMI patients treated with emergent coronary stenting, according to the CYP2C19 polymorphism.
This is a randomized, double-blind, placebo-controlled, parallel group, multi-center study to evaluate initial safety and efficacy of GW856553 in subjects with NSTEMI. Up to approximately 525 subjects will be randomized to meet the MRI recruitment target (90 subjects in substudy.) All subjects will continue to receive the local standard of care for the duration of the study.
During myocardial infarction, inflammatory response may negatively influence ventricle wall remodeling as well as endothelium-dependent vasomotor function in the coronary and systemic arterial systems. Statins have been consistently proved to attenuate inflammation and improve endothelial function. In this study, we tested the effect of different doses of statin on inflammatory response and endothelium-dependent vasodilation.
During acute coronary syndromes (ACS), the generation of inflammatory mediators negatively influences arterial wall remodeling and the endothelium-dependent vasomotor function in the coronary and systemic arterial systems. In fact, the intensity of the inflammatory upregulation is strongly related to the incidence of recurrent coronary events. The investigators previously demonstrated that high dose potent statins can rapidly reduce plasma levels of cholesterol-rich lipoproteins and inflammatory activity in subjects during ACS. In addition, such statin treatment attenuates the post-discharge endothelial dysfunction of these patients. By inference, it is plausible to hypothesize that these beneficial effects during ACS may be intensified by an additive lowering of plasma cholesterol through the treatment with ezetimibe. So far, data is unavailable to verify this assumption. In parallel, data from animal models have suggested that both statins and ezetimibe may reduce insulin sensitivity by their effect on cholesterol content and, by this way, on insulin signaling in liver cells. In this context, the present study aims to investigate the role of the addition of ezetimibe upon statin treatment on stress-induced insulin resistance and on the time-course of the inflammatory response during the acute phase of myocardial infarction and its late effect on endothelium-dependent arterial dilation.
We are doing this clinical trial in order to evaluate two different treatments for non-fluent aphasia: Melodic Intonation Therapy (MIT) and Speech Repetition Therapy (SRT). MIT uses a simple form of singing, while SRT uses intensive repetition of a set of words and phrases. We want to see which intensive form of treatment is more effective in leading to an improvement in speech output compared to a no-therapy control period, and whether either treatment can cause changes in brain activity during speaking and changes in brain structure. We will use a technique known as functional Magnetic Resonance Imaging (fMRI) to measure blood flow changes in the brain and structural MRI that assess brain anatomy and connections between brain regions. We will use fMRI to assess brain activity while a patient speaks, sings, and hums. We will assess changes in brain activity and in brain structure by comparing scans done prior to treatment to scans obtained after treatment and we will also examine changes between treatment groups. We will correlate changes in brain activity and brain structure with changes in language test scores.
The purpose of this study is to determine whether giving cardiosphere-derived stem cells (CDCs) to patients with decreased heart function and/or a large amount of damaged muscle after a heart attack is safe. CDCs are cells grown from small biopsy samples taken from the heart. Giving a patient their own CDCs is an investigational procedure that has been approved by the Food and Drug Administration for this study. In addition to determining whether this treatment is safe, the study will also examine whether it can decrease the amount of heart muscle damage and/or improve heart function after a heart attack. The amount of heart muscle damage and the function of the heart directly affects prognosis (the predicted course of the disease), and the development of heart failure and other complications some patients experience after a heart attack. By way of background, scientists and physicians believed, until just a few years ago, that heart muscle damaged after a heart attack could not be replaced. Recently, however, scientists discovered that new heart muscle can form, or be regenerated, and that this process can be enhanced (or increased) by the administration of large numbers of certain cells isolated from the heart or bone marrow. These cells can be stem cells, or cells derived from stem cells, and they may achieve their benefit by forming new heart muscle cells, becoming heart muscle cells themselves, or releasing substances which increase the ability of already existing stem cells to form new heart muscle. All of the studies conducted so far have been experimental and no cell type is approved for routine clinical care of patients with heart disease. However, studies involving bone marrow stem cells do indicate some small improvement in heart function and one large study demonstrated a decrease in clinical events in the group which received bone marrow cells. Investigators of this study decided to study CDCs because they come from a person's own body, and therefore have no foreign immune antigens which may be rejected. Since the cells come from the person's heart, they are more likely to form heart tissue. In addition, animal studies indicate no safety problems and that these cells are capable of forming heart muscle and blood vessel cells after heart attacks. The investigators are now studying whether the same is true in humans.
Patients who are hospitalized because of a heart attack are prescribed a number of medicines to help the heart heal. The investigators will examine different ways in which clinicians share information about those treatment options with patients and the impact that this can have on patients' choices and health.
The aim of this study is to: - clarify whether macrophage imaging using ferucarbotran is able to delineate the region of myocardial infarction as accurate as gadolinium-based necrosis/fibrosis imaging; - identify possible differences in infarct imaging using ferucarbotran for macrophage imaging compared to necrosis/fibrosis imaging with gadolinium-based compounds; and - evaluate which MRI pulse-sequences maximise sensitivity for macrophage imaging with ferucarbotran in the setting of acute myocardial infarction.
This clinical trial aims to find out the safety and efficacy of adult mesenchymal stem cells in patients with myocardial infarction.