Active clinical trials for "Infarction"

The present project aims to determine whether a deficit in migration of stem cells could be implicated in the failure to mount an adequate collateralization after Myocardial Infarction (MI) and thereby facilitate the development of post-ischemic heart failure (HF) and to dissect underlying molecular mechanisms. Furthermore, the investigators wish to determine the predictive value of stem cell migration assay in patients with MI.

The goal of this study is to use MCE (myocardial contrast/perfusion echocardiography) to study and compare short/long term change of myocardial perfusion abnormality and cardiac outcome in diabetic patients after nonfatal MI (heart attack), who are treated with different glucose control agents.

The investigators are developing a test that is expected to measure the amount of radiation a patient has been exposed to after a nuclear bomb. The investigator will do this by measuring the DNA in the patients blood from cells killed by the radiation. Many diseases and medical conditions can put DNA in the blood. The investigator needs to know how much DNA in order to better interpret our radiation detection test. Therefore, the investigator is collecting blood from several patients with different diseases or medical conditions and also healthy volunteers to measure their DNA content. Patients that will be included in this study are pregnant women, patients who have suffered a pulmonary embolism within the past 48 hours, patients who have suffered from myocardial infarction in the past 48 hours, patients with autoimmune diseases and health patients.

Current patterns of P2Y12 receptor inhibitor use provide an excellent opportunity to test the impact of copayment reduction on clinician choice of medication, patient adherence, and clinical outcomes. The ARTEMIS trial is a practical multicenter, cluster- randomized clinical trial that will assess the impact of copayment reduction by equalizing the copayment of clopidogrel and ticagrelor. ARTEMIS will assess prescribing patterns, patient medication adherence, and clinical outcomes up to one year. We hypothesize that reducing out--of--pocket cost for P2Y12 receptor inhibitor will lead to improved adherence. Additionally, copayment reduction of both generic and brand antiplatelet agents may lead to a reduction in MACE risk. This is in part due to greater adherence to an evidence--based secondary prevention medication. Additionally the reduction in MACE may reflect greater selection of a more potent antiplatelet agent that has been shown to reduce MACE in randomized clinical trials, as provider choice of antiplatelet therapy will be primarily driven by risk- benefit assessment rather than the cost burden to the patient.

To compare the efficacy of 2 different hydration strategies, hydration according to clinical guideline and adequate hydration, on contrast-induced nephropathy in patients with STEMI undergoing primary PCI to investigate the possible beneficial role of periprocedural adequate hydration.

There is experimental evidence that low levels of adiponectin are associated with more reperfusion injury. In addition experimental studies have demonstrated that endothelial progenitor cells may have a favorable effect on remodeling, mainly through stimulation of neo-revascularisation. Clinical data on these issues are lacking. This clinical project studies the role of adiponectin, endothelial progenitor cells and endothelial microparticles in the ischaemia-reperfusion process and the compensatory ventricular remodelling in a population of 250 infarction patients treated with primary PCI. If the role of these factors could be confirmed in this clinical setting, those factors might represent a new target for therapeutic interventions in AMI patients.

The MYSTAR-5-YEAR study controls the patients 5 years after treatment with combined (intramyocardial and intracoronary) delivery of autologous BM-MNCs. The clinical endpoint of this prospective non-randomized observational study is the MACCE, defined as major adverse cardiac and cerebrovascular events. Patients will be investigated by echocardiography, SPECT and MRI. 2D (NOGA-guided SPECT) and 3D (NOGA-guided MRI) imaging will refine the evaluation with more exact analysis of the intramyocardial injected areas (ROI).

The objective of this protocol is to use established standard criteria and methods for the collection of hMSC (human mesenchymal stromal cells) from healthy bone marrow donors. The hMSC collected from the donors will use to develop well-defined and reproducible cell banks. Standard manufacturing procedures and quality control testing methods will be used to characterize and evaluate the final cell product. After the cell banks are created, these cell products will be used in future translational or clinical research.

The purpose of this study is to prospectively observe the incidence rate of acute kidney injury (AKI), major adverse renal and cardiovascular events (MARCE) in participants who were diagnosed with ST-segment elevation myocardial infarction (STEMI) and have completed primary percutaneous coronary intervention (PCI) procedure following an injection of iso-osmolar contrast medium iodixanol (Visipaque) during the in-hospital period and up to 30 days post-PCI follow-up period. The study will provide a better safety profile of Visipaque as the contrast medium in PCI procedure.

Platelets play a key role in the athero-thrombotic process. However, the in vivo mechanism accounting for thrombus growth at site of coronary atherosclerotic lesion has not been fully elucidated. While platelet adhesion and aggregation on the thrombogenic core of atherosclerotic plaque is an established mechanism for thrombus growth, the role of systemic factors, which may contribute to thrombus via amplification and propagation of platelet aggregation, is still to be clarified. There is a growing body of evidence that lipopolysaccharides (LPS), are implicated in athero-thrombosis. Circulating levels of endotoxins have been associated with human atherosclerosis progression, particularly in smokers or in patients with infections. Furthermore, endotoxins seem to be implicated in the thrombotic process through several mechanisms including up-regulation of macrophage tissue factor expression and amplification of platelet response upon interaction with Toll-like receptor 4. The relationship between endotoxins and platelets may be relevant in the context of acute coronary syndromes as endotoxins could locally amplify platelet-derived thrombus growth but this issue is still unexplored. Previous studies demonstrated that low-grade endotoxemia is detectable in human circulation, likely as consequence of enhanced gut permeability, and may be responsible for leucocyte-platelet aggregate and eventually thrombosis. The investigators hypothesize that low-grade endotoxemia may be observed in patients with coronary heart disease and may favor, at site of coronary unstable plaque, thrombus growth. To explore this issue, Escherichia Coli (EC)-LPS concentration and biomarkers of platelet activation will be measured in coronary thrombus and intra-coronary blood of patients with STEMI and stable angina (SA), respectively, and in peripheral circulation of both patients and controls. EC DNA will be searched in serum of all patients by polymerase chain reaction (PCR). Furthermore, to substantiate that LPS could be biologically active, immune-histochemical analysis of thrombi and in vitro studies will be performed to assess the interplay between LPS and platelet activation.