View clinical trials related to Infarction.
Filter by:Troponins are sensitive and specific markers of cardiac injury. Critically ill patients frequently have elevated troponins. In this population, distinguishing patients with elevated troponins from those with myocardial infarction is difficult. However, troponin elevations on their own seem to be associated with an increased risk of death. The optimal treatment of patients with type 2 myocardial infarction or non ischemia related troponin elevations during critical illness is unclear. There are no trials in the ICU setting to guide management. This study is a 1-month pilot cohort study of troponin screening in 4 Ontario intensive care units. The objective of this pilot study is to evaluate the ability to perform a larger study, which will determine the prevalence, incidence and risk factors for elevated troponin values, how patients with elevated troponin values are treated as a baseline, and the incidence of myocardial infarction in critically ill patients. Knowing the prognostic impact of these conditions and understanding current management will thereafter guide researchers and clinicians on the importance of carefully evaluating potential risk-modifying therapies.
This is a multi-centre observational study. It will make use of the positron emission tomography (PET) tracer 18F-sodium fluoride (18F-NaF) as a marker of coronary plaque vulnerability to detect culprit and non-culprit unstable coronary plaques in patients with recent myocardial infarctions. The investigators will then perform long-term follow-up of these patients to determine the prognostic significance of coronary 18F-NaF uptake
Coronary artery disease is one of the most prevalent diseases in the western countries. A waxy substance called plaque can build up inside the coronary arteries. Over time, plaque can harden or rupture, and cause narrowing (stenosis) of the arteries and reduce the flow of oxygen-rich blood to the heart. The standard treatment of symptomatic coronary stenosis is percutaneous coronary intervention (PCI) with balloon dilation followed by stent implantation. A stent is a small metallic grid that stabilizes the coronary vessel wall after the balloon dilation. Currently, drug-eluting stents (DES) are the most widely used stent types. DESs consist of a metallic backbone and an antiprolifetive drug-coating bound by a polymer (glue). These devices have reduced the incidence of excessive formation of new tissue (in-stent restenosis) dramatically in comparison with previously used bare-metal stents. However, there are "safety concerns" with DES, since later thrombotic events have been reported. On one hand excessive tissue formation inside the stent can cause in-stent restenosis, and on the other hand insufficient coverage of the stent can cause persistently exposed metalllic material that can induce platelet aggregation and thrombus-formation. The etiology to stent thrombosis is multifactorial. Possible predisposing factors are, among others: 1) hypersensitivity towards the polymer-coating, which may induce delayed healing inside and around the stent, and 2) insufficient contact between the stent and the underlying coronary vessel wall (incomplete stent apposition), which may cause flow-disturbance and delayed healing. Delayed healing causes persistently exposed metallic material that can induce platelet aggregation and thrombus-formation. The Nobori stent is a new-generation DES, coated with a thin layer of drug and a bioabsorbable polymer. The drug is localized on the outer side of the stent, and decreases the release of drug to the blood circulation. The bioabsorbable polymer is degraded after 6-9 months after implantation, and decreases the risk of hypersensitivity-reactions in the vessel wall. The improved pharmacokinetic profile of the stent is thought to improve the healing pattern. At routine coronary angiography, a small plastic tube is inserted in the femoral artery under local anesthesia. Thin, flexible catheters are then advanced through the artery system (femoral artery and aorta) to the coronary arteries. Contrast is injected in to the blood stream by the catheters, and the arteries are depicted by a special X-ray technique during dye-release. By angiography, the outer sides of the coronary arteries are visualized, and balloon dilations and stent implantations are guided by this standard technique. Newer studies have documented that stent placement and expansion is superiorly visualized if supplementary intravascular imaging is performed during stent implantation. Small imaging catheters are wired through the vessel after stent implantation, and film the stent retrogradely through the vessel. Intravascular ultrasound (IVUS) visualizes the complete vessel wall by use of sound waves, and stent expansion is evaluated in detail. Optical coherence tomography (OCT) is a newer light-based, high-resolution technology. The technique can depict every thread (strut) from the stent, enabling visualization of both contact between struts and underlying vessel wall immediately after the procedure, and strut coverage at follow-up. The purpose of this study is to determine whether OCT-guided PCI can improve healing and coverage of the stent in comparison with routine angiographic guidance alone in patients indicating PCI due to myocardial infarction. If OCT-guidance improves coverage of the stent, this might lower the later thrombotic risk. Patients hospitalized due to myocardial infarction are randomized either to OCT-guided or angio-guided stent implantation in the present study. In both groups the Nobori stent is implanted according to standard techniques. In the angio-guided group, implantations are guided by angiography alone. OCT- and IVUS analysis are performed after an angiographic optimal result for documentary reasons. The operator is blinded towards the image findings, and analysis is performed offline later. In the OCT-guided group, both OCT and IVUS analysis is interpreted immediately after the acquisition. If stent apposition and/or expansion is deemed suboptimal, additional balloon dilation and/or stenting is performed. In case of OCT-driven stent optimization, a documentary OCT and IVUS is performed to document the final result. Patients are readmitted 6 months later for a control angiogram inclusive OCT to assess stent coverage. Furthermore, patients are readmitted 12 months after the index procedure for a control angiogram including OCT and IVUS to assess dynamic vessel wall responses.
The primary objective of the UPSTREAM Registry is to address the data gap regarding the course of NSTEMI (Non-ST-Elevation Myocardial Infarction)between ED (Emergency Department) arrival and diagnostic angiography in detail, by characterizing and following the ED and peri-ED use of advanced OAP (Oral Anti-Platelet) agents. In addition to exploring ED treatment patterns and success of both ischemic and bleeding risk stratification prior to definition of the coronary anatomy, data generated via the UPSTREAM registry will allow plausible attribution of ischemic and bleeding outcomes to pre-catheterization antiplatelet therapy in the management of NSTEMI. This registry further seeks to demonstrate that contemporary use of upstream ticagrelor is associated with an economically-sound utilization of hospital resources, and smooth transition of care into the outpatient, secondary prevention setting for the first 30 days after hospitalization. Finally, it will allow characterization of patient selection factors and processes for ticagrelor vs alternative OAP agents, carrying out that descriptive comparison through discharge. Patients transferred in to an UPSTREAM hospital are eligible for inclusion, but the timing for OAP agent administration and diagnostic catheterization begin with ED care at the first hospital.
This study aims to assess usual walking speed (4-metre gait speed) in patients undergoing primary percutaneous coronary intervention (PCI) for acute myocardial infarction and to assess whether this can predict future cardiovascular events and death.
Human urinary kallidinogenase can promote the establishment of collateral circulation in the ischemic penumbra due to the stenosis or occlusion of middle cerebral artery and then increase the perfusion.
The purpose of this study is to determine the safety and efficacy of reduced doses (10 mg and 20 mg) of intra-coronary alteplase compared with placebo as an adjunct to PCI in reducing MVO and its consequences in high risk patients with STEMI.
Oral antiplatelet therapy is a key treatment of the STEMI (ST elevation myocardial infarction). Delayed action isn't suitable and has to be elucidated. If a delayed gastric emptying time is observed during STEMI, limiting the use of morphine and encourage the use of prokinetic agents can be a first answer to optimize coronary angioplasty environment. Investigators propose a study to assess the gastric emptying times at the acute phase of myocardial infarction using a validated paracetamol absorption test. The STEMI group will be compared to in one hand, itself with measures performed 72 hours±12h after the event onset; and on the other hand, to a stable patient group referred for angioplasty for angina or non-ST-segment elevation myocardial infarction (NSTEMI). For STEMI group and stable patient group, the delay of apparition of Prasugrel or Ticagrelor efficacy will be determined by VerifyNow® test and correlated to gastric emptying times.
Massive cerebral infarction is an ischemic stroke caused by complete blockage of the internal carotid artery, middle cerebral artery, or their cortical branches. The widespread infarction, pathological severity and high fatality rate associated with massive cerebral infarction pose a major threat to affected patients. However, there is a lack of unified diagnostic criteria. Many researchers use Adams' classification, in which massive cerebral infarction is diagnosed when the following criteria are met: infarct size > 13 cm2; a major brain-feeding artery is involved; the focal site affects more than two cerebral lobes; infarct diameter line ≥ 3 cm in internal capsule of striatum. Prolonged cerebral ischemia/reperfusion can induce complex secondary changes in brain tissue, so the use of neuroprotective agents is very important. Remarkable progress has been made over the last decade in understanding the protective effect of calcium antagonists against cerebral ischemia. In particular, the liposoluble dihydropyridine Ca2+ antagonist nimodipine selectively acts on cerebral vessels and neurons and can protect ischemic brain tissue, providing a new way of treating ischemic cerebrovascular disease. Preclinical and clinical tests have shown that nimodipine has a protective effect on ischemic brain tissue, and indicate that patients should take the drug as soon as possible. However, there are no reports of double-blind, randomized, controlled clinical trials addressing the administration of nimodipine via intravenous drip within the time window for successful treatment of acute massive cerebral infarction.
At present, a variety of antithrombotic regimens are prescribed in the early postprocedure period after transcatheter aortic valve implantation (TAVI). Dual antiplatelet therapy (DAPT) using aspirin and a thienopyridine in the initial period after TAVI is the recommended strategy; however, mono antiplatelet therapy using aspirin is suggested not to be inferior. In patients with atrial fibrillation (AF) or another indication for oral anticoagulation (OAC), no recommendations on best treatment regimen currently exist although triple therapy (OAC + DAPT) is best avoided due to increased bleeding risk. We hypothesise that the omission of clopidogrel in the first 3 months after TAVI is safer and not less beneficial than the addition of clopidogrel to aspirin (cohort A) or OAC (cohort B).