View clinical trials related to Myocardial Inflammation.
Filter by:The adaptive immune response plays an important role in myocardial healing and remodeling after acute myocardial infarction in patients. Therefore, the involved lymphocytes represent a novel target for therapeutic interventions. However, there are no established blood-derived biomarkers to predict the quantity and quality of the adaptive immune response to cardiac injury. Multimodal imaging of the heart and immunologic organs might provide such information. Recent retrospective analysis of patients after MI revealed enlarged mediastinal lymph nodes associated with increased CXCR4 radiotracer accumulation, thereby indicating that CXCR4 PET-based lymph node imaging provides a non-invasive quantitative readout of the local adaptive immune response. These considerations are further fuelled by the fact that, within lymph nodes, CXCR4 is expressed almost exclusively on lymphocytes, whereas various other cell types express CXCR4 within the myocardium. This leads to the hypothesis that the size of mediastinal lymph nodes and their respective CXCR4 PET signals correlate with the adaptive immune response to cardiac injury and might provide predictive information for functional cardiac decline during follow-up. This prospective clinical study will use multimodal imaging to monitor chemokine receptor 4 (CXCR4) expression in the lymph nodes, myocardium, spleen, and bone marrow after acute MI. The combination of cardiac magnetic resonance (CMR), echocardiography, and positron emission tomography (PET) along with blood collection for immunophenotyping will allow to determine i) if the size of mediastinal lymph nodes and their respective PET-derived CXCR4 signals at baseline correlate with the adaptive immune response to acute cardiac injury; and ii) if they predict cardiac adverse remodelling during longitudinal follow-up.
The study will evaluate myocardial inflammation in cyclists after high intense and sustained exercise. Our hypothesis is that strenuous exercise in recreational cyclists may be associated with myocardial inflammation. Myocardial fibrosis in asymptomatic athletes is associated with life-threatening arrhythmic events and sudden death. Although myocarditis seems to be the most likely underlying cause, it remains unclear if strenuous and sustained physical exercise can cause myocardial inflammation with development of myocyte necrosis and possibly myocardial fibrosis in athletes. Nineteen recreational cyclists performing "L'ETAPE DU TOUR (EDT) de France" a cycling ride (175 km, 3600 m of positive altitude difference) on July 4 2021 will be included in this study. Each participant will complete a detailed questionnaire detailing their training history. All participants will have exercise testing approximately 1 week before the EDT stage to set aerobic and anaerobic gas exchange thresholds, as well as VO2max. In part 2 of the study cardiac MRI will be performed at rest before the EDT cycling ride completion. An ECG registration using a RootiRx will be realized during and up to 6 hours after the cycling ride. An echocardiography and cardiac MRI will be repeated in each cyclist between 3 and 6 hours after EDT cycling ride completion. A blood sample will be obtained at that time after the ride. This time point is chosen based on the highest troponin release that 3 to 6 hours post-exercise would allow a sufficient amount of time for inflammation to develop and be detectable, corresponding with the time when cardiac Troponin T is typically detectable and representing the liberation of enzymes from damaged myocytes. Finally, a third cardiac MRI will be repeated 24 hours after start of the cycling ride to verify the evolution of possible inflammation over this time period.
The study will evaluate myocardial inflammation in cyclists after high intense and sustained exercise. Our hypothesis is that strenuous exercise in recreational cyclists may be associated with myocardial inflammation. Myocardial fibrosis in asymptomatic athletes is associated with life-threatening arrhythmic events and sudden death. Although myocarditis seems to be the most likely underlying cause, it remains unclear if strenuous and sustained physical exercise can cause myocardial inflammation with development of myocyte necrosis and possibly myocardial fibrosis in athletes. Nineteen recreational cyclists performing "L'ETAPE DU TOUR (EDT) de France" a cycling ride (175 km, 3600 m of positive altitude difference) on July 4 2021 will be included in this study. In part 1 of the study, each participant will complete a detailed questionnaire detailing their training history and an echocardiography at rest will be performed. All participants will have exercise testing approximately 1 week before the EDT stage to set aerobic and anaerobic gas exchange thresholds, as well as VO2max.
There is increasing evidence that [18F]-2-fluoro-2-deoxy-D-glucose (18F-FDG) PET/CT is useful in the identification and treatment of disease processes that involve cardiac inflammation and infection. Current applications include imaging intra-cardiac device and prosthetic valve infections, evaluating patients with known or suspected cardiac sarcoidosis or other inflammatory cardiomyopathies. However, because normal myocardium can metabolize both glucose and free fatty acids (FFAs), physiological accumulation of FDG in the myocardium can interfere with the recognition of abnormal FDG uptake. The use of a low-carbohydrate diet with a prolonged fast ≥ 12 h nutrition followed by a fast of at least four hours is the effective preparation recommended to suppress physiological myocardial FDG uptake. However, the rate of suppression of physiological accumulation of FDG with this method in our center is only 50%.
The relationship between the immune system and the myocardium after myocardial ischemia is an evolving field of research. Crosstalk occurs between macrophages and cardiac myocytes to promote cardio-protection and resolution of inflammation after myocardial ischemia and reperfusion injury (MI/R injury). Myeloid-epithelial-reproductive tyrosine kinase (MerTK), a member of the TAM family of tyrosine kinase receptors (Tyro-Axl-MerTK), is a macrophage receptor that mediates efferocytosis, anti-inflammatory signaling, and resolution of inflammation. After MI/R injury, intact MerTK is necessary for the phagocytosis of dead cardiac myocytes and to promote anti-inflammatory signaling. Proteolytic cleavage of MerTK to its inactive form, soluble MER, restricts the capacity of macrophages to phagocytize dead cardiac myocytes and impairs MerTK-dependent anti-inflammatory signaling resulting in suppressive effects on cardiac remodeling and function. The Thorp lab at Northwestern University has previously measured soluble MER levels in both adult mice and humans and found that soluble MER concentrations increase after MI/R injury. In adult MI patients, soluble MER was measured post coronary artery reperfusion and was found to be increased (average 3200 pg/mL compared to 1700 pg/mL) compared to controls with stable cardiovascular disease. Based on murine data, the lab further postulated that reperfusion injury may directly interfere with MerTK-dependent cardiac repair as reactive oxygen species formed during reperfusion injury induce proteolytic cleavage of MerTK to soluble MER. Myocardial infarctions are rare events in pediatric patients. However, pediatric hearts are exposed to periods of hypoperfusion, ischemia, and inflammation during times of stress such as cardiac bypass and critical illness, and it is unknown how soluble MER levels change in response to these events. Thus, I was interested in investigating how soluble MER levels change after MI/R injury induced by cardiac bypass as well as in the utility of soluble MER as a biomarker of cardiac inflammation and injury in pediatric patients.
There is an unmet need for Cardiovascular Disease (CVD) risk reduction in patients with Type 2 Diabetes. In recent trials there has been promising findings of more effective glucose management and reductions in overall CVD events and hospitalization for heart failure with SGLT-2 inhibition. Using the capability of cardiac MRI with T1- and T2-mapping in assessments of myocardial fibrosis and inflammation, the investigators propose to conduct a clinical trial to investigate the effects of SGLT-2 inhibition with dapagliflozin on myocardial strain, fibrosis and inflammation as assessed by cardiac MRI with T1- and T2-mapping in patients with type-2 diabetes. Over approximately 12 months subjects will have 6 clinical visits at the investigators research clinic. During this time subjects will be randomized to receive either active 10mg dapagliflozin or a matching placebo. 2 MRI scans at one of the two University of Washington research imaging centers will take place. One at randomization and the second scan will occur approximately 12 months after the first scan.
Rheumatoid arthritis (RA) patients have a higher prevalence of subclinical atherosclerosis than the general population. In addition, RA patients experience higher rates of heart failure with preserved ejection fraction (HFpEF). There is evidence that myocardial mechanics and left ventricular diastolic function are more abnormal in the RA population and these changes occur earlier than in the general population. Recently a study suggested that RA patient have abnormal myocardial inflammation during a disease flare and that this is improved with anti-inflammatory treatment. This study is aimed at describing the prevalence of myocardial inflammation in patients during active RA disease flares and comparing that with RA patients who are in remission. Investigators hope to show that abnormalities in myocardial inflammation on PET imaging correlate with abnormalities in myocardial strain on echocardiography. Coronary CT will be performed to establish the presence of subclinical atherosclerosis and whether its presence affects changes in either myocardial inflammation or myocardial strain. The hypothesis is that patients with evidence of myocardial inflammation during the course of their RA disease are more likely to develop HFpEF during their lifetime. Although the present study will not be of a duration to assess outcome, it will provide descriptive data which may help guide future prospective study of patients with RA which may help guide appropriate cardiovascular testing in this high risk population.
This study aims to evaluate the effects of abatacept, a CTLA4-Ig fusion protein that binds cluster of differentiation antigen 80 (CD80)/86 (B7-1/B7-2), on subclinical myocarditis in rheumatoid arthritis (RA) through its effect on T cell subpopulations. RA patients without clinical CVD, biologic naïve, and with inadequate response to methotrexate (MTX), will undergo cardiac fluorodeoxyglucose (FDG) positron emission tomography (PET)/computerized tomography (CT) imaging to assess myocardial inflammation. Studies that investigate the impact of treatment on subclinical myocarditis in RA, a possible contributor to heart failure, while exploring potential underlying mechanisms (i.e., different T cell subpopulations), are needed for a better understanding of their relevance in the pathogenesis of heart failure in RA and survival improvement in these patients with excess risk for cardiovascular death. If the investigator hypothesis is confirmed and treatment with abatacept decreases and/or suppresses or prevents myocardial inflammation in RA, this will have multidisciplinary implications that could lead to changes in the current management of RA patients at high risk for cardiovascular events. Similarly, identification of T cell subpopulations in RA patients with myocardial FDG uptake will shed light into the underlying cellular mechanisms of myocardial injury and serve to guide the use of therapies that prevent their pathogenicity. The objectives of this study are to compare the change in myocardial FDG uptake in RA patients treated with abatacept vs adalimumab, and identify T cell subpopulations associated with myocardial FDG uptake in each treatment arm. RA patients will be randomized in an unblinded, 1:1 ratio to treatment with abatacept vs adalimumab. A cardiac FDG PET/CT will be performed at baseline and 16 weeks post-biologic treatment. T cell subpopulations associated with myocardial FDG uptake will be evaluated at both points in time with their transcriptional phenotype outlined by RNA sequencing.
Primary myocardial involvement is common in scleroderma, effected to pericardium, vascular, conducting defect and especially myocardium. Cardiac MRI is widely used for assessment of cardiac involvement in scleroderma, both structural and functional pathology. Cardiac MRI has a diagnostic accuracy of 85% for the detection of myocardial inflammation. Nowadays, the treatment of myocardial inflammation in scleroderma is uncertain. The investigator's study aims to define the cardiac outcome after moderate dose steroid therapy in the patients who have myocardial inflammation detection by cardiac MRI.
Patients with acute myocarditis (AM) usually experience spontaneous healing, but a considerable percentage of them evolve towards chronic long-term cardiac impairment. The evolution towards dilated cardiomyopathy (DCM) occurs in a subtle manner, frequently after an initial recover that mimics complete healing. Differences in the course of the disease may reflect the course of underlying myocardial inflammation related to viral clearance or persistence and to the following autoimmune response. Cardiac magnetic resonance (CMR) mapping parameters have been developed for the quantification of edema and necrosis, showing high diagnostic accuracy. No mapping parameter has been developed for the assessment of the third Lake Louise criteria, namely the hyperemia, and, furthermore, their prognostic role is not completely understood. The study hypothesis is that the early-enhanced T1 mapping parameter may have great diagnostic accuracy for myocarditis, and that a short-term monitoring with a complete CMR protocol at 2 month after symptoms onset may identify the subgroup of patients at high risk of progression towards DCM. The results of this study will help to significantly improve diagnostic performances of CMR and may help to manage patients with AM.