Search clinical trials by condition, location and status
The primary objective of this study is to evaluate the effect of rilonacept, added to standard therapy and compared with standard therapy alone, on improvement in myocardial inflammation in subjects with cardiac sarcoidosis after 24 weeks of therapy.
Sarcoidosis is a multisystem granulomatous disease of unknown cause that can affect any organ in the body, including the heart. Granulomatous myocarditis can lead to ventricular dysfunction and ventricular arrhythmias causing significant morbidity and mortality. Immunosuppressive therapy (IST) has been shown to reverse active myocarditis and preserve left ventricular (LV) function and in some cases improve LV function. In addition, IST can suppress arrhythmias that develop due to active myocarditis and prevent the formation of scar. The potential role of cardiac biomarkers, including brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and cardiac troponins, in detecting active myocarditis is limited and studies have been disappointing. At present, there are no biomarkers to detect active myocarditis and the use of advanced imaging modalities (FDG-PET) for assessing and monitoring active myocarditis is not feasible or practical and is associate with high radiation exposure. As such, a biomarker that is reflective of active myocarditis and that is cardiac specific will assist physicians in assessing the presence of active myocarditis to guide therapeutic decisions and to assess response to therapy which can limit further cardiac damage. Cell free DNA (cfDNA) are fragments of genomic DNA that are released into the circulation from dying or damaged cells. It is a powerful diagnostic tool in cancer, transplant rejection and fetal medicine especially when the genomic source differs from the host. A novel technique that relies on tissue unique CpG methylation patterns can identify the tissue source of cell free DNA in an individual reflecting potential tissue injury. We will be conducting a pilot study to explore the utility of this diagnostic tool to identify granulomatous myocarditis in patients with sarcoidosis.
Prospective randomized controlled trial comparing low dose Prednisone(or Prednisolone)/Methotrexate combination to standard dose Prednisone(or Prednisolone) in patients diagnosed with acute active clinically manifest cardiac sarcoidosis and not yet treated. The Investigators hypothesize that low dose Prednisone(or Prednisolone)/Methotrexate combination will be as effective as standard dose Prednisone(or Prednisolone), and result in significantly better quality of life and less toxicity than standard dose Prednisone(or Prednisolone).
This is a pilot mechanistic study of the diagnostic utility of sodium-glucose cotransporter-1/2 inhibition (SGLT1/2) on myocardial glucose suppression on FDG PET/CT. The investigators will test whether the addition of a SGLT1/2 inhibitor (SGLT1/2i) plus the standard dietary modification (ketogenic diet) will provide enhanced myocardial glucose suppression. The primary objective is to assess rates of complete myocardial glucose suppression (MGS) with 7 days of sotagliflozin 400 mg QD among healthy volunteers on a background of 1 day (N=20) or 3 days (N=20) of the KD. The secondary goal is to investigate the relationship between sotagliflozin, targeted metabolite levels, and myocardial glucose utilization on FDG-PET. Participants will be asked to: * undergo a screening visit that includes blood tests, vitals, and questions regarding health history/medications * take the provided sotagliflozin as instructed for 7 days leading up to the scan * follow a ketogenic diet as instructed for 1 or 3 days leading up to the scan * undergo an FDG PET/CT scan, which includes vitals and blood draws
Arrhythmogenic ventricular cardiomyopathy (AVC) is a genetic condition which affects the heart and can lead to heart failure and rhythm problems, of which, sudden cardiac arrest or death is the most tragic and dangerous. Diagnosis and screening of blood-relatives is very difficult as the disease process can be subtle, but sufficient enough, so that the first event is sudden death. The Mayo Clinic AVC Registry is a collaboration between Mayo Clinic, Rochester, USA and Papworth Hospital, Cambridge University Hospitals, Cambridge, UK. The investigators aim to enroll patients with a history of AVC or sudden cardiac death which may be due to AVC, from the US and UK. Family members who are blood-relatives will also be invited, including those who do not have the condition. Data collected include symptoms, ECG, echocardiographic, MRI, Holter, loop recorder, biopsies, exercise stress testing, blood, buccal and saliva samples. Objectives of the study: 1. Discover new genes or altered genes (variants) which cause AVC 2. Identify biomarkers which predict (2a) disease onset, (2b) disease progression, (2c) and the likelihood of arrhythmia (ventricular, supra-ventricular and atrial fibrillation) 3. Correlate genotype with phenotype in confirmed cases of AVC followed longitudinally using clinical, electrocardiographic and imaging data. 4. Characterize desmosomal changes in buccal mucosal cells with genotype and validate with gold-standard endomyocardial biopsies