View clinical trials related to Cardiotoxicity.
Filter by:This observational cohort will evaluate the cardiovascular effects of chemoradiation used to treat locally advanced, non-small cell lung cancer. Patients will be enrolled prior to the start of therapy and followed during and for at least 2 years after therapy with echocardiograms, nuclear stress tests, blood sampling, and quality of life surveys.
Anthracycline chemotherapies (e.g. doxorubicin, daunorubicin) are commonly given to treat pediatric cancer, and carry a risk of cardiotoxicity. Over the long term, children who receive these therapies have an increased risk of heart failure and early cardiovascular death. However, current strategies for identifying patients who are at risk prior to the development of significant changes in heart function are limited. This study will focus on imaging markers of cardiac injury and dysfunction with the goal of developing improved diagnostic tests and treatment strategies.
The purpose of the present study is to evaluate cardiotoxicity during re-challenge of a different modality of fluoropyrimidine (primary end-point S-1 and secondary any other fluoropyrimidine) after having perceived cardiotoxicity with a fluoropyrimidine based regimen previously. The patient population is being treated for solid tumors.
Aluminum phosphide (AlP) or rice tablet is a cheap pesticide. When it comes in contact with acid (gastric acid) or moisture, it releases phosphine (PH3) gas. The heart,lungs, liver are the main targets in acute Aluminum phosphide (AlP) poisoning. Most deaths occur due to cardiovascular toxicity.
The research study is being conducted to test how two different types of Positron Emission Tomography (PET/CT) scans could be used to image a type of heart disorder called amyloidosis (AL). There will be two groups in the study. One group will have PET/CT scans using an imaging drug called 18F-NOS and the other group will have PET/CT scans using a drug called Florbetaben. subject will be assigned to one of the groups when she/he agrees to be in the study.
The purpose of the present study is to investigate the effect of ACE inhibitors and the sacubitril-valsartan complex in bone marrow transplant patients by assessing cardiovascular and endothelial parameters in order to search for a potent protective role.
Advances in treatment have led to improved survival of patients with cancer, but have also increased morbidity and mortality due to cancer treatment side effects. Cardiotoxicity is one the most frequent side effect which may lead to premature morbidity and death among cancer survivors. The most concerning cardiovascular complications of cancer therapy is myocardial dysfunction, leading to heart failure, and fatal arrhythmias, especially those induced by QT-prolonging drugs. PROMETEY (PROspective Multidisciplinary obsErvational Trial of cardiotoxicity in patiEnts undergoing anticancer therapy) - is Russian multicenter observational study assessing cardiotoxicity and its clinical, biochemical and genetic factors in patients on cancer therapy. The objectives of the study are: - to reveal prevalence of cardiotoxic effects of cancer therapy in routine clinical practice in Russian Federation, - to assess contribution of these effects to mortality of patients on cancer therapy, - to evaluate clinical and economic consequences of cardiotoxicity in patients with cancer, - to develop an individualized model of cardiotoxicity risk factors based on clinical and laboratory parameters. Patients: 400 cancer patients with toxic cardiomyopathy and 100 patients with idiopathic or family dilated cardiomyopathy. Study duration: 60 months. All patients will undergo complex examination after signing informed consent form(ICF): physical exam, echocardiography with speckle tracking analysis, ambulatory 48-hours ECG monitoring, biochemistry, analysis of biomarkers of myocardial injury, fibrosis and inflammation. Primary endpoint: all-cause mortality, heart transplantation, cardioverter-defibrillator implantation, hospitalization with heart failure decompensation. Secondary endpoints: - thromboembolism, - fatal/ nonfatal myocardial infarction, stroke, - sudden cardiac death, - surgical therapy of heart failure or arrhythmias, - cardiovascular death, - all-cause mortality, - heart transplantation, - cardioverter-defibrillator implantation.
New therapies for cancer increased patient survival, but led to the recognition of adverse effects associated with cancer treatment, such as the use of chemotherapy. Cardiotoxicity is the most significant adverse effect, which affect the functional capacity and quality of life and is associated with high morbidity and mortality, regardless of the oncological prognosis. One of the manifestations of cardiotoxicity is ventricular dysfunction that can lead to heart failure. Neuro humoral hyperactivation with increased sympathetic nerve activity is a typical manifestation of heart failure and is associated with worse prognosis. Studies have shown that physical training significantly reduces sympathetic nerve activity in addition to improving muscle blood flow, reversing effects on skeletal muscle and improving quality of life. The hypothesis is that physical training may reduce sympathetic nerve activity and vasoconstrictor status in patients with heart failure caused by anthracyclines, as well as improving baroreflex and chemoreflex sensibility, mechanoreflex and metaborreflex control and skeletal myopathy.
With this study the investigators will assess early cardiac damage by means of Global Longitudinal Strain (GLS) in newly diagnosed breast cancer (BC) patients treated with anthracycline-based chemotherapy, and to investigate whether myocardial damage as measured with T1 / T2 Cardiovascular Magnetic Resonance (CMR) mapping and plasma hs-Troponin T is related to changes in GLS.
Patients enrolled in the study will receive standard of care adjuvant or definitive breast, chest wall or thoracic radiation therapy.Cardiac mitochondrial dysfunction is a hallmark of radiation-induced cardiac injury. Reactive oxygen species (ROS) produced by ionizing radiation cause oxidation of mitochondrial proteins and alter oxidative phosphorylation and pyruvate metabolism(5). The goal of this study is to detect early changes in the mitochondrial metabolism in situ as a marker for subclinical radiation-induced cardiotoxicity.