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Clinical Trials: Cardiovascular (Heart, High Blood Pressure, Etc.)
IRB No. 15-073-3 (Dr. Bruce Liang, PI): Circulating Markers and Advanced Noninvasive Cardiac Imaging Techniques That Predict Subsequent Cardiotoxicity in Cancer Patients Treated with Anthracyclines
The primary goal of this pilot study is to identify early signs of cardiotoxicity in patients with a wide range of cancers who are treated with anthracycline chemotherapy, alone or in conjunction with other chemotherapeutic or molecularly targeted cancer drugs, before there is irreversible cardiac dysfunction or clinical heart failure. We hypothesize that an elevation in apoptotic and inflammatory biomarkers and early changes in myocardial deformation as measured by strain imaging after exposure to anthracycline chemotherapy predict future development of cardiac dysfunction. By checking the levels of these biomarkers before chemotherapy, then at 3 months and at one year in cancer patients receiving anthracyclines, our goal is to determine whether those patients with a "spike" in level develop left ventricular dysfunction and/or clinical heart failure. Similarly, strain imaging by echocardiography will be performed at baseline, then every 3 months and at one year. We hypothesize that a decrease in global longitudinal strain can predict future reduction in LVEF. Our goal is to identify early those patients who are at a high risk for anthracycline-related cardiac toxicity. Early identification may lead to early institution of cardioprotective therapies (i.e. beta blockers and ACE inhibitors), which may prevent irreversible cardiac dysfunction and clinical congestive heart failure. Objectives: To determine the potential utility of biomarkers for the early identification of patients with cancer who are at risk for cardiac dysfunction. To determine whether biomarker levels, or serial changes in biomarker levels, or combination of biomarkers (activated caspase-3, troponin I, IL-6, TNF alpha, CRP, caspase-1, BNP) could predict subsequent cardiotoxicity in patients treated with anthracycline chemotherapy. To determine the utility of strain imaging in the identification of early cardiotoxicity. To determine whether cleaved caspase-3 and caspase-1 show serial changes over time during the course of cancer treatment with chemotherapy. Hypotheses: A serial increase in biomarker levels from baseline to post-chemotherapy may predict subsequent development of systolic or diastolic cardiac dysfunction. Caspase-3 as an apoptotic marker, caspase-1 as an inflammatory marker upstream of IL-1beta, IL-6 and CRP, and troponin I as cardiac injury marker can be quantified in human circulation. An elevation in the levels of these markers may indicate anthracycline-related cardiac apoptosis/ injury and associated inflammation. Strain imaging by echocardiography can identify early sub-clinical imaging evidence of cardiotoxicity. Taken together, the advanced strain imaging and novel biomarkers may identify those who are at risk of developing clinical cardiac dysfunction or heart failure. In the future, we will test whether prevention of overt heart failure can be achieved by institution of medications such as beta blocker and angiotensin converting enzyme inhibitor or angiotensin receptor blocker in these at-risk individuals.
IRB No. 16-086-1 (Dr. Kai Chen, PI): Endothelial Dysfunction in Coronary Artery Disease and Diastolic Heart Failure
Congestive Heart failure, including systolic and diastolic heart failure, is a major public health hazard and its prevalence continues to rise. While the mortality of systolic heart failure has significantly reduced over the past decade thanks to the advances in pharmacological therapy, there has not been a single therapy that has shown to be survival benefit on diastolic heart failure. A significant gap in knowledge on diastolic heart failure has to be bridged before we may design a therapeutic strategy to target this disease. Recent elegant studies have revealed evidence of systemic and myocardial inflammation in endomyocardial tissues. A new paradigm of the pathophysiology of diastolic heart failure has been proposed - systemic proinflammatory state, coronary endothelial inflammation, impairment in endothelial-cardiomyocyte nitric oxide signaling, inflammatory cell infiltration and proinflammatory cytokines, collectively lead to diastolic dysfunction. Therefore, our central hypothesis is endothelial dysfunction contributes to diastolic function and clinical exacerbation of heart failure.
IRB No. 16-234-1 (Dr. Bruce Liang, PI): UConn Health Cardiology Center Research Screening Protocol
This protocol will be used to gain permission from cardiology patients for Cardiology research staff to access health medical records in order to determine eligibility for research studies and clinical trials. The protocol does not involve actual scientific research.