Home > Search Clinical Trials > Cardiovascular (Heart, High Blood Pressure, Etc.)
Clinical Trials: Cardiovascular (Heart, High Blood Pressure, Etc.)
IRB No. 02-200-1 (Dr. Bruce Liang, PI): Molecular Correlates of Atrial Fibrillation
Study description not available
IRB No. 06-151-2 (Dr. Bruce Liang, PI): Circulating markers that underlie the transition from compensated hypertrophy to heart failure
Early detection and prevention are key features in treating subjects with heart failure. We are looking to see of caspase-3 and dystrophin can be detected in human circulation. If so, we will determine whether they are predictors for the transition between compensated and de-compensated heart failure.
IRB No. 07-252-2 (Dr. Bruce Liang, PI): Circulating Markers for Ischemic Heart Failure
The purpose of this research is to determine if two proteins in the blood are increased during acute myocardial infarction and whether their levels are higher in those who develop heart failure than those who do not. These two proteins are produced and potentially released when the heart muscle is damaged. They may then be released into the blood and be detected by standard method in the research laboratory. At this time, detection of an increase in these proteins in the blood is not know to be associated with any disease or myocardial infarction.
IRB No. 11-157-3 (Dr. Bruce Liang, PI): Circulating Caspase-3 p17 Fragment as a Novel Marker for Cardiac Apotosis
This study is an investigator initiated prospective longitudinal follow-up study with two arms (Acute STEMI subjects and Bypass surgery subjects) and collection of DNA samples. The project plans to test the hypothesis that cardiac cells undergo cell death (apoptosis) in patients during ischemic/reperfusion (I/R), and to ultimately determine the clinical significance of such cell death. By establishing the presence and importance of cardiac myocyte apoptosis the study outcomes intends to provide the rationale for developing anti-apoptotic therapy for clinically relevant I/R conditions. The research aims are to 1) Determine existence of human cardiac myocyte apoptosis under two clinically relevant ischemia/reperfusion conditions, acute ST segment elevation myocardial infarction (STEMI) with primary percutaneous coronary intervention (PCI) and cardioplegia (cardiac muscle paralysis) for bypass surgery 2) Determine the potential clinical significance of coronary and peripheral venous levels of p17 during acute STEMI with PCI and during cardioplegiaa. 68 subjects from UCHC cardiology patient base are expected to be enrolled in this study, 34 patients with anterior STEMI and 34 patients undergoing cardio-pulmonary bypass surgery. Once blood samples are obtained from each group medical records will be reviewed or follow-up calls will be made twice a year for three years to update any new cardiac events. There is no compensation to subjects participating.
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.
IRB No. 15-073-3.2 (Dr. Agnes Kim, PI): Circulating Biomarkers and Noninvasive Cardiac Imaging Techniques That predict Cancer Therapy Cardiotoxicity
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. 17-115-3.2 (Dr. Kai Chen, PI): The Risk Factors and Imaging Study of Diastolic Dysfunction
A normal heart function consists of muscle contraction during systole and muscle relaxation during diastole. Diastolic dysfunction refers to a condition in which abnormalities in mechanical function are present during diastole, namely impaired relaxation and increased stiffness. Both systolic dysfunction and diastolic dysfunction will ultimately lead to heart failure. We are specifically interested in diastolic heart failure, because the prevalence continues to rise and there is no effective therapy for this condition till today. The diagnosis of diastolic heart failure is based on echocardiographic evidence of diastolic dysfunction - signs of increased muscle stiffness and reduced relaxation. There are a number of risk factors that are believed to contribute to the development of diastoic dysfunction, including high blood pressure, diabetes and overweight. More importantly, an effective treatment of the risk factor may reverse the diastolic dysfunction. However, when diastolic heart failure is present, none of the treatment has shown the benefit. This highlights the importance of early detection and early intervention in the prevention of diastolic heart failure, by recognizing the risk factors. Therefore, the goal of this study is to identify the risk factors associated with diastolic dysfunction, by reviewing the existing chart and echocardiographic data.
IRB No. 18-154-2 (Dr. Kai Chen, PI): Left Atrial Mechanical Function and Atrial Fibrillation (LameAfib Study)
Atrial fibrillation (Afib) is the most common cardiac arrhythmias encountered in clinical practice. Afib worsens quality of life with symptoms of dyspnea, palpitation, and fatigue; and contributes to an increased risk of thromboembolic stroke and mortality. As arhythm-control strategies, direct-current cardioversion (DCCV) and catheter ablation are two therapies to restore sinus rhythm.The recurrence of Afib after DCCV or catheter ablation remains a major problem. For example, the Afib recurrence rate reached 30% at 3 months and 60% at 12 months after DCCV. A reliable prediction of the Afib recurrence will help guide the treatment strategy. Previous report has shown that left atrium (LA) size is a strong independent predictor of Afib recurrence after catheter ablation. Another report demonstrated echocardiographic diastology variables such as mitral annular velocity (e wave) and septal E/e ratio, but not LA dimensions, are the best predictors of recurrence after DCCV. Therefore, the goal of this study is to evaluate echocardiographic variables related to left atrial remodeling by strain imaging as a tool to predict atrial fibrillation recurrence after cardioversion or ablation. This is a retrospective chart review study to evaluate the echocardiographic findings in relation to Afib recurrence in the patients with Afib who underwent cardioversion or catheter ablation between 01/01/2013 and 12/31/2017.
IRB No. 18-170-1 (Dr. Sara Tabtabai, PI): Evaluation of a Guideline Directed Medication Titration (GDMT) Program in Patients with Heart Failure with Reduced Ejection Fraction
A patient newly diagnosed with heart failure with reduced ejection fraction requires close follow up for titration of medications as blood pressure, electrolytes and symptoms permit. Although the benefits of guideline directed medical therapy (GDMT) have been well studied, there remains a significant gap in the receipt of GDMT in the ambulatory and hospitalized setting. As such, we seek to assess the utility of focused GDMT clinic to reduce this gap. We hypothesize that implementation of a GDMT focused clinic will reduce the gap, improve medication compliance and in turn, improve the mean ejection fraction, and reduce hospitalization rates.
IRB No. 18-228-2 (Dr. Agnes Kim, PI): Assessment of Myocardial Deformation in Adult Patients with Type 2 Diabetes Mellitus
This retrospective case-control study aims to determine if patients with early-stage diabetic cardiomyopathy have subtle myocardial deformation usingspeckletracking echocardiogram. The two aims of the study are (1)to determine whether adult diabetic patients with preserved left ventricular ejection fraction have abnormalities in myocardial deformation and (2) to determine whether adult diabetic patients have impaired diastolic function as assessed by traditional methods as well as by novel method, i.e. left atrial strain, a measurement that has been shown to correlate with pulmonary capillary wedge pressure.