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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: 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. 22-145-2 (Dr. Christopher Pickett, PI): Effect of Beta-blocker Discontinuation on Functional Capacity and Cardiac Hemodynamics in Patients with Heart Failure with Preserved Ejection Fraction

Heart failure (HF) is a growing public health problem associated with significant mortality and healthcare cost. Heart failure (HF) can be classified into two distinct types based on cardiac muscle contractility measured as ejection fraction - HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Significant advances in the HF therapy over the past decades have substantially improved the outcome in patients with HFrEF. In contrast, there is no effective therapy available for HFpEF, which remains to be the ";single largest unmet need in cardiovascular medicine";1. Beta-blocker (BB) - The survival benefit of BB in treating HFrEF 3, but not HFpEF, has been well established. Despite of lacking evidence, BB use was shown in 80% of HFpEF patients enrolled in both TOPCAT and PARAGON-HF trials4,5, and in 66% of HFpEF patients in our observational study excluding atrial fibrillation and CAD. This pilot study is to evaluate the effect of beta-blocker withdrawal on functional capacity and cardiac hemodynamics in patients with HFpEF.

IRB No. 26-069-2 (Dr. Akif Altinbas, PI): UConn Health Cardio-Metabolic and Obesity Research Registry -- Altinbas (PI), Celi (Co-PI), Marino (Co-PI)

This registry collects comprehensive clinical information from adults receiving care for overweight or obesity, as well as those with cardio metabolic diseases such as type 2 diabetes, hypertension, dyslipidemia, metabolic syndrome, MASLD (metabolic dysfunction–associated steatotic liver disease), cardiovascular risk conditions, and related metabolic disorders. The goal is to support research that improves understanding of metabolic health, obesity related physiology, and the interplay between metabolic disease and associated conditions—including liver fibrosis, sleep apnea, frailty, sarcopenia, and cardiovascular risk progression. By integrating clinical, demographic, and physiologic data, the registry enables investigators to study disease patterns, identify high risk phenotypes, and explore how imaging modalities (such as body composition analysis, elastography, MRI based liver assessment, calcium scoring, and sleep studies) may guide management of metabolic and liver disease. Participants may also be contacted for future IRB approved studies focused on obesity, MASLD, and cardio metabolic health. (“The primary goal is to establish a biorepository and registry of clinical information… from patients who are at risk or do have cardio metabolic diseases”; “describe the clinical and demographic characteristics of individuals who are overweight or obese, or lean but with at least one described cardio metabolic disease”.

IRB No. 26-130-2 (Dr. Beiyan Zhou, PI): Type 2 diabetes impact on dysregulated immune cell function in cardiovascular diseases

Type 2 diabetes (T2DM) is the leading cause of many serious health complications, including cardiovascular diseases, chronic kidney diseases, blindness, and several types of cancers. One of the primary disease-causing factors is malfunction of the immune system, which can lead to weakened immune cell function in fighting infections and sustained low-grade systemic chronic inflammation. Through direct and indirect effects, T2DM dysregulated immune cells are pathogenic factors in various disease conditions, including atherosclerosis, infection, autoimmune diseases, and cancerous transformation. T2DM is a primary cause for the marked increase of atherosclerotic cardiovascular disease (ASCVD), accounting for 30% of symptomatic cases. Accordingly, the ASCVD risk in T2DM patients is 2-4 fold more than that in the non-T2DM population. The concomitant increase of T2DM and ASCVD in the US has prompted the urgency for more accurate ASCVD risk assessment and an effective mitigation strategy direction. Current standard-of-care therapies, addressing factors such as lipid/hypertension/glycemic control, have underachieved as indicated by recent clinical trials and extensive cohort studies. Even novel drug classes approved for ASCVD prevention in T2DM, such as SGLT2 inhibitors or GLP-1 receptor agonists, reduce disease risk by only 2%. These results warrant a new direction in the mitigation strategy, which relies on advancing our understanding of immune cell function in T2DM and T2DM-associated ASCVD. Given the volatile and central roles of monocytes in ASCVD development and progression, we recently developed a set of new algorithms to annotate their function under complex conditions with high resolution. Importantly, powered by these tools, two distinct macrophage-derived foam cell development programs were revealed (homeostatic vs. pathogenic foaming). However, mechanisms underlying T2DM-altered monocyte-derived macrophage function in ASCVD pathogenesis remain elusive. This project aims to investigate cellular and molecular mechanisms derailed by T2DM in circulating immune cells; thus, samples from healthy or T2DM patients with or without cardiovascular diseases will be needed for this study. After completing this study, we may identify new molecular targets or develop comprehensive treatments for T2DM patients to reduce their risk of comorbidities, including ASCVD.