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TUHVI Clinical Research
(504) 988-3071

Director, Clinical Research:
Roberta McDuffie, MSN

Clinical Research Coordinator:
Nana Asafu-Adjaye

Clinical Research Coordinator:
Suzanne Bowers, RN

Clinical Research Coordinator:
Andrew Myers

» Tulane Clinical Trials Website

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CURRENT CLINICAL RESEARCH STUDIES OPEN TO ENROLLMENT

CANTOS – PI: Dr. Delafontaine, Sponsor: Novartis

CANTOS is a randomized, double-blind, placebo-controlled, event-driven Phase III trial of quarterly subcutaneous canakinumab in the preventions of recurrent cardiovascular events among stable post-myocardial infarction (MI) patients with evelevated hsCRP. Canakinumab (ACZ885) is a fully human monoclonal anti-human IL-1β antibody of the IgG1/k isotype, being developed for the treatment of IL-1β driven inflammatory diseases. It is designed to bind to human IL-1β and thus blocks the interaction of this cytokine with its receptors. The antagonism of the IL-1β  mediated inflammation using canakinumab in lowering high sensitivity C-reactive protein (hsCRP) and other inflammatory marker levels has shown an acute phase response in patients with Cryopyrin-Associated Periodic Syndrome (CAPS) and rheumatoid arthritis. This evidence has been replicated in patients with type 2 diabetes mellitus (T2DM) using canakinumab, and with other IL-1β antibody therapies in development.

TAO – PI: Dr. Delafontaine, Sponsor: Sanofi-Aventis
Randomized, double-blind, triple-dummy trial to compare the efficacy of otamixaban with Unfractionated Heparin + eptifibatide, in patients with Unstable angina/Non ST segment Elevation Myocardial infarction scheduled to undergo an early invasive strategy. Subjects, presenting with acute coronary syndrome, are invited to participate in this research study designed to compare intravenous otamixaban to unfractionated heparin and eptifibatide on top of aspirin and clopidogrel or another oral antiplatelet agent.

COAG – PI: Dr. Delafontaine, Sponsor: NIH
The purpose of COAG is to determine whether the use of genetic and clinical information to guide the initial dosing of warfarin will improve anticoagulation control, as compared to the use of only clinical information (without genetics) to guide the initial dosing of warfarin. By comparing the two strategies in this trial, the study will be able to determine if genetic information provides added benefit above and beyond what can be done simply with clinical information. The investigational part of this study is the dose calculation using genetic and clinical factors (e.g., age, body size). There are three known variants in genes CYP2C9 that affect metabolism of warfarin, while variants in VKORC1 affect the body's sensitivity to warfarin. Clinical and genotype data will be collected on all participants, who will then be randomized to one of two study dosing intervention arms: genotype-guided dosing arm or clinical-guided dosing arm. The intervention will be applied over these first 4-5 days of treatment. Thereafter, dose adjustments until stable dose is reached will be based on INR measurements according to standardized warfarin treatment protocol. Study visits will be followed according to the protocol visit schedule for duration of 24 weeks. The first 4 weeks of treatment duration is a blinded study phase with 20 weeks of unblinded follow-up.

DIVA – PI: Dr. Irimpen, Sponsor: VA
Subjects who have had a saphenous vein graft (SVG) during coronary bypass surgery will qualify to participate in this study. Subjects will have an angiogram to see if your SVG has narrowed or blocked areas and to determine whether a Percutaneous Coronary Intervention (PCI) is needed. If the subject needs a PCI and meets other conditions, they may be eligible to be in this study. If you need to have a PCI, this can be done whether or not you decide to be in the study. Your doctor will explain that procedure to you, including the risks, and you will sign a separate consent form before the procedure is done. We will use two types of stents in this study. One type is bare metal (BMS). The other type is drug-eluting (DES). The drug-eluting stent is coated with medication that slowly releases into the wall of the blood vessels to help keep scar tissue from growing and re-narrowing the blood vessels. The two types of stents have different advantages and disadvantages, but doctors do not know which type of stent is better. Drug-eluting stents might reduce the risk of the blood vessels re-narrowing compared to bare metal stents. But patients who get drug-eluting stents need to take medications longer, which might increase the risk of side effects. Both BMS and DES, together with medications that are normally prescribed after getting a stent placed (blood thinners, cholesterol lowering and blood pressure lowering medications, etc.) are commonly used in SVGs, so these risks are the same whether or not you participate in the study. Neither BMS (except for an outdated model that is not used very much anymore) nor DES are approved by the U.S. Food and Drug Administration (FDA) for use in SVGs, but both are commonly used in SVGs. The purpose of this study is to see if one type of stent works better in SVGs.

Skeletal Muscle – PI: Dr. Delafontaine, Sponsor: Investigator Initiated
In addition to regulating blood pressure and salt and water balance, the renin-angiotensin system (RAS) plays an important role in the pathogenesis of all stages of cardiovascular disease, ranging from early endothelial dysfunction to target-organ damage, congestive heart failure (CHF), renal or cerebrovascular disease1. Patients with advanced disease, such as CHF or end-stage renal disease (ESRD), often have cachexia and skeletal muscle wasting, which independently worsens outcome2. Yet, little is known about how perturbations in the RAS affect skeletal muscle. The overall goal of this project is to understand how angiotensin II (Ang II) alters the biology of skeletal muscle and how its effects are counteracted by insulin-like growth factor 1 (IGF-1). The study hypothesis is that Angiotensin causes alterations in AMPK activity and metabolic signaling that lead to skeletal muscle wasting and that normal regenerative processes are inhibited by Angiotensin II.


 

 

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