Look at Way the Heart Functions in People With Pulmonary Hypertension (PH) Who Have Near Normal Right Ventricle (RV) Function and People With Pulmonary Hypertension Who Have Impaired RV Function. Using Imaging Studies PET Scan and Cardiac MRI.
The purpose of this study to look at differences in the way the heart functions in people with pulmonary hypertension (PH) who have near normal right ventricle (RV) function and people with pulmonary hypertension who have impaired RV function. The right ventricle is a chamber of the heart that pumps blood into the pulmonary artery (the artery that carried blood from the heart to the lungs). Learning more about how the heart is working in people with pulmonary hypertension may help researchers to understand how to better treat pulmonary hypertension and prevent the disease from getting worse.
To do this, we will use two imaging techniques, MRI (Magnetic Resonance Imaging) and PET/CT (Positron Emission Tomography/Computed Tomography). MRI uses a strong magnet and radio waves to take pictures of your heart. A PET/CT scan combines a PET and CT scan into one machine. A CT scan uses x-0rays to take a 3-day picture of the inside of your body, while a PET scan measures small amounts of radiation from a dye called a "tracer" that we inject into your veins.
You will be given two tracers as part of the PET/CT scan. A tracer is a special type of dye with a small amount of radioactivity in it. The tracers that are used in this study are called [18F]fluorodeoxyglucose (FDG) and [11C]-acetate.
In order to take part in this study, you must also have agreed to take part in a companion study. In the companion study, we are trying to learn whether the drug ranolazine is safe and effective in people with PH.
Pulmonary Arterial Hypertension
Chronic Thromboembolic Pulmonary Hypertension
|Study Design:||Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Diagnostic
|Official Title:||11C-acetate/18Fluorodeoxyglucose-FDG PET/Cardiac MRI in Pulmonary Hypertension|
- 1. To demonstrate that there are differences in metabolism and function between subjects with near normal RV function and persistent RV dysfunction as defined by CMR Right Ventricular Ejection Fraction (RVEF) of <= 40%. [ Time Frame: baseline and 6 months ] [ Designated as safety issue: No ]Compare myocardial oxygen consumption, FDG uptake, and myocardial perfusion at baseline for subjects with near normal right ventricular function and those with persistent right ventricular dysfunction.
- 2. To measure changes in RV energy and contractility in subjects with persistent RV dysfunction using serial 11C-acetate and 18F-FDG PET/CT and CMR. perfusion [ Time Frame: Baseline to 6 months ] [ Designated as safety issue: No ]Compare myocardial oxygen consumption, FDG uptake, and myocardial perfusion at baseline for subjects with near normal right ventricular function and those with persistent right ventricular dysfunction.
- Changes in myocardial structure and function [ Time Frame: 6 months ] [ Designated as safety issue: No ]Using CMR, comparing myocardial structure and function in patients treated with ranolazine or placebo.
|Study Start Date:||September 2013|
|Estimated Study Completion Date:||June 2015|
|Estimated Primary Completion Date:||June 2015 (Final data collection date for primary outcome measure)|
Experimental: 11c-acetate and 18F-FDGI
For each PET/CT imaging session subjects will receive a 15-25 millicurie intravenous injection of 11C-acetate and 10 millicurie injection of 18F-FDG at baseline/6months follow-up, a cardiac MRI will be performed.
For each PET/CT imaging session subject will receive a 15-25 millicurie intravenous injection of 11C-acetateDrug: [18F]Fluoro-2-deoxy-2-D-glucose
For each PET/CT imaging session subjects will receive a 10 millicurie injection of 18F-FDGDrug: MultiHance
Cardiac MRI is performed at 6 months to measure any change in structure and function of the treatment groups. MultiHance is the contrast that will be given to subjects.
Historically, RV failure had been described as a stereotyped response to hemodynamic overload. More recent large patient cohort data suggests that RV, independently from Pulmonary Arterial Pressure (PAP), predicts mortality. Thus, a recent hypothesis suggests that individual genetic differences dysregulate cardiomyocyte function and, in doing so, predispose to RV failure in humans, control patient-specific manifestations of disease, and thus would represent key diagnostic markers and therapeutic targets. In fact, multiple key metabolic regulatory factors have been found to be altered in RV failure, any one of which could contribute to individual predisposition to RV failure. Based on their established functions in left ventricular injury and metabolism19 and known alterations in right ventricular failure20, we propose to evaluate metabolic dysfunction of the RV using positron emission topography (PET) and cardiac magnetic resonance imaging (CMR).
Please refer to this study by its ClinicalTrials.gov identifier: NCT01953965
|Contact: Laurie Lawler, RNemail@example.com|
|Contact: Aaron Waxman, MD, PhDfirstname.lastname@example.org|
|United States, Massachusetts|
|Brigham and Women's Hospital||Recruiting|
|Boston, Massachusetts, United States, 02115|
|Contact: Laurie Lawler, RN 617-525-9731 email@example.com|
|Principal Investigator: Aaron Waxman, MD,PhD|
|Principal Investigator:||Aaron Waxman, MD, PhD||Brigham and Women's Hospital|