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.

Pulmonary Arterial Hypertension Clinical Trial

Official title: 11C-acetate/18Fluorodeoxyglucose-FDG PET/Cardiac MRI in Pulmonary Hypertension

Status Terminated

Clinical Trial Summary

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.

Clinical Trial Description

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). ;

Study Design

Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Diagnostic

Related Conditions & MeSH terms

• Chronic Thromboembolic Pulmonary Hypertension
• Familial Primary Pulmonary Hypertension
• Hypertension
• Hypertension, Pulmonary
• Pulmonary Arterial Hypertension

• NCT number: NCT01953965
• Study type: Interventional
• Source: Brigham and Women's Hospital
• Status: Terminated
• Phase: Phase 2
• Start date: September 2013
• Completion date: July 2016