Body Volume Regulation in Pulmonary Arterial Hypertension With Right Ventricular Failure
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT00811486|
Recruitment Status : Withdrawn (Only 1 patient recruited, and he withdrew)
First Posted : December 19, 2008
Last Update Posted : January 28, 2013
|Condition or disease||Intervention/treatment||Phase|
|Right Heart Failure Pulmonary Hypertension||Drug: Spironolactone and conivaptan||Not Applicable|
Much has been learned about the pathophysiological state that underlies the development of increased total body volume and edema in left ventricular failure. Very little, however, is known about the mechanism underlying systemic hypervolemia in patients with isolated right ventricular dysfunction. Patients with pulmonary arterial hypertension (PAH) represent a model of isolated right ventricular dysfunction in which these mechanisms may be elucidated. Aldosterone has now been shown to have many properties that are likely to be detrimental in congestive heart failure (CHF) and that are not shared by angiotensin II. Aldosterone blockade has been associated with improved mortality in patients with left ventricular failure, already receiving an angiotensin converting enzyme inhibitor. But its role in isolated right ventricular failure has not been elucidated. The plasma arginine vasopressin levels are disproportionately elevated for the degree of serum osmolarity in patients with heart failure and result in water retention and hyponatremia. Conivaptan, a vasopressin receptor antagonist, appears to reduce body weight and improve signs of left heart failure, though there is no study to evaluate its role in right ventricular failure with edema.
This study will examine the role of spironolactone and conivaptan in patients with right ventricular failure and pathophysiology of sodium and water retention in these patients.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||0 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||None (Open Label)|
|Official Title:||Body Volume Regulation in Pulmonary Arterial Hypertension With Right Ventricular Failure|
|Study Start Date :||January 2009|
|Actual Primary Completion Date :||July 2010|
|Actual Study Completion Date :||December 2010|
U.S. FDA Resources
No Intervention: Usual care
Experimental: Spironolactone and conivaptan
Drug: Spironolactone and conivaptan
Tablet, 50 mg to 200 mg, daily, orally 20 mg intravenously one time over 30 minutes
- Cross sectional study [ Time Frame: 18 months ]Correlation between severity of pulmonary hypertension and neurohumoral activation, Regional Blood Flow (RBF) & Transcatheter Pulmonary Valve (TPV). Acute study:electrolyte-free water and sodium excretion. Cohort Study: Composite of Cardiac index (CI),brain natriuretic peptide (BNP) and Right Atrial Pressure (RAP)
- Cross-sectional Study [ Time Frame: 18 months ]Correlations between mean pulmonary artery pressure, pulmonary vascular resistance; and neurohumoral activation, glomerular filtration rate (GFR) and Transcatheter Pulmonary Valve (TPV). Acute study:correlation between response to drug and severity of disease.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00811486
|United States, Colorado|
|University of Colorado at Denver and Health Sciences Center General Clinical Research Center|
|Denver, Colorado, United States, 80262|
|Principal Investigator:||Shweta Bansal, MD||UCHSC|