Impact of Polymorphism on Pulmonary Pressure in Subjects With Pulmonary Hypertension of Different Cause

The recruitment status of this study is unknown because the information has not been verified recently.
Verified September 2011 by University of Leipzig.
Recruitment status was  Recruiting
Sponsor:
Information provided by (Responsible Party):
Sven Möbius-Winkler, University of Leipzig
ClinicalTrials.gov Identifier:
NCT00893178
First received: May 1, 2009
Last updated: September 2, 2011
Last verified: September 2011

May 1, 2009
September 2, 2011
December 2007
July 2012   (final data collection date for primary outcome measure)
Correlation of the Expression of Glu 298ASP Polymorphism with pulmonary pressure [ Time Frame: Dec. 2010 ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT00893178 on ClinicalTrials.gov Archive Site
Rate of G308A TNF alpha polymorphism within the different groups [ Time Frame: Dec. 2010 ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Impact of Polymorphism on Pulmonary Pressure in Subjects With Pulmonary Hypertension of Different Cause
Impact of Different Genetic Polymorphism on the Pulmonary Pressure in Patients With Pulmonary Hypertension of Different Cause With Special Focus on Patients With Chronic Heart Failure

Pulmonary Hypertension (PH) is a disease that is characterized by vasoconstriction of small vessels of the lung. Many cases do have proliferation of endothelial cells within these vessels. A possible influence of polymorphisms of genes relevant for inflammatory and endothelial processes is suspected.

Especially patients with chronic heart failure can develope PH. The reasons therefore are lacking.

The researchers investigate different polymorphism and the influence of these on pulmonary artery pressure (measured invasively) in patients with congestive heart failure (CHF) and patients with primary pulmonary hypertension.

The study consists of 3 arms-patients with CHF and PH, patients with CHF without PH and patients without CHF and PH.

The PH measurement is due to routine catheterization, thereafter we measure different vasoactive polymorphism.

Observational
Observational Model: Case Control
Time Perspective: Prospective
Not Provided
Retention:   Samples With DNA
Description:

EDTA Blood, Serum

Probability Sample

CHF elevated pulmonary hypertension

  • Congestive Heart Failure
  • Pulmonary Hypertension
Not Provided
  • CHF with elevated PAP
    CHF patients (LVEF > 35%) with elevated mean pulmonary pressure( > 20 mmHg ) measured by pa catheter
  • CHF patient without elevated PAP
    CHF patients (LVEF > 35%) with normal mean pulmonary pressure
  • Normal EF with elevated PAP
    Patients with normal LVEF < 60% with elevated mean pulmonary pressure
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
600
December 2012
July 2012   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • CHF with or without pulmonary hypertension or
  • patients with normal LVEF and pulmonary hypertension
  • right heart catheterization due to routine
  • informed consent

Exclusion Criteria:

  • no right heart catheterization
  • no informed consent
  • elevated pulmonary pressure due to valve diseases or congenital heart disease
Both
18 Years and older
No
Germany
 
NCT00893178
SMW 03
No
Sven Möbius-Winkler, University of Leipzig
University of Leipzig
Not Provided
Principal Investigator: Sven Möbius-Winkler, M.D University Leipzig-Heart Center
University of Leipzig
September 2011

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP