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

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. Identifier: NCT00893178
Recruitment Status : Active, not recruiting
First Posted : May 5, 2009
Last Update Posted : March 15, 2017
Heartcenter Leipzig GmbH
Information provided by (Responsible Party):
Sven Möbius-Winkler, University of Leipzig

May 1, 2009
May 5, 2009
March 15, 2017
December 2007
July 2018   (Final data collection date for primary outcome measure)
Correlation of the Expression of Glu 298ASP Polymorphism with pulmonary pressure [ Time Frame: Dec. 2010 ]
Same as current
Complete list of historical versions of study NCT00893178 on Archive Site
Rate of G308A TNF alpha polymorphism within the different groups [ Time Frame: Dec. 2010 ]
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 Model: Case-Control
Time Perspective: Prospective
Not Provided
Retention:   Samples With DNA
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 Identifier (NCT Number) in Medline.
Active, not recruiting
Same as current
December 2018
July 2018   (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
Sexes Eligible for Study: All
18 Years and older   (Adult, Older Adult)
Contact information is only displayed when the study is recruiting subjects
SMW 03
Not Provided
Not Provided
Sven Möbius-Winkler, University of Leipzig
University of Leipzig
Heartcenter Leipzig GmbH
Principal Investigator: Sven Möbius-Winkler, M.D University Leipzig-Heart Center
University of Leipzig
March 2017