Now Available for Public Comment: Notice of Proposed Rulemaking (NPRM) for FDAAA 801 and NIH Draft Reporting Policy for NIH-Funded Trials

Inhaled Nitric Oxide in Pulmonary Embolism

This study has been completed.
Sponsor:
Information provided by:
Medical University of Vienna
ClinicalTrials.gov Identifier:
NCT00565253
First received: November 28, 2007
Last updated: June 22, 2010
Last verified: June 2010

November 28, 2007
June 22, 2010
March 2005
July 2009   (final data collection date for primary outcome measure)
right ventricular size and arterial oxygenation [ Time Frame: 2 hours ]
Same as current
Complete list of historical versions of study NCT00565253 on ClinicalTrials.gov Archive Site
blood pressure, central venous pressure, right ventricular function, pulmonary artery pressure [ Time Frame: 2 hours ]
Same as current
Not Provided
Not Provided
 
Inhaled Nitric Oxide in Pulmonary Embolism
Inhaled Nitric Oxide in Pulmonary Embolism, a Randomized, Double-Blind Placebo-Controlled Study

The purpose of the study is to determine if inhaled nitric oxide, a potent and selective pulmonary vasodilator, is beneficial in patients with acute pulmonary embolism causing increased right ventricular afterload.

The early phase of severe pulmonary embolism is associated with high mortality. Right ventricular failure induced by the increase in right ventricular afterload is the final cause of deterioration leading to circulatory failure in patients who die from severe pulmonary embolism. Therefore, reduction of right ventricular afterload remains the central therapeutic strategy. In acute pulmonary embolism, the increase in pulmonary vascular resistance is caused by reduction in the cross-sectional area of the pulmonary vascular bed from obstructing emboli. Pulmonary arterial constriction further increases pulmonary vascular resistance, whereby vasoactive humoral factors may be contributing, which are released from activated platelets accumulating at the site of the clot. Consequently, administration of vasodilators of the pulmonary circulation may be regarded as a therapeutic option to antagonize increased pulmonary vasoconstriction or compensate for impaired vasodilation. Inhaled nitric oxide (NO) acts as a powerful selective pulmonary vasodilator. The aim of the study is to determine, if short-term inhalation of NO is beneficial in respiratory compromised patients with right ventricular dysfunction after acute pulmonary embolism.

Interventional
Phase 2
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
Pulmonary Embolism
Drug: Inhaled nitric oxide (NO)
20 ppm for 15 minutes
Not Provided
Capellier G, Jacques T, Balvay P, Blasco G, Belle E, Barale F. Inhaled nitric oxide in patients with pulmonary embolism. Intensive Care Med. 1997 Oct;23(10):1089-92.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
30
December 2009
July 2009   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Patients with acute pulmonary embolism within 24 hours after onset of symptoms.
  • Patients with hypoxaemia not present before pulmonary embolism and acute right ventricular dysfunction.

Exclusion Criteria:

  • Age < 18 years.
  • Chronic lung disease, left heart failure, suspected or documented intracranial bleeding.
  • Pregnancy, Methaemoglobinaemia.
  • Patients who previously needed thrombolysis or surgical embolectomy.
  • Negative D-Dimer test.
Both
18 Years and older
No
Contact information is only displayed when the study is recruiting subjects
Austria
 
NCT00565253
3052001
No
Not Provided
Medical University of Vienna
Not Provided
Principal Investigator: Peter Schenk, Prof MD MSc Dpt. of Internal Medicine III, Medical University Vienna, Austria
Medical University of Vienna
June 2010

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