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Endothelial Progenitor Cells and Pulmonary Idiopathic Arterial Hypertension

The Determination of Endothelial Progenitor Cells in Pulmonary Idiopathic Arterial Hypertension.

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT00551408
Enrollment
20
Registered
2007-10-31
Start date
2007-08-31
Completion date
2016-10-31
Last updated
2018-10-16

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Pulmonary Idiopathic Arterial Hypertension

Brief summary

Endothelial dysfunction ultimately represents an imbalance between the magnitude of injury and the capacity for repair. Current evidence established that endothelial progenitor cells (EPC) participate in several models of vascular disease as acute coronary syndromes, stroke, diabetes, peripheral artery disease, etc. However EPC in the setting of PAH is less well established. The target of this study is to demonstrate if the number of EPC is increased in a mexican population of patients with PAH.

Interventions

None listed

Sponsors

Unidad de Investigacion Clinica en Medicina S.C.
Lead SponsorNETWORK

Study design

Observational model
CASE_CONTROL
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to 70 Years
Healthy volunteers
No

Inclusion criteria

* Patients were included in the study if they were in The WHO functional class II to III, and had a mean pulmonary artery pressure \>30 mm Hg on right heart catheterization. The ability to walk \>50 m during a standardized 6-min walk test.

Exclusion criteria

* Pulmonary hypertension as a result of heart disease, pulmonary disease, sleep-associated disorders, chronic thromboembolic disease, autoimmune or collagen vascular disease, HIV infection, liver disease, major bleeding requiring blood transfusion,renal dysfunction, and evidence for malignant diseases were excluded.

Countries

Mexico

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026