Elevated Basic Fibroblast Growth Factor Levels: Materials and Methods

Although abnormal expression of bFGF and VEGF has been noted in animal models of pulmonary hypertension, their contribution to human PAH is not well understood. The detection of elevated growth factors in affected patients may help clarify the underlying mechanisms involved in the disease process. One area in which research on angiogenesis may have clinical application is the quantitation of angiogenesis. Quantitation of angiogenic proteins in body fluids has been used as an indirect measure of angiogenic growth factor activity in certain patients with tumors, as well as nonneoplastic diseases. We hypothesized that angiogenic growth factors may have a role in the cellular proliferation seen in the small vessels of the lung in PAH. We therefore measured bFGF and VEGF levels in the blood and urine of a large cohort of these patients. my canadian pharmacy

Study Population
We studied a cohort of 117 patients with PAH (Table 1). The study was approved by the institutional review committee of the participating centers, and the patients gave informed consent. The control population consisted of 60 normal volunteers (median age, 37.5 ± 10.2 years [± SD]; female gender, 62%) from the participating centers without known cardiopulmonary disease or malignancy. Diagnosis of PAH was established by World Health Organization (WHO) criteria. Other causes of pulmonary hypertension were confirmed using patient histories, serologic testing, abdominal ultrasonographic findings, pulmonary function testing, lung/perfusion scintigraphy, echocardiography, chest CT, and cardiac catheterization, as appropriate. Covariates of interest including age, gender, etiology, WHO functional class, current medication, and hemodynamics were collected for each patient. Exclusion criteria included the following: age < 8 years old, pregnancy, neoplasia, pulmonary venous hypertension, pulmonary hypertension associated with disorders of the respiratory system and/or hypoxemia, and pulmonary hypertension due to chronic thromboembolic disease. Our procedures were in accordance with institutional guidelines for human subjects research.
Table 1—Patient Characteristics (n = 117)

Etiology PPH

(n = 67)

CHD

(n = 34)

CTD (n = 16)
Female gender 88 74 88
Age, yrf 44 (10-74) 33 (12-56) 52(31-75)
Pulmonary vascular resistance,

Wood units/m2

12(3-37) 20 (5.2-31.6) 7 (2.2-21)
Cardiac output, L/min 4.5 (1.7-7.4) 4 (1.8-7.7) 4.8 (1.8-9.2)
Mean PAP, mm Hgf 53(23-89) 71 (34-102) 54 (32-71)
Mean right atrial pressure, mm Hg 8(1-25) 8 (4-19) 11 (1-18)
WHO class 3 (1 -4) 2 (2-4) 3 (2-4)
Warfarin 59.4 66.7 55.5
Calcium-channel blockerf 31.0 18.2 41.7
Prostacyclin f 65.2 25.8 71.4
This entry was posted in Hypertension and tagged angiogenesis, growth substances, pulmonary heart disease.