BACKGROUND: Basic fibroblast growth factor (bFGF) is a mitogenic polypeptide that demonstrates enhanced expression and promotes angiogenesis in animal models of myocardial ischemia and infarction. Elevated levels of bFGF are present in the urine of humans with metastatic tumors, but its expression in human myocardial ischemia is unknown. Thus, we sought to determine whether urine levels of bFGF are altered by exercise-induced ischemia in humans. METHODS AND RESULTS: Eighty-six patients underwent exercise thallium studies for evaluation of anginal symptoms. Urine levels of bFGF (corrected for urine creatinine) were determined by ELISA immediately before and between 2 and 4 hours after exercise. The change in urine bFGF level was compared between 43 patients with and 43 patients without exercise-induced ischemia. Patients with ischemia had an increase in urine bFGF compared with nonischemic patients (1052 +/- 245 versus -278 +/- 130 pg/g creatinine, P < .0001). Exercise, demographic, and clinical variables were assessed and analyzed for possible effect on bFGF response to exercise. By univariate analysis, a history of hypertension was negatively associated with a change in bFGF level (P < .05). No other variables were associated. By multivariate analysis, only bFGF response (P < .001) and age (P < .05) were independently related to exercise-induced ischemia. CONCLUSIONS: Significantly increased levels of bFGF are detected in the urine within hours of exercise-induced ischemia. Further studies are warranted to determine whether bFGF might serve as a useful circulating marker of myocardial ischemia in humans.
BACKGROUND:Basic fibroblast growth factor (bFGF) is a mitogenic polypeptide that demonstrates enhanced expression and promotes angiogenesis in animal models of myocardial ischemia and infarction. Elevated levels of bFGF are present in the urine of humans with metastatic tumors, but its expression in humanmyocardial ischemia is unknown. Thus, we sought to determine whether urine levels of bFGF are altered by exercise-induced ischemia in humans. METHODS AND RESULTS: Eighty-six patients underwent exercise thallium studies for evaluation of anginal symptoms. Urine levels of bFGF (corrected for urine creatinine) were determined by ELISA immediately before and between 2 and 4 hours after exercise. The change in urine bFGF level was compared between 43 patients with and 43 patients without exercise-induced ischemia. Patients with ischemia had an increase in urine bFGF compared with nonischemic patients (1052 +/- 245 versus -278 +/- 130 pg/g creatinine, P < .0001). Exercise, demographic, and clinical variables were assessed and analyzed for possible effect on bFGF response to exercise. By univariate analysis, a history of hypertension was negatively associated with a change in bFGF level (P < .05). No other variables were associated. By multivariate analysis, only bFGF response (P < .001) and age (P < .05) were independently related to exercise-induced ischemia. CONCLUSIONS: Significantly increased levels of bFGF are detected in the urine within hours of exercise-induced ischemia. Further studies are warranted to determine whether bFGF might serve as a useful circulating marker of myocardial ischemia in humans.