Search

Plasma levels and 24-hour urine excretion of fibrinopeptide A were measured in a consecutive series of 179 patients with angina pectoris. Sixty-four patients had stable angina and 115 patients had unstable angina. Urine was collected over 24 hours the day before coronary arteriography, and blood samples were taken at the end of urine collection. When the values of fibrinopeptide A in plasma and in the 24-hour urine specimens were compared, no significant correlation was found in patients with either stable (rs = 0.16, difference not significant) and unstable (rs = 0.07, difference not significant) angina. The concentrations of fibrinopeptide A in the plasma did not differ significantly when patients with stable angina (range 0.1 to 82.6, median 7.4 ng/mL) were compared with patients with unstable angina (range 0.2 to 61.7, median 14 ng/mL, p = 0.055), whereas fibrinopeptide A 24-hour urinary excretion was significantly higher in patients with unstable angina (range 0.3 to 38.1, median 11.8 micrograms/24 hr) than in patients with stable angina (range 0.4 to 38.1, median 3.8 micrograms/24 hr, p less than 0.001). Twenty-four-hour urine excretion of fibrinopeptide A in patients with unstable angina and angiographically documented intracoronary thrombi were higher than the corresponding values in patients with unstable angina without such angiographic characteristic (p less than 0.001). The largest increase in plasma and urine concentration of fibrinopeptide A was observed in patients whose first episode of angina at rest occurred within the previous 48 hours. We conclude that the cumulative thrombin activity, assessed by 24-hour urinary excretion of fibrinopeptide A, is a more useful index, compared with single fibrinopeptide A measurement in plasma, for discriminating between patients with stable and with unstable angina pectoris.

To assess the prevalence of abnormal coronary vasoconstriction in stable exertional angina and to evaluate whether the presence of increased coronary tone may have therapeutic implications, we studied 83 consecutive patients with typical exertional angina, positive response to exercise stress testing and documented coronary artery disease. Abnormal coronary vasoconstriction was induced by a hyperventilation test in 16 patients (group I) while the remaining 67 had a negative response (group II). No differences were observed between the 2 groups with regard to clinical, exercise and angiographic data. All group I patients and 16 patients in group II repeated hyperventilation and exercise tests after the administration of dihydropyridine-type calcium antagonists (7 patients nifedipine, 9 patients felodipine). After treatment 15 of 16 group I patients had a negative response to the hyperventilation test. The total exercise duration was significantly increased (278 +/- 183 vs 554 +/- 248 seconds; p less than 0.001) with higher values of rate pressure product at peak exercise (168 +/- 47 vs 235 +/- 67 mm Hg x beats/min/100; p less than 0.0025). In group II no significant differences were observed between pre- and posttreatment values for total exercise duration (244 +/- 210 vs 308 +/- 243 seconds) and rate pressure product at peak exercise (170 +/- 46 vs 188 +/- 56 mm Hg x beats/min/100). These data show that the hyperventilation test can be used to select a subset of patients with stable exertional angina and detectable abnormal coronary vasoconstriction who will improve their exercise tolerance with coronary vasodilator treatment.