Lack of evidence for alpha-adrenergic receptor-mediated mechanisms in the genesis of ischemia in syndrome X.

Patients with syndrome X (typical angina pectoris, positive exercise tests [greater than or equal to 1 mm of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) have a reduced coronary flow reserve due to inappropriate dilatation of small resistive vessels. To assess whether alpha-adrenergic mechanisms play a role in the genesis of ST-ischemic changes in syndrome X, 12 patients with this syndrome (2 men and 10 women, mean age 50 +/- 6 years) underwent exercise testing and 24-hour ambulatory electrocardiographic monitoring. They were done off treatment and after alpha blockade with prazosin and clonidine on 2 separate weeks. Despite treatment, all exercise tests remained positive and patients were stopped because of progressive angina pain. Compared to the off-treatment tests, exercise duration and heart rate-blood pressure product at 1 mm of ST-segment depression did not change significantly after prazosin (617 +/- 203 vs 663 +/- 203 seconds and 23,857 +/- 6,125 vs 22,098 +/- 4,816 beats/min X mm Hg, respectively) and clonidine (684 +/- 148 vs 649 +/- 80 seconds and 25,514 +/- 2,386 vs 24,567 +/- 2,001 beats/min X mm Hg, respectively). Ambulatory monitoring showed similar results regarding number of episodes of ST-segment depression greater than or equal to 0.1 mV during control and after prazosin (39 vs 38) or clonidine (26 vs 23) treatment. None of the 8 patients who also underwent provocative testing with phenylephrine had ischemic electrocardiographic changes; only 2 experienced chest pain during the test.(ABSTRACT TRUNCATED AT 250 WORDS)