The results suggest that aging selectively impairs endothelium-dependent coronary microvascular function and that this impairment can be restored by administration of L-arginine, a precursor of nitric oxide.

These findings demonstrate that both endothelium-dependent and endothelium-independent dilatation of the coronary microvasculature is impaired in syndrome X.

No abstract

Transcutaneous electrical nerve stimulation can increase resting coronary blood flow velocity. The findings suggest that the site of action is at the microcirculatory level and that the effects may be mediated by neural mechanisms.

Esophageal acid stimulation can cause animal attacks and significantly reduce coronary blood flow in patients with coronary artery disease. The lack of any significant effect in heart transplant recipients with heart denervation suggests a neural reflex.

Objectives-To assess the effect of hyperventilation and mental stress on coronary blood flow and symptom production in patients with syndrome X. Design-A prospective study. Hyperventilation and mental stress tests were performed on the ward and were repeated in the cardiac catheter laboratory where coronary blood flow velocity was also measured with an intracoronary Doppler catheter in the left anterior descending coronary artery. Oesophageal manometry studies were also performed. Patients-29 patients with syndrome X

The results of our study suggest that abnormal cardiac pain perception is a fundamental abnormality in syndrome X.

Patients with syndrome X who present with unstable angina have a significantly better functional prognosis than those presenting with symptoms of stable angina. This may reflect differences in underlying pathophysiological mechanisms.