Cardiological syndrome X. Non-invasive assessment of endothelial function and arterial compliance

Mechanisms responsible for cardiological syndrome X are complex and not well understood. It has been postulated that impaired endothelial function and abnormal reactivity of coronary vessels may play a role in the pathogenesis of this condition.

To assess mechanical properties of peripheral arterial vessels and both endothelium-dependent and endothelium-independent vessel reactivity in patients with or without atherosclerotic lesions in coronary arteries.

The study group consisted of 100 patients with typical angina and positive exercise test who underwent coronary angiography. Based on angiographic results, the patients were divided into two groups: 50 patients with normal coronary angiograms and 50 age- and gender-matched patients with at least one significant coronary artery lesion (coronary artery disease (CAD) group). The control group consisted of 40 healthy volunteers without risk factors of atherosclerosis. The compliance of arterial vessels was assessed by automatic measurement of pulse wave velocity (PWV). Endothelial function was examined by ultrasonographic measurement of the diameter of brachial artery following passive hyperaemia (endothelium-dependent vessel distension) and following nitroglycerine (endothelium-independent mechanism).

Among all three studied groups, the PWV values were the highest in patients with CAD. Patients with syndrome X had significantly higher PWV than in controls. A cut-off PWV value of 10.5 m/s distinguished patients with syndrome X from those with CAD. Endothelium-dependent arterial distensibility was significantly lower in patients with syndrome X than in controls; the lowest values were observed in patients with CAD. Among patients with syndrome X, the endothelium-dependent arterial vessel distensibility was the only parameter significantly influencing PWV results.

PWV was significantly increased in patients with syndrome X which suggests a decreased arterial vessel compliance. These results and the impairment of endothelium-dependent relaxation suggest a similar pathomechanism of altered arterial reactivity in patients with syndrome X and in patients with CAD.