Elevated circulating inflammatory markers in female patients with cardiac syndrome X.

Background: The pathophysiological mechanism in cardiac syndrome X has been suggested as impairment in normal endothelial function of the coronary microvasculature, resulting in inadequate flow reserve. However, despite the extensive studies, the precise mechanisms in cardiac syndrome X remain unclear.

Purpose: The present study was, therefore, to investigate whether inflammatory cells and markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) might be involved in the pathogenesis of cardiac syndrome X.

Coronary restenotic reduction of drug-eluting stenting may be due to its anti-inflammatory effects.

The development of coronary stent has revolutionized the field of interventional cardiology by reducing the incidence of restenosis after balloon angioplasty. However, the stent has still associated with a serious complication, namely, in-stent restenosis. Although, restenosis following coronary stenting has long been attributed to neointimal proliferation, thrombosis, and negative remodeling, the inflammation may be a trigger for those vascular reactions following coronary stenting.