“…Although the pathophysiological mechanism of SCF has not been determined consistently, several potential hypotheses have been suggested, such as an earlier form of atherosclerosis, platelet aggregability, the organic or functional dysfunction of small coronary arteries, and an imbalance between vasoconstricting and vasodilating factors [18,19]. Inflammation has been reported to be a major contributing factor in many cardiovascular events and is associated with different clinical settings of CAD, which may be involved in the development of SCF.…”