Coronary slow flow phenomenon: a local or systemic disease?

Coronary slow flow phenomenon (CSFP) is an important, angiographic entity characterized by delayed progression of the contrast medium injected into the coronary tree. Since definition of this phenomenon in 1972, there has not been any clear-cut etiology. Original data often focused on histological or pathological changes in coronary artery itself. It was confirmed that small vessel structural defect as well as an underlying residual microvascular resistance abnormality coexists in the coronary microcirculation. Early atherosclerosis was also detected in epicardial coronary arteries by intravascular ultrasound (IVUS). Taken together, it can be suggested that a combination of morphological and functional abnormalities in small vessels and epicardial coronary arteries contributes to the pathogenesis of CSFP. CSFP may be defined as a local disease confined to coronary arteries. However, another feature of CSFP is its frequent occurrence in association with more widespread vascular abnormalities. Reduced endothelial function is implicated in CSFP as measured by flow-mediated dilatation (FMD) of the brachial artery, suggesting that endothelial dysfunction appears to be a generalized process affecting both coronary and peripheral vasculature. In addition, several studies have now demonstrated that carotid intima-media thickness (IMT) is significantly increased in patients with CSFP and there was a significant correlation between coronary intima-media thickness and carotid IMT. Therefore, we hypothesize that CSFP is not an isolated finding but may be part of a systemic vascular disturbance. CSFP is not an infrequently detected finding typically observed in patients presenting with an acute coronary syndrome, usually unstable angina. The subsequent clinical course is characterized by high frequency of relapsing chest pain resulting in considerable impairment in quality of life. Accordingly, further experimental investigations and clinical studies are warranted to shed light into the pathogenesis as well as therapeutics of CSFP.