LAUSR

Introduction: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in chronic kidney disease (CKD) patients and it has been shown that its level declines as eGFR decreases. Most studies have found that the decreased level of TWEAK was seen in atherosclerosis and was also associated with calcification of the plaque. This prospective study was designed to clarify any relationship between coronary slow flow (CSF) and TWEAK levels. Hypothesis: Our hypothesis was to show that the higher level of TWEAK might be seen in the setting of CSF due to lack of calcium deposits and TWEAK is not a reflection of healthy vessels. Methods: This prospective study included 93 consecutive patients undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020 (Table 1). A total of 93 patients were divided into two groups with regard to having CSF (n=35) or no-CSF (n=58). Results: Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, the TWEAK level was increased statistically significant (r:0.635/ p<0.001). The TWEAK level of 516 pg/mL was found for the prediction of CSF in ROC analysis. Conclusions: Our study has shown that plasma TWEAK level is an independent predictor for the CSF in patients with CKD (Table 2). Our study have found that elevated TWEAK levels may not reflect the healthy vessels as it was hypothesized in the past.