Since its discovery by Tambe et al in 1972, exact mechanism or pathogenesis of delayed distal opacification of angiographically normal coronary artery or slow coronary flow phenomenon is still unknown. Although its long term prognosis is good, it can even lead to sudden cardiac death and can occur up to 25% incidence. It was thought to be due to small vessel disease, endothelial dysfunction, inflammation, hyperviscosity, hemoconcentration, increased Plaque & Platelet activity, systolic & diastolic dysfunction, anatomic factors or diffuse atherosclerosis until now. We like to report the results of our recent randomized controlled trial about finding the most influential mechanism(s) of this phenomenon. From October 2012 to April 2013, this approved and consented randomized trial was conducted at our cath labs of First Affiliated Hospital of Zhengzhou University by analyzing the theories mentioned before in one randomized controlled retrospective study. Among the approximately 2000 patients who had consecutively done coronary angiogram, 100 patients (81 male, 19 female; mean age 57 ± 10 years) were randomized and enrolled as SCF group from 212 patientswith slow coronary flowwithout significant lesion and another 100 patients (45male, 55 female;mean age 58 ±10 years) with neither slow coronary flow nor significant lesion were also randomized and enrolled as Control group. Patients with previous MI/PCI, renal dysfunction, connective tissue disease, obstructive coronary artery disease, coronary vasospasm, coronary ectasia or aneurysm were excluded. Slow coronary flow was diagnosed by standard TIMI Frame Counts and confirmed by other two cardiologists. Tortuosity status, patient demographic parameters and investigations (UA, RDW, MPV, Platelet Count, Fibrinogen, Gamma GT, Hb, HCT, Calculated Osmolarity, Lipid Profile, BNP, Troponin, CKMB, EF, LVEDD, EDV) were retrospectively recorded and compared within two groups. Calculated Osmolarity was calculated by the equation: Osmolarity = 2Na + Glucose + BUN. Tortuosity was defined whenever there was less than 125 degree angled three or more turns in slow coronary flow affected artery or two or more normal coronary arteries. Patient gender, HDL, hemoglobin, hematocrit and Uric Acid had strongest strength of correlation (all p = 0.000 and r N 0.31)with SCF group [Table 1]. But, only Uric Acid (p = 0.000, CI = 2.266–13.242), Tortuosity (p = 0.000, CI = 2.373–14.655), End Diastolic Volume (p = 0.041, CI = 1.061–15.231) and Calculated Osmolarity (p = 0.003, CI = 0.131–0.658) were left as independent determinant factors for slow coronary flow after multivariable logistic regression [Table 1]. After ROC curve analysis Uric Acid got the highest area under curve (AUC = 0.720) with the best cut off point of 286 μmol/L (Sensitivity = 69%, Specificity = 69%) [Fig. 1A, C] followed by Tortuosity, End Diastolic Volume and Calculated Osmolarity [Fig. 1B]. Whenwe analyzed our data, only Uric Acid and Tortuosity were the top determinant factors. Among them, confidence interval of Uric Acid was much less than that of Tortuosity although odds ratio of Uric Acid and Tortuosity were very similar [Table 1]. Moreover, Uric Acid had stronger strength of correlationwith slowcoronary flow thanTortuosity [Table 1]. Furthermore, after ROC curve analysis, Uric Acid got the highest area under curve [Fig. 1A]. Therefore we concluded that Uric Acid was the most determinant factor for slow coronary flow phenomenon in our study. Uric Acid (UA) is the inevitable by-product of cellular degradation which is converted from xanthine by xanthine oxidase (XO). It plays a role in inflammation. It is detectable in almost all inflammatory diseases. Moreover, the higher the Uric Acid, the more other inflammatory markers are increased. Serum UA is associated positively with IL-6, CRP and TNF-α and negatively with IL-1β, particularly in women [1]. It also plays a role in endothelial dysfunction although there are still controversies [2,3]. Uric Acid lowering drug, a xanthine oxidase inhibitor, allopurinol can improve endothelial dysfunction. We can also hypothesize that Uric Acid induces endothelial dysfunction because there is an inverse circadian relationship between serum UA levels and NO in healthy persons [4]. It should be noted that hyperuricemia itself is not a risk factor but a risk marker for presence of risk for the development of severe clinical complications. Most damages found with hyperuricemia are not directly caused byUA but by superoxide free radical produced by the enzyme XO [5]. Integrating above discussion with our results, we found that inflammation and endothelial dysfunction may be the most influential mechanism of slow coronary flow phenomenon according to our study. Although we didn't have a chance to record hsCRP, hCYand IL6 because of lack of consent, this study is the first study analyzing all the previously reported theories to find the most influential mechanism of slow coronary flow phenomenon in our knowledge. With better understanding about etiopathogenesis of slow coronary flow phenomenon, patients will be beneficial with newer therapies and implications.