Background Slow coronary flow(SCF) was first discovered and reported by Tambe, according to Mohammad’s latest data, about 6.6% population had SCF in patients underwent coronary artery angiography. The patients with SCF can have cheat discomfort without definite cause, stable angina pectoris, acute coronary syndrome, malignant arrhythmia or sudden death and so on. With the increased incidence and diversity clinical manifestation of SCF, it was becoming more and more attention. In spite of numerous study about SCF, its physiopathologic mechanism was not specific. So far, the treatment of SCF had no definite guideline recommendation, only to give the corresponding treatment according to clinical symptoms. Integrating the present study the possible physiopathologic mechanism of SCF was impaired endothelial function, microvascular dysfunction, inflammation and the early stage of atherosclerosis. The impaired endothelial cells lead to the disorganized secretion of vasoactive substance and microvascular dysfunction, meanwhile it was also the key step of arteriosclerosis. Because microvascular is a major source of blood flow resistance, therefore, microvascular lesions can lead to the increased blood flow resistance and the congestion state of great vessels. This would result in the aggregation and rouleaux formation of blood cells. The increased blood viscosity onone hand furthered the blood flow resistance, on the other hand induced leukocyte to adhere to vascular wall, which result in the inflammation and injury of endothelial cells. The inflammatory response can first lead to the imbalance of endothelial injury and repair mechanisms, then result in the pathological changes such as intimal thickening and smooth muscle proliferation, which occurred in the remodeling of vascular and the increased blood flow resistance. So the factors of SCF were interactive rather than single. Peripheral blood cells were composed of white blood cells, red blood cells and platelets. White blood cells were the major participants in the process of inflammatory reaction, they can release various of inflammatory cytokine to accelerate this process. The immune adherence function of red blood cells can cause adhesion among red blood cells or between red blood cells and platelets, which then lead to increased microvascular emb-olization, blood flow resistance. In addition to coagulation and hemostasis, platelets can also protect the vascular endothelium, involve in endothelial repair and prevent atheros-clerosis, but the excessive activation of platelets can induce thrombosis, causing vascular embolization. Based on the function of peripheral blood cells and combined with the current relevant research, we speculated that some components of peripheral blood cells might involve in the pathophysiological process of SCF in a certain extent. Therefore, by comparing the indexes of peripheral blood cells between the normal group and SCF group, we want to clarify the relation between the indexes of peripheral blood cells and slow coronary flow, in order to provide basis for clinical diagnosis.Objective To investigate the correlation between the indexes of peripheral blood cells and slow coronary flowMethods We studied 195 patients with angiographically no more than one stenosis < 40% in each major coronary artery who had admitted to the department of cardiology ofthe First Affiliated Hospital of Zhengzhou university, including 99 cases(male 52, female 47) of SCF group, 96 cases(male 45, female 51) of normal blood group(NCF). SCF was defined as the image acquisition speed of 30 frame/s, contrast agent through at least one coronary artery frame number > 27 frame. Recording the basic clinical data of patients, then extracting fasting elbow venous blood to measure the blood routine, blood lipid, blood glucose, uric acid, urea and creatinine the hospital the next day morning and calculating the neutrophil to lymphocyte ratio(NLR). Using SPSS17.0 statistical software for statistical analysis of the data of the two groups.Results 1. There was no statistical difference compared to the baseline data of the two groups(P > 0.05); 2. The white blood cell count, neutrophil count, red cell distribution width(RDW), high sensitive C-reactive protein(hs-CRP), mean platelet volume(MPV), uric acid(UA) and NLR of SCF group were significantly higher than those in NCF group(6.76±1.31 vs. 6.32±1.39,P = 0.024;4.24±1.12 vs. 3.79±1.16,P = 0.007;13.47±1.93 vs. 12.88±1.90,P = 0.034;2.20±0.69 vs. 2.01±0.61,P = 0.041;9.04±1.11 vs. 8.55±1.42,P = 0.008;287.55±67.46 vs. 262.26±80.46,P = 0.018;2.45±0.80 vs. 2.06±0.70,P < 0.001),the difference was statistically significant(P < 0.05); 3. Pearson correlation analysis showed that NLR was positively correlated with hs-CRP, r = 0.871, P < 0.001; 4. Binary logistic regression analysis showed that the increased NLR(OR = 1.885,95% CI:1.254-2.835,P = 0.002) and MPV(OR = 1.381,95% CI:1.085-1.757,P = 0.009) may be independent risk factors of SCF; 5. ROC curve showed that the NLR(AUC = 0.635, sensitivity 59.6%, specificity 61.5%) and MPV(AUC = 0.612, sensitivity 80.8%, specificity 46.9%) had great value in predicting the occurrence of SCF.Conclusion 1.White blood cells, neutrophils, hs-CRP and UA were involved in the pathophysiology of SCF; 2.NLR was positively correlated with the serum level of hs-CRP, which may be used as a marker of inflammation, NLR and increased hs-CRP may indicate that SCF was an inflammatory condition; 3.NLR and MPV might be the independent risk factors of SCF, which could be used as important indexes for clinical noninvasive prediction SCF. |