title: Clinical analysis of the risk factors of slow coronary flow.
abstract: Slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized by the delayed passage of contrast in the absence of obstructive epicardial coronary disease, and is an important clinical entity because it may be the cause of precordial pain when the body is at rest and/or during exercise. Although clinical and pathological features of SCF have been previously described, its etiopathogenesis remains unclear. The present study aims to investigate the risk factors of slow coronary flow, in order to provide the foundation for further exploration of potential mechanisms of SCF. A total of 47 consecutive patients with documented slow coronary flow, and 33 patients with normal coronary flow--as defined by TIMI frame count (TFC)--were recruited for this study. Clinical information was collected, and biochemical indicators including high-sensitivity C-reactive protein (hs-CRP), and a marker of systemic inflammation were detected. Logistic regression analysis was performed for statistical analysis. SCF patients had a higher level of serum uric acid (323.2 ± 79.3 vs. 282.8 ± 82.4 μmol/l, p = 0.03), 2-h postprandial blood glucose (8.6 ± 2.7 vs. 7.5 ± 1.8 mmol/l, p = 0.04), platelet count (165.9 ± 51.6 × 10(3) vs. 127.0 ± 32.0 × 10(3) cells/μl, p = 0.0003) and hs-CRP (3.4 ± 0.8 vs. 2.0 ± 0.9 mg/l, p < 0.0001) than those of patients in the control group. No marked differences in other variables were observed between the two groups. Logistic regression showed serum uric acid level (χ(2) = 3.84, β = 0.007, p = 0.049), 2-h postprandial blood glucose (χ(2) = 5.02, β = 0.277, p = 0.025) and blood platelet count (χ(2) = 12.16, β = 0.026, p = 0.001) were independent predictors of SCF. When hs-CRP was included in the multivariate model, hs-CRP (χ(2) = 21.19, β = 1.90, p < 0.0001) was the only independent predictor of SCF. These findings suggested that an elevation of serum uric acid level, 2-h postprandial blood glucose, and blood platelet count might be the causes of SCF, and inflammation was likely to be implicated in the causal pathway leading to SCF.
authors.affiliation: Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, 74 Lingjiang Road, Chongqing, China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Xia
authors.forename: Song-Bai
authors.initials: SB
authors.lastname: Deng
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Xiao
authors.forename: Jian-Lin
authors.initials: JL
authors.lastname: Du
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xi-Chun
authors.initials: XC
authors.lastname: Wang
authors.forename: Ye-Qing
authors.initials: YQ
authors.lastname: Li
authors.forename: Rui
authors.initials: R
authors.lastname: Zhao
authors.forename: Li
authors.initials: L
authors.lastname: He
authors.forename: Yu-Luan
authors.initials: YL
authors.lastname: Xiang
authors.forename: Qiang
authors.initials: Q
authors.lastname: She
mesh_terms: D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002681:China; D017023:Coronary Angiography; D003326:Coronary Circulation; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D016015:Logistic Models; D008833:Microcirculation; D054318:No-Reflow Phenomenon / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D015588:Observer Variation; D010976:Platelet Count; D019518:Postprandial Period; D011237:Predictive Value of Tests; D015203:Reproducibility of Results; D018570:Risk Assessment; D012307:Risk Factors; D014527:Uric Acid / Q000097:blood
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D018836:Inflammation Mediators; D014527:Uric Acid; D002097:C-Reactive Protein