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      Could neutrophil/lymphocyte ratio be an indicator of coronary artery disease, coronary artery ectasia and coronary slow flow?

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          Abstract

          Objective

          To determine whether neutrophil/lymphocyte ratio (NLR) differed between patients with isolated coronary artery disease (CAD), isolated coronary artery ectasia (CAE), coronary slow flow and normal coronary anatomy.

          Methods

          Patients who underwent coronary angiography were consecutively enrolled into one of four groups: CAD, coronary slow flow, CAE and normal coronary anatomy.

          Results

          The CAD ( n = 40), coronary slow flow ( n = 40), and CAE ( n = 40) groups had similar NLRs (2.51 ± 0.7, 2.40 ± 0.8, 2.6 ± 0.6, respectively) that were significantly higher than patients with normal coronary anatomy ( n = 40; NLR, 1.73 ± 0.7). Receiver operating characteristics demonstrated that with NLR > 2.12, specificity in predicting isolated CAD was 85% and sensitivity was 75%, with NLR > 2.22 specificity in predicting isolated CAE was 86% and sensitivity was 75%. With NLR > 1.92, specificity in predicting coronary slow flow was 89% and sensitivity was 75%. Multivariate logistic regression analyses identified NLR as an independent predictor of isolated CAE (β = −0.499, 95% CI −0.502, −0.178; P <  0.001), CAD (β = −0.426, 95% CI −1.321, −0.408; P <  0.001), and coronary slow flow (β = −0.430, 95% CI −0.811, −0.240; P = 0.001 Table 2).

          Conclusions

          NLR was higher in patients with CAD, coronary slow flow and CAE versus normal coronary anatomy. NLR may be an indicator of CAD, CAE and coronary slow flow.

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          Most cited references40

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          Association between admission neutrophil to lymphocyte ratio and outcomes in patients with acute coronary syndrome.

          The neutrophil/lymphocyte ratio (NLR) has recently been described as a predictor of mortality in patients who undergo percutaneous coronary intervention. The aim of this study was to investigate the utility of admission NLRs in predicting outcomes in patients with acute coronary syndromes (ACS). A total of 2,833 patients admitted to the University of Michigan Health System with diagnoses of ACS from December 1998 to October 2004 were followed. Patients were divided into tertiles according to NLR. The primary end point was all-cause in-hospital and 6-month mortality. The ACS cohort comprised 564 patients with ST-segment elevation myocardial infarctions and 2,269 patients with non-ST-segment elevation ACS. Patients in tertile 3 had higher in-hospital (8.5% vs 1.8%) and 6-month (11.5% vs 2.5%) mortality compared with those in tertile 1 (p <0.001). After adjusting for Global Registry of Acute Coronary Events risk profile, patients in the highest tertile were at an exaggerated risk for in-hospital (odds ratio 2.04, p = 0.013) and 6-month (odds ratio 3.88, p <0.001) mortality. Admission NLR is an independent predictor of in-hospital and 6-month mortality in patients with ACS. This relatively inexpensive marker of inflammation can aid in the risk stratification and prognosis of patients diagnosed with ACS.
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            TIMI frame count: a quantitative method of assessing coronary artery flow.

            Although the Thrombolysis in Myocardial Infarction (TIMI) flow grade is valuable and widely used qualitative measure in angiographic trials, it is limited by its subjective and categorical nature. In normal patients and patients with acute myocardial infarction (MI) (TIMI 4), the number of cineframes needed for dye to reach standardized distal landmarks was counted to objectively assess an index of coronary blood flow as a continuous variable. The TIMI frame-counting method was reproducible (mean absolute difference between two injections, 4.7 +/- 3.9 frames, n=85). In 78 consecutive normal arteries, the left anterior descending coronary artery (LAD) TIMI frame count (36.2 +/- 2.6 frames) was 1.7 times longer than the mean of the right coronary artery (20.4 +/- 3.0) and circumflex counts (22.2 +/- 4.1, P < .001 for either versus LAD). Therefore, the longer LAD frame counts were corrected by dividing by 1.7 to derive the corrected TIMI frame count (CTFC). The mean CTFC in culprit arteries 90 minutes after thrombolytic administration followed a continuous unimodal distribution (there were not subpopulations of slow and fast flow) with a mean value of 39.2 +/- 20.0 frames, which improved to 31.7 +/- 12.9 frames by 18 to 36 hours (P < .001). No correlation existed between improvements in CTFCs and changes in minimum lumen diameter (r=-.05, P=.59). The mean 90-minute CTFC among nonculprit arteries (25.5 +/- 9.8) was significantly higher (flow was slower) compared with arteries with normal flow in the absence of acute MI (21.0 +/- 3.1, P < .001) but improved to that of normal arteries by 1 day after thrombolysis (21.7 +/- 7.1, P=NS). The CTFC is a simple, reproducible, objective and quantitative index of coronary flow that allows standardization of TIMI flow grades and facilitates comparisons of angiographic end points between trials. Disordered resistance vessel function may account in part for reductions in flow in the early hours after thrombolysis.
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              Leukocyte count and coronary heart disease: implications for risk assessment.

              Inflammation is a key feature of atherosclerosis and its clinical manifestations. The leukocyte count is a marker of inflammation that is widely available in clinical practice. This paper reviews the available epidemiologic evidence for a relationship between the leukocyte count and coronary heart disease (CHD). Numerous epidemiologic and clinical studies have shown leukocytosis to be an independent predictor of future cardiovascular events, both in healthy individuals free of CHD at baseline and in patients with stable angina, unstable angina, or a history of myocardial infarction. This relationship has been observed in prospective and retrospective cohort studies, as well as in case-control studies. It is strong, consistent, temporal, dose-dependent, and biologically plausible. The relationship persists after adjustment for multiple CHD risk factors, including smoking. Elevated differential cell counts, including eosinophil, neutrophil, and monocyte counts, also predict the future incidence of CHD. Leukocytosis affects CHD through multiple pathologic mechanisms that mediate inflammation, cause proteolytic and oxidative damage to the endothelial cells, plug the microvasculature, induce hypercoagulability, and promote infarct expansion. In summary, leukocytosis has been consistently shown to be an independent risk factor and prognostic indicator of future cardiovascular outcomes, regardless of disease status. The leukocyte count is inexpensive, reliable, easy to interpret, and ordered routinely in inpatient and outpatient settings. However, its diagnostic and prognostic utility in CHD is widely unappreciated. Further studies are needed to assess the true impact of leukocytosis on CHD, compare it with other inflammatory markers such as C-reactive protein and lipoprotein phospholipase A(2) levels, and promote its use in CHD prediction.
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                Author and article information

                Journal
                J Int Med Res
                J. Int. Med. Res
                IMR
                spimr
                The Journal of International Medical Research
                SAGE Publications (Sage UK: London, England )
                0300-0605
                1473-2300
                7 November 2016
                December 2016
                : 44
                : 6
                : 1443-1453
                Affiliations
                [1 ]Department of Cardiology, Elazığ Training and Research Hospital, Elazığ, Turkey
                [2 ]Department of Cardiology, Fırat University School of Medicine, Elazığ, Turkey
                Author notes
                [*]Mücahid Yılmaz, Department of Cardiology, Elazığ Training and Research Hospital, Elazığ, Turkey. Email: mucahid.yilmaz@ 123456mynet.com
                Article
                10.1177_0300060516664637
                10.1177/0300060516664637
                5536743
                28322100
                fc280a41-871f-47f3-ad73-924f7f4e3793
                © The Author(s) 2016

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License ( http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 29 March 2016
                : 26 July 2016
                Categories
                Clinical Reports

                coronary artery disease,coronary artery ectasia,coronary slow flow,neutrophil/lymphocyte ratio

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