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      Anatolian Journal of Cardiology
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          Abstract

          To the Editor, We thank the authors for their valuable evaluation of our article entitled “Relationship between the presence of left atrial thrombus in patients with mitral stenosis and platelet-to-lymphocyte ratio” published in Anatol J Cardiol 2016; 16: 673-7 (1). The aim of our study was to examine the relationship between the presence of left atrial (LA) thrombus and platelet-to-lymphocyte ratio (PLR), a marker of inflammatory process, in patients with rheumatic mitral valve stenosis (RMVS). This prospective cross-sectional study included patients with a mitral valve area less than 2 cm2. Patients were divided into two groups: those with and without LA thrombus. Because of the pathophysiological properties of the disease, it is normal for variables, such as atrial fibrillation (AF), mitral valve area, mean gradient, and left atrial volume, to be different between the groups. The relationship between AF and LA thrombus formation is also strong in patients with RMVS. It is known that rheumatic heart diseases are autoimmune inflammatory pathologies and that inflammation subclinically continues (2, 3). One of the primary aims of the study was to examine the relationship between thrombus formation and PLR, which is a marker of inflammatory activity. While the presence of AF was associated with LA thrombus formation, this was independent of PLR levels. While its role of inflammation in the pathophysiology of AF is known, the presence of paroxysmal AF, ambulatory ECG recordings, or time of AF were not recorded as they were not the primary aim of the study. Even though the relationship between inflammation and thrombus formation does not mean that there should be a relationship between PLR and AF, the presence of a link between AF and PLR may have been affected by the lack of these prelated parameters. At the same time, regression analysis results demonstrated that the relationship between PLR levels and AF continued to be independent of variables, such as AF, mitral valve area, mean gradient, and left atrial volume.

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          Increased levels of high sensitive C-reactive protein in patients with chronic rheumatic valve disease: evidence of ongoing inflammation.

          The precise pathogenetic mechanism(s) of rheumatic fever and rheumatic heart disease have never been defined. C-reactive protein (CRP) is increased in patients with acute rheumatic fever, but it is not known whether plasma levels increase in patients with chronic rheumatic valve disease. The aim of this study was to determine the role of inflammation detected by high sensitivity CRP (hs-CRP) levels in the progression of chronic rheumatic valve disease. A total of 113 patients with chronic rheumatic valve disease (81 women, 32 men; mean age 40+/-14 years, range 13-70), 51 patients with prosthetic valve(s) (31 women, 20 men; mean age 48+/-13 years, range 21-71) and 102 healthy subjects (68 women, 34 men, mean age 41+/-12 years, range 25-73), as a control group, were assessed. Patients with acute rheumatic fever, acute infection, inflammatory disease, malignancy, acute myocardial infarction and trauma were excluded. hs-CRP was determined using latex-enhanced immunonephelometric assays on a BN II analyzer (Behring). Transthoracic echocardiography was performed in all patients in order to evaluate valvular disease. Levels of hs-CRP were significantly higher in patients with chronic rheumatic heart disease than in patients with prosthetic valve(s) and healthy subjects (0.62+/-0.64 vs. 0.35+/-0.41 vs. 0.24+/-0.18 mg/l, P<0.01 and P<0.001 respectively). No correlation was observed between CRP and age, sex or functional capacity. We found that hs-CRP is increased in chronic rheumatic heart disease; this may indicate that inflammatory response still persists in the chronic phase. Copyright 2002 European Society of Cardiology
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            Further evidence of inflammation in chronic rheumatic valve disease (CRVD): high levels of advanced oxidation protein products (AOPP) and high sensitive C-reactive protein (hs-CRP).

            Chronic rheumatic valve disease (CRVD) is a late sequel of Rheumatic Fever (RF) which appears in approximately 30% of RF patients, leading to valve injury. Advanced Oxidation Protein Products (AOPP) and high sensitive C-Reactive Protein (hs-CRP) plasma levels were measured in patients with CRVD in order to evaluate the presence of oxidative stress and systemic inflammation. A total of 90 patients (70 female, 20 male, mean age 46.01 +/- 11.72 years, range 24-69 years) with CRVD, who have or have not undergone valve replacement due to rheumatic etiology, and 46 healthy subjects (27 female, 19 male, mean age 41.89 +/- 9.02 years range 28-60 years) were studied. Levels of AOPP were measured by the determination of optical density (OD) at 340 nm under acidic conditions and hs-CRP by enhanced immunonephelometric assays. Significantly elevated levels of AOPP and hs-CRP were observed in CRVD patients when compared to the controls (AOPP 212.62 +/- 34.14 umol/l vs. 126.97 +/- 27.74 umol/l p < 0.00006 and for hs-CRP 5.40 +/- 1.98 mg/l vs. 2.66 +/- 1.36 mg/l p < 0.05). In addition, high levels of AOPP were associated to the presence of prosthetic valve and time after surgery (p < 0.0008 and p < 0.005, respectively). No correlation was observed between the levels of AOPP and hs-CRP with age, sex and degree of mitral valve stenosis. No correlation was found between AOPP and hs-CRP plasma values. These results suggest the involvement of oxidative stress and systemic inflammation in the pathogenesis of CRVD.
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              Relationship between the presence of left atrial thrombus in patients with mitral stenosis and platelet-to-lymphocyte ratio

              Objective: Rheumatic carditis-induced mitral valve disease is associated with a chronic inflammatory process. The close relationship between inflammation and prothrombotic processes is known. Our goal was to examine the relationship between the presence of left atrial (LA) thrombus in patients with rheumatic mitral valve stenosis (RMVS) and platelet-to-lymphocyte ratio (PLR), which is an inflammatory marker. Methods: This cross-sectional study included 351 consecutive patients diagnosed with RMVS upon presentation to the cardiology polyclinic. All patients were evaluated using transthoracic and transesophageal echocardiography and were divided into 2 groups: those with and without LA thrombus. In addition to echocardiographic and biochemical parameters, PLR was compared between the groups. Student’s t-test, Mann–Whitney U test, logistic regression analysis, and receiver operating characteristic (ROC) curve analysis were used for statistical analysis. Results: No significant differences in terms of age, gender, body mass index, and comorbidities were found between the groups with and without LA thrombus. In the group with LA thrombus, higher red cell distribution width, mean platelet volume, and platelet count and lower lymphocyte count were detected. In addition, C-reactive protein levels were significantly higher in the LA thrombus group (4.7 vs. 2.7 mg/L, p<0.001). PLR was significantly higher in patients with thrombus than in those without (133±38 vs. 119±31, p=0.001). Higher PLR was identified as independently associated with the presence of LA thrombus (odds ratio: 1.03, 95% confidence interval: 1–1.06, p=0.016). Conclusion: Higher PLR was detected in the LA thrombus group of patients with RMVS.
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                Author and article information

                Journal
                Anatol J Cardiol
                Anatol J Cardiol
                Anatolian Journal of Cardiology
                Kare Publishing (Turkey )
                2149-2263
                2149-2271
                December 2016
                : 16
                : 12
                : 993
                Affiliations
                [1]Department of Cardiology, Okmeydanı Training and Research Hospital; İstanbul- Turkey
                Author notes
                Address for Correspondence: Dr. Erdal Belen Okmeydanı Eğitim ve Araştırma Hastanesi Kardiyoloji Bölümü, Darülaceze Cad. No: 25 34384 Okmeydanı, Şişli, İstanbul- Türkiye E-mail: belenerdal@ 123456gmail.com
                Article
                AJC-16-993
                5324926
                28005020
                2d7ba3d4-4d56-4b1f-9e95-a1805e704ab6
                Copyright © 2016 Turkish Society of Cardiology

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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