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Research Article - Volume 2 - Issue 3

Diagnostic value of the Neutrophil-to-Lymphocyte Ratio (NLR) In Predicting Mortality of Heart Failure

Marjan Hajahmadi1; Mohammad Sadegh Rajabian2* ; Soroush Rad3; Sima Zahedi4; Amirali Kamyab Rajabi5

1Cardiologist, Fellowship in Heart failure and cardiac transplantation, Cardiovascular department ,Rasoul Akram General Hospital,Iran University of medical science, Tehran, Iran.
2Resident of General Surgery, Shiraz University of Medical Science, Shiraz, Iran.
3Hematologist and Medical Oncologist, Tehran University of Medical Sciences, Hematology-Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Iran.
4Medical Doctor, Department of Medicine, Arak University of Medical Sciences, Iran.
5Islamic Azad University, Tehran Medical Branch, Tehran, Iran.

Received Date : Apr 12, 2022
Accepted Date : May 25, 2022
Published Date: Jun 09, 2022
Copyright:© Mohammad Sadegh Rajabian 2022

*Corresponding Author : Mohammad Sadegh Rajabian, Resident of General Surgery, Shiraz University of Medical Science, Shiraz, Iran.
Email: m.s.rajabian@live.com
DOI: Doi.org/10.55920/2771-019X/1166

Abstract

Introduction: The role of inflammatory processes in exacerbating fibrotic and atherosclerotic processes has been confirmed, such as increased neutrophil count. Some evidence identified the prognostic role of the neutrophil to the lymphocytic ratio (NLR) in predicting adverse outcomes of heart diseases. A review of the literature indicates controversial results about the role of this index in predicting mortality of heart failure (HF). In this comprehensive review, we aimed to evaluate the role of NLR in predicting mortality in patients with HF.

Methods: Initial search identified 67 studies from databases such as PubMed, Web of Knowledge, Google Scholar, SCOPUS, and Iranian databases, including SID and Magiran, and articles in non-English or non-Farsi languages case studies, review articles were excluded. At the final stage, 10 studies remained.

Results: Overall, 5 cases of acute heart failure and 5 cases of chronic heart failure were included. Totally, 5979 patients (3462 acute, and 2517 chronic) were studied. The mean follow-up time was 18 months (11.3 to 26 months). The mortality rate in patients with acute heart failure was 23.8% (22.4% to 25.2%), and in patients with chronic heart failure was 27.1% (24.9% to 29.5%), with a high heterogeneity among studies.

Conclusion: NLR was able to predict mortality among patients with acute and chronic heart failure, with a hazard ratio of 1.61 and 1.44, respectively. The NLR values above 4.4, have relatively good sensitivity and specificity to predict mortality in patients with acute heart failure.

 Keywords: Heart failure; NLR; predictive value; mortality; myocardial infarction.

Introduction

Acute heart failure is a term used to describe the sudden onset or change in the signs and symptoms of heart failure [1]. The prevalence of this syndrome is increasing due to the increased incidence of coronary heart disease, particularly in older people. In addition, acute heart failure has a high mortality and morbidity [2]. Therefore, early and timely diagnosis and identification of patients at high risk is critical. Each year 5,000,000 people in the United States suffer from heart failure, and the prevalence of this disease worldwide is increasing, especially in developed countries [3]. Although the prevalence of heart failure with reduced ejection fraction is decreasing (due to increasing lifespans in developed societies and increased risk factors such as diabetes and hypertension) the proportion of patients with heart failure with maintained or near normal ejection fraction is increasing [4].

Many prognostic factors have been proposed for predicting mortality associated with acute heart failure [4-12]. Most of these factors were related to inflammation. Furthermore, the pathophysiological role of inflammatory factors in the progression of heart failure has been well established [13-15]. The ratio of neutrophil to lymphocyte or NLR in the peripheral circulatory system is one of the factors that is easily measured in the blood. Increased neutrophil counts have been suggested as a primary component in the activity of inflammatory pathways, and lymphopenia is also known to be a predictor of physiological stress. Some evidence has been published that Neutrophil Lymphocyte Ratio (NLR) can predict cardiovascular disease risk [16-23]. However, the relationship between NLR and hospital mortality in patients with acute heart failure is a valuable question. This study aims to analyze and summarize studies on the role of NLR in predicting hospital mortality in patients with acute and chronic heart failure.

The role of neutrophils and lymphocytes in heart failure

Both types of heart failure - with reduced ejection fraction or ejection fraction close to normal- have also been associated with chronic inflammation [24, 25] . In this respect, some evidence suggests that neutrophils play a key role in the pathophysiology of heart failure [26, 27]. Neutrophils are leukocytes at the forefront of the host defense against pathogens and play as an important mediator in inflammatory processes caused by tissue damage [27]. Along with the proven role of neutrophils in counteracting microorganisms, neutrophils also play an essential role in triggering natural or acquired immune responses [26]. The importance of neutrophil involvement in inflammatory processes was obtained by assessing these cells' capacity to release neutrophilic extracellular ducts or NETs and their associated microparticles or MPs [28].

Physiologically, neutrophils play a major role in myocardial injury and are always infiltrated in the injured myocardium [26]. Due to natural and acquired immune responses, neutrophils can affect these responses and affect dendritic cell function and lymphocytes. Recent evidence suggests that neutrophils play a major role in the cardiac repair after myocardial infarction. Suppression of neutrophil function in animal models by inducing acute myocardial infarction has led to decreased cardiac function, the emergence of cardiac fibrosis, and a faster progression to HF [11]. Although the timing of neutrophil infiltration and following cardiac tissue repair after myocardial infarction has been evaluated and determined [29], the functional properties of neutrophils in heart failure remain unclear. Few studies have shown that neutrophils play an essential role in myocarditis [30, 31]. However, their role in the transition from inflammation to heart failure remains unclear. Several etiologies are involved in the incidence and development of myocarditis.

In some cases, for example in the myocarditis, giant cells plays a significant role in the induction of the myocarditis process [31, 32]. In most types of myocarditis, a natural immune response mediated by monocytes and macrophages and neutrophils plays a role in the autoimmune process. These cells can also play a role in promoting both injuries and repairing it [31]. In right ventricular failure due to transient pulmonary hypertension, increased expression of some interleukins, such as IL-1β, IL-6, and IL-10, along with infiltration of both neutrophil and macrophage cell lines, has strongly emphasized the role of myocardial inflammation in heart failure [33]. On the other hand, neutrophils and neutrophil-dependent oxidative stress are also involved in exacerbating the toxic cardiomyopathy process. In animal models, histological and staining evaluations for MPO activity have demonstrated high accumulation of neutrophils in the infarcted and myocardial fibrotic area with decreased myocardial contractility [34]. Both high-risk patients and patients with heart failure have shown an increase in normal immune activity [35]. In some studies, neutrophil counts are significantly associated with severity of heart failure. They have been less related to peripheral vascular disease, cardiac death, abdominal aortic aneurysm, and non-lethal myocardial infarction [35]. Both neutrophil counts and neutrophil phenotype have been related to negative outcomes in patients with reduced EF heart failure [35]. Some reports reported an increase in the total leukocyte count and neutrophil count in expired patients, who had ventricular function abnormalities in heart failure [36]. Recent studies have also shown a significant relationship between increased neutrophil function, increased plasma CRP levels, and severity of heart failure [37, 38]. However, this relationship was only applicable to patients with heart failure with reduced EF.

When looking at inflammatory tissue, neutrophil counts may be far beyond other leukocytes, such as lymphocytes. Inflammation can occur in various time sequences and shapes of typical disorder. As a result, diagnostic biomarkers, clinical, pathological, and radiological, should be considered in a systematic way [39]. Given that increased neutrophil counts are an important factor in predicting the outcome of heart failure [40, 41], the ratio of neutrophils to lymphocytes is another factor in evaluating inflammation severity in patients with heart failure. Recent comprehensive data-based observations involving patients with heart failure, have shown that the neutrophil-to-lymphocyte ratio or NLR is associated with outcomes from some disorders, such as chronic kidney disease, major cardiovascular events, and readmissions due to heart failure [41]. This ratio is a prognostic factor in coronary heart disease and a significant predictor of mortality in patients with acute coronary syndrome [42]. This parameter has also been associated with an increased risk of ventricular arrhythmias and mortality in patients undergoing PCI [43]. Similarly, increased NLR was significantly correlated with increased mortality in patients with non-ST elevation MI (NSTEMI) [44]. It was also related to the outcome of the CRT procedure [44]. Finally, both NLR indices and platelet-to-lymphocyte count ratios correlated with mortality in patients undergoing heart transplantation [45].

Neutrophils are activated by hypoxia and a decrease in nitric oxide concentration along with the activity of prothrombotic and proatherogenic profiles [46]. Through the interaction between neutrophils and atherogenic cells such as monocytes, macrophages, and endothelial cells, neutrophils can influence the inflammatory response to atherosclerotic response, by maintaining and promoting proinflammatory and atherosclerotic processes [47].

Other evidence for the role of neutrophils has been related to the polarization of these cells after myocardial infarction. After myocardial injury, proinflammatory atherosclerotic processes will be observable [48]. Increased neutrophils after myocardial infarction lead to polarization of these cells, which coincides with the differentiation of M1 and M2 macrophages [49]. Numerous cytokines released by injured myocardial and endothelial cells in HF can lead to rise in neutrophil counts. Overall, it’s exciting that we can use ancient pathological biomarkers in new diagnostic criteria. For example, a previous markers of inflammation - Mast Cell Density- have link with inflammation Tumor Grade in Carcinoma [50]. Also, expression patterns of DNA repair proteins, such as microsatellite instability (MSI), have recently can be useful to predicting the prognosis of some tumor and inflammation [51]. In a clinical setting, these pathological correlations can be crucial. In patients with respiratory distress, for example, a good correlation was found between end-tidal carbon dioxide and partial arterial carbon dioxide pressure [52].

Routine analysis of blood biomarkers is very useful in evaluating patients with heart failure and determining their risk level. The role of inflammatory and proinflammatory factors has been well established [53-57]. Many of these markers and proteins have been identified as predictors of these patients' adverse risk and inappropriate outcomes. Therefore many of them are considered as therapeutic targeting factors [58]. Some biomarker in tumor and inflammation, in specific ages such as children, can changes the course of treatment [59]. Some of these inflammatory factors contribute to the progression and pathophysiology of heart failure and play a key role in the prognosis of the disease [5].

Project Results and Findings

Characteristics of the evaluated studies: A total of 10 studies about patients with heart failure (whether acute or chronic) were included in the project. According to the study population, 5 cases were about acute heart failure and 5 cases regarded chronic heart failure. Overall, 5979 patients (including 3462 cases with acute form and 2517 patients with chronic disease) were studied. The mean age of patients in acute form was 66.2 years and 69.4 years in chronic form. The mean follow-up time was 11.3 to 26 months, with an average of 18 months.

Figure 1: Pathway of literatures review.

Mortality rate calculation based on studies

According to the meta-analytic analysis, the overall mortality rate for patients with heart failure was estimated to be 22.2% (18.1% to 23.3%) over the 18-month follow-up (Table 2 and Figure 1). Further, the mortality rate among patients with acute heart failure was 23.8% (from 22.4% to 25.2%) (Table 3 and Chart 2) and among patients with chronic heart failure was 27.1% (24.9% to 29.5%) (Table 4 and Chart 3). Overall, studies had high heterogeneity, in assessing both acute mortality rate (82.932% heterogeneity coefficient) and chronic mortality rate (91.02% heterogeneity coefficient). However, publication bias in mortality rate analysis in acute and chronic failure was not significant (Charts 4 and 5).

 

Relationship between NLR Ratio and Mortality due to Heart Failure

The mean NLR ratio in patients with acute heart failure in both groups with and without mortality was 5.9 and 3.5, respectively. According to analysis, NLR was able to predict mortality among patients with acute and chornic heart failure with a hazard ratio of 1.61. Based on the results of three studies of five studies focusing on acute heart failure, NLR values ​​were higher than 4.4 was able to predict 18-month mortality in patients with acute heart failure, with a sensitivity of 67.2% and a specificity of 67.1% (Table 5). Also, the mean NLR ratio in patients with chronic heart failure in both groups with and without mortality was estimated to be 4.7 and 2.3, respectively. Accordingly, NLR was able to predict mortality among patients with chronic heart failure, with a hazard ratio equal to 1.44 (Table 5).

Table 1: Details of the studies.

Table 2 and Chart 1: Total mortality rate in patients with heart failure.

Table 3 and Chart 2: Total mortality rate in patients with acute heart failure.

Table 4 and Chart 3: Total mortality rate in patients with acute heart failure.

Figure 4: Publication bias in determining the mortality rate due to acute heart failure.

Figure 5: Publication bias in the determination of mortality rate due to acute heart failure.

Table 5: Details of the relationship between NLR and mortality rate.

Discussion

The role of inflammatory processes in exacerbating fibrotic and atherosclerotic processes in various studies has been confirmed. Increased neutrophil count as one of the immune and inflammatory systems mediators has also been emphasized. Some evidence has emphasized the prognostic role of the NLR ratio in predicting adverse outcomes in heart disease, including acute coronary syndrome and heart failure. However, a review of the literature indicates contradictory results regarding the role of this index in predicting medium- and long-term mortality.

In the 2017 study by Huang et al., 1923 patients with acute heart failure were investigated. The age of individuals in the study was 76 years (68% male). Consequently, 875 cases expired during a follow-up of 28.6 months. Through evaluation via regression modeling, NLR had a high value in predicting the mortality of these patients with a risk ratio of 1.166 [60]. In another study by Yu et al., the NLR ratio of 942 patients was divided into two groups: those experiencing heart failure and normal subjects. Patients were followed for 4.26 years. The study found that NLR was able to predict the risk of acute heart failure (risk ratio equal to 1.697). Additionally, NLR with a high-risk ratio of 4.26 was able to predict mortality in patients with heart failure [61].

Tasal et al. (2014), investigated 553 patients with a mean age of 63.4 years (368 men) with heart failure. In this study, the NLR ratio was a mortality predictor with a probability ratio of 1.310. Using the area under the rock curve (AUC = 0.737), this ratio was still a predictor of mortality from heart failure [62]. Also, Uthamalingam et al. (2011) studied 1212 patients with heart failure who were monitored. During the 26-month follow-up period, 284 cases (23.4%) expired. Mortality rates in the three tertiles experienced NLR ratios of 32.8%, 23.2%, and 14.2%, respectively. Multivariate regression analysis showed that the NLR ratio with a risk ratio of 2.23 was able to predict mortality in these patients [63].

In this study, we aimed to evaluate and summarize the analytical results on the role of NLR in predicting mortality in patients with heart failure. Initially, the evaluation focused on two studies based on acute and chronic heart failure. First, our evaluation of mortality from acute and chronic heart failure over an 18-month follow-up showed a mortality rate of 23.8% and 27.1%, respectively. Of course, this mortality depends on many factors, such as duration of follow-up, patients' LVEF status (reduced or compensatory), and inclusion criteria such as the distribution of cardiac risk factors, sex distribution, age, and the acute or chronic manifestations of failure. These factors led to high heterogeneity between studies in the computation of total mortality. However, publication bias was favorably low. Publication bias in medical science journals refers to the publication of more articles that contain positive or statistically significant conclusions. This bias indicates that articles containing statistically negative or nonsignificant results are less likely to print. Based on our analysis, the journals we evaluated did not have such a bias (or tendency) among the editors of the various journals.

As a major finding, our study demonstrated the high role of NLR in predicting mortality in patients with acute and chronic heart failure. While all studies evaluated by our analysis have emphasized the role of the NLR in predicting mortality, the strengths and weaknesses of studies in this regard have varied. First, the NLR in the expired group was significantly higher than in living patients in all studies. Second, the relative mortality risk in patients with acute and chronic heart failure was estimated to be 1.6 and 1.4, respectively. In this regard, only three studies determined the best cutoff point for NLR to predict mortality (including in patients with acute heart failure). In summary, it was evident that NLR values above 4.4 with relatively good sensitivity and specificity were able to predict mortality in patients with acute heart failure. However, there have been no studies of the predictive value of NLR in predicting mortality in patients with chronic heart failure, and such studies based on analysis of the area under the ROC curve are essential.

Notably, the markers studied in the study, including neutrophils, lymphocytes, and even platelets, are affected by underlying conditions such as inflammation or infection. Evaluation of the relationship between markers and outcome of heart disease should be done with these confounding factors or exclusion of the patients under study, which was not mentioned in any of the studies studied, so this should be addressed in future studies.

Conclusion

Overall, the incidence of mortality from acute and chronic heart failure during the 18-month follow-up was estimated to be 23.8% and 27.1%, respectively, with high heterogeneity among studies. The NLR values above 4.4 with relatively good sensitivity and specificity were able to predict mortality in patients with acute heart failure.

References

  1. Kurmani S, Squire I. Acute Heart Failure: Definition, Classification and Epidemiology. Current heart failure reports. 2017; 14(5): 385-92.
  2. Savarese G, Lund LH. Global Public Health Burden of Heart Failure. Cardiac failure review. 2017; 3(1): 7-11.
  3. Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation. 2012; 125(1): e2-e220.
  4. Dhingra A, Garg A, Kaur S, Chopra S, Batra JS, Pandey A, et al. Epidemiology of heart failure with preserved ejection fraction. Current heart failure reports. 2014; 11(4): 354-65.
  5. Paulus WJ, Tschope C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. Journal of the American College of Cardiology. 2013; 62(4): 263-71.
  6. McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Bohm M, Dickstein K, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. European heart journal. 2012; 33(14): 1787-847.
  7. Turfan M, Erdoğan E, Tasal A, Vatankulu MA, Jafarov P, Sönmez O, et al. Neutrophil-to-lymphocyte ratio and in-hospital mortality in patients with acute heart failure. Clinics (Sao Paulo, Brazil). 2014; 69(3): 190-3.
  8. Savic-Radojevic A, Radovanovic S, Pekmezovic T, Pljesa-Ercegovac M, Simic D, Djukic T, et al. The role of serum VCAM-1 and TNF-α as predictors of mortality and morbidity in patients with chronic heart failure. Journal of clinical laboratory analysis. 2013; 27(2): 105-12.
  9. Dzudie A, Kengne AP, Thienemann F, Sliwa K. Predictors of hospitalisations for heart failure and mortality in patients with pulmonary hypertension associated with left heart disease: a systematic review. BMJ open. 2014; 4(7): e004843.
  10. Cooper LB, Mentz RJ, Stevens SR, Felker GM, Lombardi C, Metra M, et al. Hemodynamic Predictors of Heart Failure Morbidity and Mortality: Fluid or Flow? Journal of cardiac failure. 2016; 22(3): 182-9.
  11. Keteyian SJ, Patel M, Kraus WE, Brawner CA, McConnell TR, Piña IL, et al. Variables Measured During Cardiopulmonary Exercise Testing as Predictors of Mortality in Chronic Systolic Heart Failure. Journal of the American College of Cardiology. 2016; 67(7): 780-9.
  12. Baydemir C, Ural D, Karaüzüm K, Balci S, Argan O, Karaüzüm I, et al. Predictors of Long-Term Mortality and Frequent Re-Hospitalization in Patients with Acute Decompensated Heart Failure and Kidney Dysfunction Treated with Renin-Angiotensin System Blockers. Medical science monitor: international medical journal of experimental and clinical research. 2017; 23: 3335-44.
  13. Hermansen SE, Kalstad T, How OJ, Myrmel T. Inflammation and reduced endothelial function in the course of severe acute heart failure. Translational research: the journal of laboratory and clinical medicine. 2011; 157(3): 117-27.
  14. Silvestre-Roig C, Braster Q, Ortega-Gomez A, Soehnlein O. Neutrophils as regulators of cardiovascular inflammation. Nature reviews Cardiology. 2020.
  15. Wrigley BJ, Lip GY, Shantsila E. The role of monocytes and inflammation in the pathophysiology of heart failure. European journal of heart failure. 2011; 13(11): 1161-71.
  16. Akpek M, Kaya MG, Lam YY, Sahin O, Elcik D, Celik T, et al. Relation of neutrophil/lymphocyte ratio to coronary flow to in-hospital major adverse cardiac events in patients with ST-elevated myocardial infarction undergoing primary coronary intervention. The American journal of cardiology. 2012; 110(5): 621-7.
  17. Azab B, Zaher M, Weiserbs KF, Torbey E, Lacossiere K, Gaddam S, et al. Usefulness of neutrophil to lymphocyte ratio in predicting short- and long-term mortality after non-ST-elevation myocardial infarction. The American journal of cardiology. 2010; 106(4): 470-6.
  18. Gibson PH, Cuthbertson BH, Croal BL, Rae D, El-Shafei H, Gibson G, et al. Usefulness of neutrophil/lymphocyte ratio as predictor of new-onset atrial fibrillation after coronary artery bypass grafting. The American journal of cardiology. 2010; 105(2): 186-91.
  19. Dogdu O, Akpek M, Yarlioglues M, Kalay N, Ardic I, Elcik D, et al. Relationship between hematologic parameters and left ventricular systolic dysfunction in stable patients with multi-vessel coronary artery disease. Turk Kardiyoloji Dernegi arsivi: Turk Kardiyoloji Derneginin yayin organidir. 2012; 40(8): 706-13.
  20. Tanriverdi Z, Gungoren F, Tascanov MB, Besli F, Altiparmak IH. Comparing the Diagnostic Value of the C-Reactive Protein to Albumin Ratio With Other Inflammatory Markers in Patients With Stable Angina Pectoris. Angiology. 2019: 3319719897490.
  21. Ye M, Qian X, Guo X, Wang H, Ni Q, Zhao Y, et al. Neutrophil-Lymphocyte Ratio and Platelet-Lymphocyte Ratio Predict Severity and Prognosis of Lower Limb Arteriosclerosis Obliterans. Annals of vascular surgery. 2019.
  22. Jaszczura M, Gora A, Grzywna-Rozenek E, Barc-Czarnecka M, Machura E. Analysis of neutrophil to lymphocyte ratio, platelet to lymphocyte ratio and mean platelet volume to platelet count ratio in children with acute stage of immunoglobulin A vasculitis and assessment of their suitability for predicting the course of the disease. Rheumatology international. 2019; 39(5): 869-78.
  23. Meshaal MS, Nagi A, Eldamaty A, Elnaggar W, Gaber M, Rizk H. Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) as independent predictors of outcome in infective endocarditis (IE). The Egyptian heart journal: (EHJ): official bulletin of the Egyptian Society of Cardiology. 2019; 71(1): 13.
  24. Mann DL. Innate immunity and the failing heart: the cytokine hypothesis revisited. Circulation research. 2015; 116(7): 1254-68.
  25. Vitiello D, Harel F, Touyz RM, Sirois MG, Lavoie J, Myers J, et al. Changes in cardiopulmonary reserve and peripheral arterial function concomitantly with subclinical inflammation and oxidative stress in patients with heart failure with preserved ejection fraction. International journal of vascular medicine. 2014: 917271.
  26. Soehnlein O, Steffens S, Hidalgo A, Weber C. Neutrophils as protagonists and targets in chronic inflammation. Nature reviews Immunology. 2017; 17(4): 248-61.
  27. Kolaczkowska E, Kubes P. Neutrophil recruitment and function in health and inflammation. Nature reviews Immunology. 2013; 13(3): 159-75.
  28. Dalli J, Montero-Melendez T, Norling LV, Yin X, Hinds C, Haskard D, et al. Heterogeneity in neutrophil microparticles reveals distinct proteome and functional properties. Molecular & cellular proteomics: MCP. 2013; 12(8): 2205-19.
  29. Horckmans M, Ring L, Duchene J, Santovito D, Schloss MJ, Drechsler M, et al. Neutrophils orchestrate post-myocardial infarction healing by polarizing macrophages towards a reparative phenotype. European heart journal. 2017; 38(3): 187-97.
  30. Woudstra L, Biesbroek PS, Emmens RW, Heymans S, Juffermans LJ, van Rossum AC, et al. Lymphocytic myocarditis occurs with myocardial infarction and coincides with increased inflammation, hemorrhage and instability in coronary artery atherosclerotic plaques. International journal of cardiology. 2017; 232: 53-62.
  31. Bracamonte-Baran W, Cihakova D. Cardiac Autoimmunity: Myocarditis. Advances in experimental medicine and biology. 2017; 1003: 187-221.
  32. Błyszczuk P. Myocarditis in Humans and in Experimental Animal Models. Frontiers in Cardiovascular Medicine. 2019; 6(64).
  33. Dewachter L, Dewachter C. Inflammation in Right Ventricular Failure: Does It Matter? Frontiers in physiology. 2018; 9: 1056.
  34. Strassheim D, Dempsey EC, Gerasimovskaya E, Stenmark K, Karoor V. Role of Inflammatory Cell Subtypes in Heart Failure. Journal of immunology research. 2019; 2164017.
  35. Shah AD, Denaxas S, Nicholas O, Hingorani AD, Hemingway H. Neutrophil Counts and Initial Presentation of 12 Cardiovascular Diseases: A CALIBER Cohort Study. Journal of the American College of Cardiology. 2017; 69(9): 1160-9.
  36. Ferrari JP, Lueneberg ME, da Silva RL, Fattah T, Gottschall CAM, Moreira DM. Correlation between leukocyte count and infarct size in ST segment elevation myocardial infarction. Archives of medical sciences Atherosclerotic diseases. 2016; 1(1): e44-e8.
  37. Avci A, Alizade E, Fidan S, Yesin M, Guler Y, Kargin R, et al. Neutrophil/lymphocyte ratio is related to the severity of idiopathic dilated cardiomyopathy. Scandinavian cardiovascular journal: SCJ. 2014; 48(4): 202-8.
  38. Sproston NR, Ashworth JJ. Role of C-Reactive Protein at Sites of Inflammation and Infection. Frontiers in immunology. 2018; 9: 754.
  39. Mortezazadeh M, Vahedifard F, Ahmadi-Renani S, Salimzadeh A. A woman with a bamboo spine in the thoracic vertebra and normal sacroiliac joint; a 5-years undiagnosed ankylosing spondylitis: Case report and literature review. Rheumatology Research. 2020; 5(1): 33-8.
  40. Yıldız A, Yüksel M, Oylumlu M, Polat N, Akıl MA, Acet H. The association between the neutrophil/lymphocyte ratio and functional capacity in patients with idiopathic dilated cardiomyopathy. Anatolian journal of cardiology. 2015; 15(1): 13-7.
  41. Yan W, Liu C, Li R, Mu Y, Jia Q, He K. Usefulness of the Neutrophil-to-Lymphocyte Ratio in Predicting Adverse Events in Elderly Patients With Chronic Heart Failure. International heart journal. 2016; 57(5): 615-21.
  42. Dong CH, Wang ZM, Chen SY. Neutrophil to lymphocyte ratio predict mortality and major adverse cardiac events in acute coronary syndrome: A systematic review and meta-analysis. Clinical biochemistry. 2018; 52: 131-6.
  43. Chatterjee S, Chandra P, Guha G, Kalra V, Chakraborty A, Frankel R, et al. Pre-procedural Elevated White Blood Cell Count and Neutrophil-Lymphocyte (N/L) Ratio are Predictors of Ventricular Arrhythmias During Percutaneous Coronary Intervention. Cardiovascular & hematological disorders drug targets. 2011; 11(2): 58-60.
  44. Boros AM, Széplaki G, Perge P, Jenei Z, Bagyura Z, Zima E, et al. The ratio of the neutrophil leucocytes to the lymphocytes predicts the outcome after cardiac resynchronization therapy. Europace: European pacing, arrhythmias, and cardiac electrophysiology: journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2016; 18(5): 747-54.
  45. Seropian IM, Romeo FJ, Pizarro R, Vulcano NO, Posatini RA, Marenchino RG, et al. Neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio as predictors of survival after heart transplantation. ESC heart failure. 2018; 5(1): 149-56.
  46. Adua E, Danso FO, Boa-Amponsem OM, Adusei-Mensah F. Effect of Neutrophils on Nitric Oxide Production from Stimulated Macrophages. Iranian journal of immunology: IJI. 2015; 12(2): 94-103.
  47. Swirski FK, Nahrendorf M. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Science (New York, NY). 2013; 339(6116): 161-6.
  48. Ma Y, Yabluchanskiy A, Iyer RP, Cannon PL, Flynn ER, Jung M, et al. Temporal neutrophil polarization following myocardial infarction. Cardiovascular research. 2016; 110(1): 51-61.
  49. Puhl S-L, Steffens S. Neutrophils in Post-myocardial Infarction Inflammation: Damage vs. Resolution? Frontiers in Cardiovascular Medicine. 2019; 6(25).
  50. Moradi Tabriz H, Obohat M, Vahedifard F, Eftekharjavadi A. Survey of Mast Cell Density in Transitional Cell Carcinoma. Iranian Journal of Pathology. 2020; 16(2): 119-27.
  51. Salari S, Ghadyani M, Karimi M, Mortezazadeh M, Vahedifard F. Immunohistochemical Expression Pattern of MLH1, MSH2, MSH6, and PMS2 in Tumor Specimen of Iranian Gastric Carcinoma Patients. Journal of Gastrointestinal Cancer. 2022; 53(1): 192-6.
  52. MASOOMI GR, Noyani A, DEHGHANI A, AFRASIABI A, KIANMEHR N. Brief Communication: Investigation of the relationship between end-tidal carbon dioxide and partial arterial carbon dioxide pressure in patients with respiratory distress. MEDICAL JOURNAL OF THE ISLAMIC REPUBLIC OF IRAN (MJIRI). 2020; 34(1).
  53. Albert MA. Biomarkers and heart disease. Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine. 2011; 7(5): S9-11.
  54. Pasini E, Aquilani R, Testa C, Baiardi P, Angioletti S, Boschi F, et al. Pathogenic Gut Flora in Patients With Chronic Heart Failure. JACC Heart failure. 2016; 4(3): 220-7.
  55. Held C, White HD, Stewart RAH, Budaj A, Cannon CP, Hochman JS, et al. Inflammatory Biomarkers Interleukin-6 and C-Reactive Protein and Outcomes in Stable Coronary Heart Disease: Experiences From the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) Trial. Journal of the American Heart Association. 2017; 6(10).
  56. Nymo SH, Aukrust P, Kjekshus J, McMurray JJ, Cleland JG, Wikstrand J, et al. Limited Added Value of Circulating Inflammatory Biomarkers in Chronic Heart Failure. JACC Heart failure. 2017; 5(4): 256-64.
  57. Sharma A, Stevens SR, Lucas J, Fiuzat M, Adams KF, Whellan DJ, et al. Utility of Growth Differentiation Factor-15, A Marker of Oxidative Stress and Inflammation, in Chronic Heart Failure: Insights From the HF-ACTION Study. JACC Heart failure. 2017; 5(10): 724-34.
  58. Moayedi Y, Ross HJ. Advances in heart failure: a review of biomarkers, emerging pharmacological therapies, durable mechanical support and telemonitoring. Clinical science (London, England: 1979). 2017; 131(7): 553-66.
  59. Vahedifard F, Mortezazadeh M, Mofidi A, Kashani M, Sharifi Rayeni A. Focal nodular hyperplasia in a 14-year-old child: A case report. Caspian Journal of Internal Medicine. 2021; 12(0): 460-3.
  60. Huang WM, Cheng HM, Huang CJ, Guo CY, Lu DY, Lee CW, et al. Hemographic indices are associated with mortality in acute heart failure. Scientific reports. 2017; 7(1): 17828.
  61. Yu C, Chen M, Chen Z, Lu G. Predictive and prognostic value of admission neutrophil-to-lymphocyte ratio in patients with CHD. Herz. 2016; 41(7): 605-13.
  62. Tasal A, Erturk M, Uyarel H, Karakurt H, Bacaksiz A, Vatankulu MA, et al. Utility of the neutrophil to lymphocyte ratio for predicting in-hospital mortality after levosimendan infusion in patients with acute decompensated heart failure. Journal of cardiology. 2014; 63(6): 418-23.
  63. Uthamalingam S, Patvardhan EA, Subramanian S, Ahmed W, Martin W, Daley M, et al. Utility of the neutrophil to lymphocyte ratio in predicting long-term outcomes in acute decompensated heart failure. The American journal of cardiology. 2011; 107(3): 433-8.

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