Association Of Monocyte Count Research Articles

Association of Monocyte Count With Lung Function and Exercise Capacity Among Hospitalized COVID-19 Survivors: A 2-Year Cohort Study.

Abnormal changes of monocytes have been observed in acute COVID-19, whereas associations of monocyte count with long COVID were not sufficiently elucidated. A cohort study was conducted among COVID-19 survivors discharged from hospital. The primary outcomes were core symptoms of long COVID, distance walked in 6 min, and lung function, and the secondary outcomes were health-related quality of life and healthcare use after discharge. Latent variable mixture modeling was used to classify individuals into groups with similar trajectory of monocyte count from discharge to 2-year after symptom onset. Multivariable adjusted generalized linear regression models and logistic regression models were used to estimate the associations of monocyte count trajectories and monocyte count at discharge with outcomes. In total, 1389 study participants were included in this study. Two monocyte count trajectories including high to normal high and normal trajectory were identified. After multivariable adjustment, participants in high to normal high trajectory group had an odds ratio (OR) of 2.52 (95% CI, 1.44-4.42) for smell disorder, 2.27 (1.27-4.04) for 6-min walking distance less than lower limit of normal range, 2.45 (1.08-5.57) for total lung capacity (TLC) < 80% of predicted, 3.37 (1.16-9.76) for personal care problem, and 1.70 (1.12-2.58) for rehospitalization after discharge at 2-year follow-up compared with those in normal trajectory group. Monocyte count at discharge showed similar results, which was associated with smell disorder, TLC < 80% of predicted, diffusion impairment, and rehospitalization. Monocyte count may serve as an easily accessible marker for long-term management of people recovering from COVID-19.

Association of Monocyte Count and Monocyte/Lymphocyte Ratio with the Risk of Cardiovascular Outcomes in Patients with CKD.

Emerging evidence suggests an association of higher monocyte count and monocyte/lymphocyte ratio (MLR) with the risk of cardiovascular disease (CVD) in individuals without chronic kidney disease (CKD); however, limited studies have examined if this association translates to the CKD population. This study examined whether monocyte count and MLR are associated with the risk of CVD, CVD death, and all-cause death in patients with nondialysis CKD who participated in the Chronic Renal Insufficiency Cohort observational study. Baseline monocyte count and MLR were categorized into tertiles and also modeled continuously. Cox proportional hazards models were used to examine the association between monocyte count (primary predictor) and MLR (secondary predictor) at baseline and time to a composite of CVD events, including heart failure, myocardial infarction, ischemic stroke, and peripheral artery disease (primary outcome). Secondary outcomes were time to CVD death and all-cause death. The median follow-up time was 9 years for CVD events and 11.7 years for death. In the fully adjusted model, participants with a higher monocyte count and MLR had a greater risk of CVD events (hazard ratio [HR] per doubling of monocyte count=1.2 [95% CI, 1.1 to 1.31]; HR per doubling of MLR=1.26 [95% CI, 1.16 to 1.36]), CVD death (HR=1.18 [95% CI, 0.99 to 1.41]; HR=1.27 [95% CI, 1.1 to 1.48]), and all-cause death (HR=1.17 [95% CI, 1.06 to 1.3]; HR=1.18 [95% CI, 1.09 to 1.29]). These results suggest that monocyte count and MLR may have the potential to be cost-effective, clinically available indicators of CVD risk in the CKD population.

Increased Monocyte Count is Related to the Development of Atrial Fibrillation in Subjects with Heart Failure

Determining subjects with heart failure (HF), who have a high risk of developing atrial fibrillation (AF), is crucial since it is related to an increase in morbidity and mortality. The importance of an increase in inflammatory response cannot be ignored in developing AF in subjects with HF. This study’s goal was to evaluate the relationship between the development of AF and monocyte count, the main components of the inflammatory response, in subjects with HF. Medical data of 158 subjects in total with sinus rhythm, admitted to the emergency department and hospitalized with systolic HF between January 2009 and February 2014, were analyzed prospectively. All the subjects followed up in terms of the development of AF. The subjects separated into two groups according to their rhythm at the end of the follow-up period. Group 1 included subjects who maintained sinus rhythm, while Group 2 included subjects with AF. Echocardiographic findings and laboratory data were collected. No statistically significant difference was determined between the groups concerning age, sex (p=0.056), hypertension, diabetes mellitus, and smoking status. The two groups differed significantly regarding the presence of moderate-to-severe mitral regurgitation (MR) [32 (28%) vs. 22 (51%), p=0.010] and monocyte count [560 (20-3100) vs. 800 (380-1510) μL, p&lt;0.001]. The multivariate Cox regression model demonstrated that an association of monocyte count (HR=2.397, 95% CI =1.397-4.112, p=0.002) and moderate-to-severe MR (HR= 2.347, 95% CI=1.276-4.316, p=0.006) with the development of AF remained following the adjustment for the variables, which had determined to be statistically significant as a result of the univariate analysis and related to monocyte count. The present study concludes that increased monocyte count in subjects with HF is related to the development of AF. However, further large-scale research required for confirming the findings, as mentioned above.

Increased Monocyte Count is Related to the Development of Atrial Fibrillation in Subjects with Heart Failure

Determining subjects with heart failure (HF), who have a high risk of developing atrial fibrillation (AF), is crucial since it is related to an increase in morbidity and mortality. The importance of an increase in inflammatory response cannot be ignored in developing AF in subjects with HF. This study’s goal was to evaluate the relationship between the development of AF and monocyte count, the main components of the inflammatory response, in subjects with HF. Medical data of 158 subjects in total with sinus rhythm, admitted to the emergency department and hospitalized with systolic HF between January 2009 and February 2014, were analyzed prospectively. All the subjects followed up in terms of the development of AF. The subjects separated into two groups according to their rhythm at the end of the follow-up period. Group 1 included subjects who maintained sinus rhythm, while Group 2 included subjects with AF. Echocardiographic findings and laboratory data were collected. No statistically significant difference was determined between the groups concerning age, sex (p=0.056), hypertension, diabetes mellitus, and smoking status. The two groups differed significantly regarding the presence of moderate-to-severe mitral regurgitation (MR) [32 (28%) vs. 22 (51%), p=0.010] and monocyte count [560 (20-3100) vs. 800 (380-1510) μL, p&lt;0.001]. The multivariate Cox regression model demonstrated that an association of monocyte count (HR=2.397, 95% CI =1.397-4.112, p=0.002) and moderate-to-severe MR (HR= 2.347, 95% CI=1.276-4.316, p=0.006) with the development of AF remained following the adjustment for the variables, which had determined to be statistically significant as a result of the univariate analysis and related to monocyte count. The present study concludes that increased monocyte count in subjects with HF is related to the development of AF. However, further large-scale research required for confirming the findings, as mentioned above.

Association of Monocyte Count on Admission with the Angiographic Thrombus Burden in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

BackgroundThe intracoronary high-thrombus burden during the primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. Monocytes have been described to play an important role in thrombotic disorders.ObjectivesThis study aimed to investigate the relationship between admission monocyte count and angiographic intracoronary thrombus burden in patients receiving primary percutaneous coronary intervention (PPCI).MethodsA total of 273 patients with acute STEMI who underwent PPCI were enrolled. The patients were divided into two groups according to the thrombolysis in myocardial infarction (TIMI) thrombus grade: low-thrombus burden group with a grade of 0-2 and high-thrombus burden group with a grade of 3-4. The monocyte count and other laboratory parameters were measured on admission before PPCI. P-value < 0.05 was considered significant.ResultsThere were 95 patients (34.8%) in the high-thrombus burden group, and 178 patients (65.2%) in the low-thrombus burden group. Patients with high-thrombus burden had significantly higher admission monocyte count (0.61 ± 0.29×109/L vs. 0.53 ± 0.24×109/L, p = 0.021). In multivariate analysis, monocyte count was the independent predictor of angiographic high-thrombus burden (odds ratio 3.107, 95% confidence interval [CI] 1.199-7.052, p = 0.020). For the prediction of angiographic high-thrombus burden, admission monocyte count at a cut-off value of 0.48×109/L yielded 0.59 ROC-AUC (71.9% sensitivity, 46.9% specificity).ConclusionsMonocyte count on admission was an independent clinical predictor of high-thrombus burden in patients with STEMI undergoing PPCI. Our findings suggest that admission monocyte count may be available for early risk stratification of high-thrombus burden in acute STEMI patients and might allow the optimization of antithrombotic therapy to improve the outcomes of PPCI.

Can monocytosis act as an independent variable for predicting deep vein thrombosis?

IntroductionDeep venous thrombosis (DVT) is a manifestation of venous thromboembolism (VTE). It has been estimated that there are 900,000 cases of pulmonary emboli (PE) and DVT per year resulting in 60,000 to 300,000 deaths. About two-thirds of VTE cases are associated with prolonged hospitalizations, emphasizing the importance of major surgery or immobilization as risk factors. MethodsRetrospective study conducted in a Metropolitan Hospital. A total of 46 records were obtained from the hospital database following the established inclusion and exclusion criteria. For the control group a total of 42 records were selected. Patients included in this study were admitted with the diagnosis of deep venous thrombosis identified either by lower leg Doppler. ResultsMonocytosis with DVT, p-value was <0.001, with an Odd Ratio (OR) 9.35 and Interval Confidence (IC) 95% (3.2–27.3). The p-value for eosinophilia with DVT was 0.092, for males with DVT the p-value was 0.35 and age related groups with DVT value was 0.720. Sensitivity of monocytosis was 67.3%, specificity 80%, positive predictive value (PPV) 79.49% and negative predictive value (NPV) 63.9%. ConclusionThis study revealed the association between monocytosis and DVT, thus patients with monocytosis are more likely to develop DVT. This evidence is consistent with previous studies establishing that monocytes could have an important role with the coagulation cascade activation and the formation of DVT. The association of monocyte count and DVT can be used in the future as a significant tool in those patients with suspected DVT to increase diagnostic yield.

Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction

The no-reflow phenomenon during primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. It has been shown that the monocytes may be involved in the pathogenesis of coronary artery disease and associated with high risk of myocardial infarction. To assess the relation between admission monocyte count and angiographic no-reflow after pPCI. A total of 236 patients with acute STEMI, who underwent pPCI, were enrolled. The patients were divided into two groups (no-reflow and normal reflow) based on post-pPCI Thrombolysis in Myocardial Infarction (TIMI) flow grade. No reflow was defined as TIMI flow grades ≤ 2, and normal reflow was defined as TIMI 3 flow grade. The monocyte count and other laboratory parameters were measured on admission before pPCI. There were 43 (18.2%) patients in the no-reflow group and 193 (81.8%) patients in the normal-reflow group. Patients with no-reflow had significantly higher admission monocyte count (0.76 ± 0.48 × 109/L vs. 0.55 ± 0.29 × 109/L, p = 0.004). Also, white blood cell and neutrophil counts were significantly higher while haemoglobin was significantly lower in the no-reflow group. In multivariate analysis, monocyte count remained an independent predictor of angiographic no-reflow phenomenon (odds ratio [OR] 2.665, 95% confidence interwal [CI] 1.102-6.445, p = 0.030) together with low haemoglobin concentration (OR 0.978, 95% CI 0.961-0.995, p = 0.013). Monocyte count on admission and low haemoglobin concentration were independent clinical predictors of no-reflow following pPCI in patients with STEMI. Our findings suggest that admission monocyte count may be available for early risk stratification of no-reflow after pPCI and might allow the improvement of strategies to prevent this phenomenon.