Impact Of Inflammatory Markers Research Articles

Impact of Inflammatory Markers and Senescence-Associated Secretory Phenotype in the Gingival Crevicular Fluid on the Outcomes of Periodontal Regeneration.

The aim of this study was to test the molecular expression profile (senescence-associated secretory phenotype; SASP) in gingival crevicular fluid (GCF) prior to surgery in relation to the distribution of clinical success of periodontal regeneration. Forty consecutive patients presenting sites with residual probing pocket depth (PPD) ≥ 6 mm and intrabony defects ≥ 3 mm were treated through a minimally invasive surgical technique. Pre-operatively, GCF was sampled for inflammatory biomarker analysis related to SASP [interleukin (IL)-1β, IL-6, and IL-12; matrix-metalloproteinases (MMP)-8 and -9]. Better or worse responders were classified depending on the achievement of a composite outcome measure at 1-year [COM; PPD ≤ 4 mm and clinical attachment gain (CAL) gain ≥ 3 mm]. Correlation analyses and logistic regression models were performed. Periodontal regeneration led to significant improvements in mean clinical and radiographic parameters. Teeth achieving COM presented significantly lower amounts of SASP factors compared with non-successful teeth. Higher CAL gain, PPD reduction, and radiographic bone fill were negatively correlated with IL-1β and MMP-8 and -9 (p < 0.001), while IL-12 showed a direct relationship with CAL gain (p = 0.005) and PPD reduction (p = 0.038). Sites expressing higher SASP expression in the GCF before periodontal regeneration achieved worse clinical and radiographic outcomes.

Impact of inflammatory markers, dread diseases and cycle threshold (Ct) Values in COVID-19 progression

The link between the inflammatory marker and SARS-CoV-2 cycle threshold (Ct) with disease progression remains undefined, mainly in coronavirus disease-2019 (COVID-19). Therefore, this study aimed to identify several inflammatory markers (Ferritin, LDH, and D-dimer), and Ct values to predict outcomes in hospitalized COVID-19 Iraqi patients. A case study was performed on 426 patients to guess cutoff values of inflammatory markers that were detected by a real-time polymerase chain reaction (RT-PCR) and specific auto-analyzer instrument. Significantly increased levels of inflammatory markers in critical and severe patients compared with mild-moderate (p &lt; 0.001). Compared with aging and disease severity, inflammatory markers and Ct values are significantly related to the aging and severity in critical and severe COVID-19 patients (p &lt; 0.001). Finding the Ct value was negatively associated with Ferritin, LDH, and D-dimer (p &lt; 0.001); moreover, inflammatory markers concentrations and Ct values were significantly higher during the first ten days. The Ct values correlate with some relevant clinical parameters of inflammation. Higher levels of D dimer, S. Ferritin and LDH were associated with older age and the severity of COVID-19. The area under the ROC curve indicates that serum ferritin was the highest and excellent predictor for disease severity. Keywords: Coronavirus disease 2019; Inflammation; D-dimer; Ferritin; Lactate dehydrogenase; Cycle threshold (Ct).

Inflammation as a Prognostic Marker in Heart Failure.

Background: Heart failure (HF) is a chronic cardiac disease of great importance worldwide and responsible for one-fifth of hospitalizations for cardiovascular disease in Brazil. Pro-inflammatory mediators are involved in the pathophysiology of HF. However, the impact of inflammatory markers on the prognosis of the disease remains uncertain.Objective: We aimed to evaluate inflammation as a prognostic marker in chronic HF.Methods: In this prospective, single-center, observational cohort study conducted from June 2018 through December 2019, we included outpatients with HF from a specialized service of a teaching hospital. Patients with decompensated HF requiring hospitalization in the last 30 days were excluded. At the time of inclusion, serum C-reactive protein (CRP) and albumin were collected and the presence of inflammation was defined as CRP/albumin ≥1.2. Patients with CRP/albumin ratio <1.2 (group A) and CRP/albumin ratio ≥1.2 (group B) were compared. The primary outcome was all-cause mortality. The secondary outcomes were hospitalization for decompensated HF, number of hospitalizations, and number of days of hospitalization in the 12-month follow-up.Results: We included 77 patients, 49 (63.3%) in group A and 28 (3.4%) in group B. Six patients in group A (12.2%) and 10 patients in group B (35.7%) required at least one hospitalization during follow-up (p=0.01). The rate of hospitalizations for decompensated HF for every 100 patients was 16.3 in group A vs 50.0 in group B (p=0.0001) and the average in-hospital length of stay was 12.2 vs 14.2 days per hospitalized patient (p=0.36) in groups A and B, respectively. The mortality rate was 6.1% in group A vs 7.1% in group B (p=0.86).Conclusion: In HF outpatients with inflammation evidentiated by the CRP/albumin ratio ≥1.2, the risk of death was similar to patients without inflammation criteria. However, the presence of inflammation led to a three-fold higher risk of hospitalization for HF decompensation.

Impact of Inflammatory Markers in Predicting Outcomes of SARS-CoV-2 Patients: The why’s and how’s of Diabetic Hypertensive Patients

Background: Hypertension and Diabetes Mellitus, the most frequent co-morbidities in SARS-Cov-2 patients are considered as risk factors for disease severity and mortality. And the role of inflammatory biomarkers on these patients is still under evaluation. Methods: Retrospective data was collected study in 3 independent groups each with 24 patients: diabetes, hypertension and with concomitant diabetes and hypertension respectively of critically ill SARS-CoV-2 patients admitted in the CCM. The data of age, gender, diabetic and hypertensive history, inflammatory marker, duration of stay was obtained from electronic patient data repository of the hospital and compared with Mortality. Results: The mean CRP levels in diabetes was 78.81 ± 16.8, in hypertension 82.23 ± 13.98 and in group with both the co morbidities was 79.05 ± 16.38. Serum ferritin levels were high in hypertensive group 731 ± 621.12, were as in diabetes population it was 560.31 ± 319.81, and 629.37 ± 350.8 in both diabetic and hypertensive population. The mean and SD of D-dimer it was 3726.4 ± 2411.86 in diabetic group, 2861.28 ± 2041.36 in hypertensive group and 2755.6 ± 1980.67. CRP levels and D-dimer were positively correlated with mortality and duration of stay. Conclusion: Our study concluded inflammatory markers CRP and D-dimer levels were elevated in both comorbid patients and this was statistically significant. Correlation of ferritin to the outcome was not significant and understanding the molecular mechanism of infection in co-morbid patients and assessing the inflammatory markers can provide necessary assistance at earliest, for a better clinical outcome.

Impact of inflammatory markers on the relationship between sleep quality and diabetic kidney disease.

Both poor sleep and diabetic kidney disease are closely associated with inflammation. However, the correlation between poor sleep and diabetic kidney disease has not been wellclarified. Thus, the aim of this study was to determine the mediating role that inflammatory markers play in the pathogenic effectof poor sleep on the severity of diabetic kidney disease (DKD). A cross-sectional survey was conducted on 336 patients withtype 2 diabetes (T2D). DKD was diagnosed according to the guidelines of the National Kidney Foundation-Kidney Disease Outcome Quality Initiative (NKF-K/DOQI). The Pittsburg Sleep Quality Index (PSQI) score was applied to assess patients for the quality of their sleep. Patients with a PSQIscore of more than 5 were assigned to the poor sleep group, and the rest of the patients were assigned to the good sleep group. Circulating levels of six inflammatory biomarkers related to poor sleep and DKD were measured. The prevalence of DKD was higher in patients with poor sleepquality than in those with good sleepquality (42% vs. 25%, P = 0.002). After adjustment, poor sleepquality (PSQI score OR 1.075 [95%CI 1.018-1.135], P = 0.009) remained independently associated with DKD. PSQI score was found to be positively related to fibroblast growth factor (FGF23), interleukin 6 (IL-6), P-selectin, and intercellular adhesion molecule-1 (ICAM-1) (P < 0.01), rather than fibrinogen and C-reactive protein (CRP) in linear regression models. As revealed by multiple mediation analysis, FGF23 and IL-6 mediated 26% and 23% of the relationship between PSQI score and urinary microalbumin (UMA), respectively. Similarly, the FGF23 and ICAM-1, instead of IL-6 and P-selectin, mediated 32% and 24% of the association between PSQI and estimated glomerular filtration rate (eGFR), respectively. Poor sleepquality is independently associated with DKD. These results suggest that inflammatory markers contribute to a pathogenic connection between poor sleep and DKD.

P76.12 Impact of Inflammatory Markers and Body Mass Index on TKI Toxicity in Patients With Non-Small Cell Lung Cancer Harboring an EGFR Mutation

The standard treatment for patients with advance EGFR mutated NSCLC are Tirosine Kinasa inhibitors (TKI), these treatment has been linked with different profile of toxicity; there is limited data of Inflammatory markers in this especial population. The aim of our study is to determine whether neutrophil lymphocyte ratio (NLR), lymphocyte platelet ratio (PLR) and body mass index (BMI) are related to the develop of this toxicity. We retrospectively analyzed data of patients with EGFRm NSCLC at Aliada Clinic between January 2016 to December 2019. Inflammatory markers were obtained from laboratory tests performed during the first visit as outpatient. The BMI kg/m2 at the start of the treatment was defined as the weight (kg) divided by the height (m) squared. Adverse event (AE) were graded according CTCAE v5.0. A total of 164 patients were diagnosed with advanced NSCLC, of these 50 patients were assessed, 29 women and 21 men. The average age was 58.9 years, median of 59.5 ( 38 to 83; SD: 11.7). The most frequent EGFR mutation was deletion 19 (59.6%) followed by L858R mutation ( 23.1%). The median BMI was 25.18 (16.2 to 41.3 kg/m2) 46.2% were normal, 36.5% were overweight, and 11.5 % were obese. 80% present any grade of AE. The most frequent AE was skin related: 75% (90 % grade I or II) follow by gastrointestinal: 57.6% (74 % grade I or II). There were no significant differences between NLR according to toxicity grade I-II vs III-IV (media: 3.44 and 4.32; P = 0.46); PLR according toxicity grade I-II vs III-IV (media: 229.41 and 251-50; P = 0.78). Similarly, no significant differences were observed among toxicity profiles in relation to BMI (p = 0.2). Finally, there was no impact of severity of toxicity on progression-free survival (p = 0.64) or overall survival 24,33 months (IC 95% 16,05 – 32,6; p = 0.9). There was no impact of inflammatory markers according to the grade of toxicity in patients with EGFRm advance NSCLC receiving TKIs. We recommend increase the population to validate our results.

Impact of inflammatory markers on survival in patients with limited disease small-cell lung cancer undergoing chemoradiotherapy.

BackgroundSystemic inflammation appears to play a role in the progression of numerous solid tumors by promoting tumor proliferation. Our current study aimed to evaluate the role of inflammatory markers in limited disease (LD) small-cell lung cancer (SCLC) patients undergoing thoracic chemoradiotherapy (TCR).Patients and methodsWe retrospectively analyzed a total number of 350 SCLC patients diagnosed with LD SCLC who received TCR between 1999 and 2017 and had available blood tests within 2 weeks prior to the start of TCR. Serum C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), lactate dehydrogenase (LDH), hemoglobin (Hb) levels, and platelet count (Pc) were evaluated as potential inflammatory markers. Kaplan–Meier survival analysis was performed for overall survival (OS). For comparison of survival curves, the log-rank (Mantel–Cox) test was used. Univariate and multivariate Cox proportional HRs were used to assess the influence of cofactors on OS.ResultsUnivariate analysis for OS revealed a statistically significant effect for LDH >400 U/L (HR 2.05 U/L; 95% CI 1.29–3.26 U/L; P=0.002), prophylactic cranial irradiation (PCI; HR 0.58; 95% CI 0.40–0.85; P=0.005), CRP >50 mg/L (HR 1.49 mg/L; 95% CI 1.05–2.10 mg/L; P=0.026), and Karnofsky performance scale (KPS) <70% (HR 1.35%; 95% CI 1.02–1.80%; P=0.035). NLR, age (>70 years), Hb levels, and Pc did not influence survival. In multivariate analysis, OS was significantly affected by PCI (HR 0.64; 95% CI 0.43–0.94; P=0.026), LDH >400 U/L (HR 1.91 U/L; 95% CI 1.21–3.05 U/L; P=0.006), and CRP >50 mg/L (HR 1.43 mg/L; 95% CI 1.01–2.04 mg/L; P=0.045). KPS (≤70%) did not influence survival in multivariate analysis.ConclusionElevated CRP and LDH seem to be the independent prognostic factors for OS in LD SCLC patients undergoing TCR. However, elevated NLR was not found to be an independent prognostic factor for OS if taken prior to TCR. LDH and CRP are easily available blood tests and do not require additional resources for routine use and could be useful for clinical decision making.

Stillbirth, Inflammatory Markers, and Obesity: Results from the Stillbirth Collaborative Research Network.

Obesity is associated with increased risk of stillbirth, although the mechanisms are unknown. Obesity is also associated with inflammation. Serum ferritin, C-reactive protein, white blood cell count, and histologic chorioamnionitis are all markers of inflammation. This article determines if inflammatory markers are associated with stillbirth and body mass index (BMI). Additionally, we determined whether inflammatory markers help to explain the known relationship between obesity and stillbirth. White blood cell count was assessed at admission to labor and delivery, maternal serum for assessment of various biomarkers was collected after study enrollment, and histologic chorioamnionitis was based on placental histology. These markers were compared for stillbirths and live births overall and within categories of BMI using analysis of variance on logarithmic-transformed markers and logistic regression for dichotomous variables. The impact of inflammatory markers on the association of BMI categories with stillbirth status was assessed using crude and adjusted odds ratios (COR and AOR, respectively) from logistic regression models. The interaction of inflammatory markers and BMI categories on stillbirth status was also assessed through logistic regression. Additional logistic regression models were used to determine if the association of maternal serum ferritin with stillbirth is different for preterm versus term births. Analyses were weighted for the overall population from which this sample was derived. A total of 497 women with singleton stillbirths and 1,414 women with live births were studied with prepregnancy BMI (kg/m2) categorized as normal (18.5-24.9), overweight (25.0-29.9), or obese (30.0 + ). Overweight (COR, 1.48; 95% confidence interval [CI]: 1.14-1.94) and obese women (COR, 1.60; 95% CI: 1.23-2.08) were more likely than normal weight women to experience stillbirth. Serum ferritin levels were higher (geometric mean: 37.4 ng/mL vs. 23.3, p < 0.0001) and C-reactive protein levels lower (geometric mean: 2.9 mg/dL vs. 3.3, p = 0.0279), among women with stillbirth compared with live birth. Elevated white blood cell count (15.0 uL × 103 or greater) was associated with stillbirth (21.2% SB vs. 10.0% live birth, p < 0.0001). Histologic chorioamnionitis was more common (33.2% vs. 15.7%, p < 0.0001) among women with stillbirth compared with those with live birth. Serum ferritin, C-reactive protein, and chorioamnionitis had little impact on the ORs associating stillbirth with overweight or obesity. Adjustment for elevated white blood cell count did not meaningfully change the OR for stillbirth in overweight versus normal weight women. However, the stillbirth OR for obese versus normal BMI changed by more than 10% when adjusting for histologic chorioamnionitis (AOR, 1.38; 95% CI: 1.02-1.88), indicating confounding. BMI by inflammatory marker interaction terms were not significant. The association of serum ferritin levels with stillbirth was stronger among preterm births (p = 0.0066). Maternal serum ferritin levels, elevated white blood cell count, and histologic chorioamnionitis were positively and C-reactive protein levels negatively associated with stillbirth. Elevated BMIs, both overweight and obese, were associated with stillbirth when compared with women with normal BMI. None of the inflammatory markers fully accounted for the relationship between obesity and stillbirth. The association of maternal serum ferritin with stillbirth was stronger in preterm than term stillbirths.

Longitudinal effects of systemic inflammation markers on periodontitis.

Systemic low-grade inflammation represents a central hallmark of chronic diseases and has been proposed as the underlying mechanism linking factors like obesity or diabetes with periodontitis. However, the impact of inflammatory markers on periodontitis has not yet been investigated. The study population comprised 1784 subjects from the Study of Health in Pomerania with complete 11-year follow-up. Fibrinogen and white blood cell (WBC) counts were measured as markers of inflammation. Periodontitis was assessed by probing depth (PD), clinical attachment loss (CAL) and the CDC/AAP case definition. Multilevel regression analyses revealed significant coefficients for the impact of both inflammation markers on the percentage of sites with PD/CAL≥3mm. Increases in fibrinogen about 1g/l were associated with 3.0% and 2.7% more sites with PD/CAL≥3mm respectively. Consistent associations were found using mean values of PD/CAL but not using missing teeth or caries. Regarding the CDC/AAP case definition, 11-year changes in fibrinogen and WBC counts were significantly associated with ≥1 category progression (OR: 1.36 and 1.11). Fibrinogen levels and WBC counts showed consistent long-term associations with PD, CAL and the CDC/AAP case definition. Results indicate that systemic low-grade inflammation might indeed represent one possible pathway for effects of obesity, diabetes or other chronic inflammatory conditions on periodontitis.

Impact of inflammatory markers on the relationship between sleep quality and incident cardiovascular events in type 2 diabetes

AimsTo analyze relevance of sleep quality with CVD in T2D patients and determine whether inflammation prompted by poor sleep has impact on the CVD. Methods332 T2D patients were recruited and their sleep qualities were evaluated by PSQI. The patients with PSQI score >7 were in the poor sleep group, and the others were in the good sleep group. Plasma samples of the patients were obtained to measure inflammatory markers. Correlation analyses and regression analyses were performed to examine the cross-sectional relationships among the poor sleep, inflammatory markers and CVD. ResultsThe morbidity of CVD was significantly higher in the poor sleep patients compared to the good sleep patients (P=0.000). PSQI score ORs were both >1 for CVD in model 1 and model 2 (P<0.05). PSQI score were positively related to IL-6 and ICAM-1(P<0.05), negatively to FBI (P<0.05), but not related to CRP in linear regression models. Multiple logistic regression analysis showed IL-6 and ICAM-1, but not FBI and CRP, were related to CVD (P<0.05). ConclusionsPoor sleep is regarded as a plausible risk factor for CVD in T2D patients, and may be mediated by certain inflammatory markers.

Admission leukocytosis, C-reactive protein and erythrocyte sedimentation rate in acute noncardioembolic cerebral ischemia: influence on early outcome

Background There is growing evidence regarding the role of inflammation in the pathogenesis of ischemic stroke, especially nonembolic types of ischemic stroke. Despite this, there is a need to investigate the direct impact of inflammatory markers on the early outcome in nonembolic ischemic stroke. Objective The aim of the present study was to determine whether positive inflammatory markers such as raised erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and leukocytosis could be used as biochemical predictors for poor early outcome in patients with acute noncardioembolic ischemic stroke. Patients and methods A total of 60 patients(40 men and 20 women; median age: 64.5 years) with first attack of noncardioembolic ischemic stroke were included in the study. Full clinical assessment and routine laboratory investigation were conducted for all patients. MRI of brain, ECG, and cardiac echo were carried out to confirm the diagnosis and exclude cases with embolic stroke. Blood samples for all patients within the first 24 h of onset of symptoms were taken for assessment of ESR, qualitative CRP, and leukocyte count on admission. National Institute of Health Stroke Scale was used for all patients after 7 days. On the basis of their scores patients were divided into two groups: 40 patients with favorable outcome were included in the first group and 20 patients with bad outcome in the second group. Results There was significant difference between the two groups regarding ESR value, and the leukocyte count was higher in the group with bad prognosis. In addition, positive CRP was associated more with the same group in statistically significant way. Conclusion Inflammatory markers play an important role in detecting the early outcome of noncardioembolic stroke.

Assessment of the validity of the 28-joint disease activity score using erythrocyte sedimentation rate (DAS28-ESR) as a disease activity index of rheumatoid arthritis in the efficacy evaluation of 24-week treatment with tocilizumab: subanalysis of the SATORI study

As tocilizumab (TCZ) greatly inhibits inflammatory markers, methods of evaluating rheumatoid arthritis (RA) disease activity that include inflammatory markers may overestimate the effect of TCZ treatment. We have evaluated the impact of inflammatory markers on the efficacy of TCZ by comparing the efficacy indicated by the 28-joint disease activity score using erythrocyte sedimentation rate (DAS28-ESR) with that indicated by the clinical and simplified disease activity indexes (CDAI and SDAI, respectively) and the American College of Rheumatology (ACR) core set criteria in a double-blind study of TCZ—the SATORI study. The Spearman correlation coefficient between DAS28-ESR and CDAI was comparable between that at week 24 and that at baseline [correlation coefficient at baseline and week 24 was 0.823 (p < 0.0001) and 0.818 (p < 0.0001), respectively]. A large difference between the DAS28 remission rate and CDAI remission rate was observed at week 24. However, these results are comparable to those of a previous study conducted with non-TCZ-treated patients. Moreover, the same results were obtained in the comparison between the DAS28-ESR and SDAI, even though the SDAI includes an inflammatory parameter as a component. These results confirm that the DAS28-ESR has a validity comparable to that of other methods in terms of evaluating the RA treatment efficacy of TCZ, despite its strong inflammatory marker-inhibiting effects.

Impact of inflammatory markers on platelet inhibition and cardiovascular outcome including stent thrombosis in patients with symptomatic coronary artery disease

Background There is cumulative evidence that the degree of inflammation correlates with prognosis after percutaneous coronary interventions (PCI). Additionally, there is a cross-link between platelet activation and inflammatory pathways. The aim of the present analysis was to evaluate the association of inflammatory markers and effects of dual antiplatelet therapy on platelet function and outcome in patients undergoing PCI. Methods and results In a pilot study, 157 patients with symptomatic coronary artery disease (CAD) undergoing PCI were consecutively evaluated. Platelet response to clopidogrel and acetylsalicylic acid was assessed using whole blood multiple electrode aggregometry (MEA). Baseline levels of IL-6, RANTES and MCP-1 were measured by Bio-Plex Cytokine assay. C-reactive protein (CRP) was determined by Immunoassay. Levels of IL-6, RANTES, and CRP correlated well with ADP and arachidonic acid (AA)-induced MEA. In a second step, a retrospective analysis of a cohort of 903 PCI-patients was performed to evaluate the association of on-treatment residual platelet aggregation (RPA) and baseline CRP levels on the incidence of myocardial infarction (MI), death and stent thrombosis (ST). Patients suffering a subsequent event had a significantly higher level of baseline CRP and higher RPA compared to patients without events. After multivariate adjustment high baseline CRP and high RPA were independent predictors for combined major events and ST after PCI. Conclusion To our knowledge this is the first study linking inflammation, antiplatelet drug responsiveness and outcome in a large CAD-patient cohort. The results suggest a relevant interaction of these parameters and encourage multimodal therapeutic approaches to treat cardiovascular risk after PCI.

Prognostic impact of hs‐CRP and IL‐6 in patients with persistent atrial fibrillation treated with electrical cardioversion

Objective. The aim of this study was to assess the role of inflammatory processes in the development of atrial fibrillation (AF) and the prognostic impact of inflammatory markers in predicting long‐term risk of AF recurrence after electrical cardioversion (CV). Methods. High‐sensitivity C‐reactive protein (hs‐CRP) and interleukin‐6 (IL‐6) were measured in 56 patients with persistent AF (lasting mean 128 days (range 14–960), mean age 65 years (34–84)), 19 healthy volunteers and 19 patients with permanent AF. Patients with persistent AF underwent CV. Blood samples were taken prior to CV and after 1, 30 and 180 days. Results. The immediate success rate of CV was 88 %, while the total recurrence rate after 180 days was 68 %. Patients with permanent AF had significantly higher levels of hs‐CRP and IL‐6 than patients with persistent AF (p = 0.0011, p<0.001). Patients in sinus rhythm (SR) after 180 days had significantly lower baseline hs‐CRP (1.25 mg/L (0.5–2.4) versus 2.0 mg/L (0.9–3.3), p<0.001) and IL‐6 (1.96 pg/mL (1.35–2.7) versus 2.75 pg/mL (1.55–3.62), p<0.001) than patients with recurrent AF. Baseline IL‐6 was the only independent predictor of recurrent AF (p = 0.04) in a multivariate Cox analysis. Patients in the lowest hs‐CRP quartile (<0.8 mg/L) had significantly lower AF recurrence rates after 180 days (50 % versus 74 % in the other three quartiles combined; p = 0.0069). Conclusion. Patients with AF had elevated levels of inflammatory markers. Low hs‐CRP and IL‐6 prior to CV are associated with a lower risk of AF recurrence after CV.

Impact of inflammatory markers on cardiovascular mortality in patients with metabolic syndrome

Recent investigations suggest the inclusion of inflammatory markers in the definition of the metabolic syndrome (MS). The aim of this study was to address the role of C-reactive protein, fibrinogen, interleukin-6 (IL-6) and IL-18 (IL-18) on cardiovascular prognosis in accordance to MS. A total of 1263 patients with documented coronary artery disease were prospectively included. We defined MS (MS yes: N=533, 42.2%) as the presence of at least three of the following criteria: triglycerides>or=150 mg/dl; low high-density lipoprotein cholesterol (men: <40 mg/dl women: <50 mg/dl); body mass index greater than 30 kg/m; blood pressure>or=130/85 mmHg; fasting glucose>or=100 mg/dl. In addition, we determined C-reactive protein, fibrinogen, IL-6 and IL-18 levels. Follow-up data (median 6.1 years) were available for 1257 patients (99.5%). 139 patients (11.1%) died from cardiovascular causes. Cardiovascular mortality was related to MS (MS yes: 15.1% versus MS no: 8.1%, P<0.0001) and was further increased by elevation of each inflammatory marker. To address whether elevation of inflammatory markers provides additional prognostic information, a subgroup analysis was performed including patients with MS. In a multivariate-adjusted model including all four inflammatory markers, only IL-18 could be identified as an independent predictor of cardiovascular mortality. The measurement of inflammatory markers, especially IL-18, adds important prognostic information with regard to the long-term prognosis of patients with MS.

Impact of Inflammatory Markers, Anemia and Renal Dysfunction in Elderly Patients with Chronic Heart Failure

Introduction: Several studies showed that renal disease, anemia and inflammation are markers of poor prognosis in patients with chronic heart failure (HF). Objective: Analyze some important risk factors in patients with advanced HF and its influence on morbidity and mortality. Methods: In a prospective cohort of 59 patients with CHF, the mean age = 61.3 ± 12.08 y/o; 67.8% were males; 59.3% were caucasians; 25.4% were diabetic; 61% had history of hypertension; 50.8% had smoking history, ischaemic etiology = 61%; and mean left ventricular ejection fraction (LVEF) was 0.32 ± 0.09.