Objective Smoking has been proven to increase systemic inflammation in previous studies using different biomarkers. The eosinophil-to-lymphocyte ratio (ELR), neutrophil-to-lymphocyte ratio (NLR), and lymphocyte-to-monocyte ratio (LMR) are new indicators of systemic inflammation that are used as predictors of systemic inflammation, morbidity, and mortality associated with many diseases. We investigated the effects of smoking on these inflammatory indicators. Methods In total, 616 consecutive smoking healthy subjects and 387 age-matched nonsmoking healthy subjects were enrolled. White blood cell counts (neutrophils, lymphocytes, basophils, eosinophils, and monocytes) were determined by electrical impedance with an automatic blood cell counting device. The ELR, LMR, and NLR were calculated based on these cell counts. Smoking habits of participants were calculated as pack/year. Results The NLR and ELR were significantly higher and the LMR was significantly lower in smokers than nonsmokers. The pack-years were positively correlated with the NLR and ELR and negatively correlated with the LMR. Conclusion A high NLR and ELR and low LMR are associated with cigarette smoking and may be useful indicators of systemic inflammation activity, even in healthy smokers. Smokers with a high NLR and ELR and low LMR can easily be identified during routine blood analysis and might benefit from preventive treatment.

The heart rate variability (HRV), which can provide information about the balance between the sympathetic and the parasympathetic system, is accepted as an indicator of autonomic tone, which is effective on the heart. Neural remodeling developing in hearts that are affected by various diseases leads to imbalance in the autonomic activity. These changes that may occur in the autonomic nervous system may lead to ventricular arrhythmia and sudden cardiac death through negatively affecting the cardiac rhythm. HRV has been evaluated in many cardiac, neurological and rheumatological diseases in recent years and has come into the foreground as an important marker of mortality. In this review, we aimed to introduce the parameters used in HRV measurements and analyze the conditions that could influence these measurements (maneuver, diseases or drugs, etc).

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OBJECTIVE:The aim of this study was to investigate the performance of controlling nutritional status (CONUT) index, geriatric nutritional risk index (GNRI), and prognostic nutritional index (PNI) scores in predicting the long-term prognosis of patients with non-ST-elevated myocardial infarction (NSTEMI) who underwent percutaneous coronary intervention (PCI). METHODS: A total of 915 patients with NSTEMI (female: 48.4%; mean age: 73.1±9.0 years) who underwent PCI at Adana Numune Training and Research Hospital, Cardiology Clinic between January 2014 and January 2015 were included in this cross-sectional and retrospective study. CONUT, GNRI, and PNI scores were calculated based on the admission data derived from samples of peripheral venous blood. The mean follow-up duration was 64.5±15.4 months. RESULTS:During follow-up (mean 64.5±15.4 months), 179 patients (19.6%) died. The mean GNRI and PNI scores were significantly lower in the nonsurvivor group; however, the median CONUT score was significantly higher in the nonsurvivor group compared with the survivor group. The receiver operating characteristic (ROC) curve analyses have shown that GNRI score has similar performance to the CONUT score and has better performance than PNI score in predicting 5-year mortality. The Kaplan-Meier curve analysis has shown that patients with lower PNI or GNRI had higher cumulative mortality than the patients with higher PNI or GNRI. Also, the patients with higher CONUT scores had higher cumulative mortality compared with those with lower scores. The multivariate analyses have shown that GNRI (HR: 0.973), PNI (HR: 0.967), CONUT score (HR: 1.527), and body mass index (BMI) (HR: 0.818) were independent predictors of the 5-year mortality in patients with NSTEMI. CONCLUSION:In this study, we have shown that CONUT score, GNRI, and PNI values were associated with the long-term mortality in patients with NSTEMI who underwent PCI, and GNRI yielded similar results to CONUT score but was better than PNI.

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Atrial fibrillation (AF) is an arrhythmia caused by disorganized electrical activity in the atria, and it is an important cause of mortality and morbidity. There is a limited data about Rho/Rho-kinase (ROCK) pathway contribute to AF development. The aim of the present study was to elucidate leukocyte RHO/ROCK gene expressions in patients with non-valvular AF (NVAF). A total of 37 NVAF patients and 47 age and sex-matched controls were included in this study. mRNA was extracted from leukocytes, and real-time polymerase chain reaction was used for gene expression analysis. A marked increase in ROCK1 and ROCK2 gene expressions in patients with NVAF was observed (P<0.0001). The present study detected significant elevations in RHOBTB2, RND3 (RHOE), RHOC, RHOG, RHOH, RAC3, RHOB, RHOD, RHOV, RHOBTB1, RND2, RND1 and RHOJ gene expressions (P<0.01). However, there were marked decreases in CDC42, RAC2, and RHOQ gene expressions in patients with NVAF. No significant modifications were seen in the other Rho GTPase proteins RHOA, RAC1, RHOF, RHOU and RHOBTB3. To the best of our knowledge, the present study is the first to provide data that gene expression of leukocyte RHO/ROCK may contribute to the NVAF pathogenesis through activated leukocytes, which promotes the immune or inflammatory cascade.

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Carbon monoxide (CO) poisoning could cause significant cardiac injury. This study aimed to evaluate patients with CO poisoning by using speckle tracking echocardiography (STE), a potentially more sensitive technique, to identify left systolic ventricular dysfunction for the first time in the literature. Seventy-two patients who were exposed to CO poisoning were studied. Blood collection and echocardiography were performed at admission and after patients' discharge on days 10-15 (mean 12 days). Global longitudinal strain (GLS) and global circumferential strain (GCS) were calculated using STE. In order to find the normal strain levels and to compare it to the patient with CO poisoning, 35 healthy subjects were included in the study. Left ventricular ejection fraction was analyzed according to Simpson's method. Patients were divided into two groups based on their LVEF values. LVEF < 55%, Group 1 (n = 24); LVEF ≥ 55%, Group 2 (n = 48). The reduction in Group 1 strain levels decreased in correlation with LVEF (p < 0.001) while in Group 2, there were no significant changes in LVEF but strain levels were significantly reduced (p = 0.091; p < 0.001). Compared with the control group patients, admission GLS and GLC values of CO-poisoned patients were significantly low both in Group 1 and 2. On the contrary, no significant difference was observed when compared with follow-up GLS value. For prediction of CO cardiotoxicity, the cutoff value of GLS was ≥ - 19.1 with a sensitivity of 70.3% and a specificity of 100% [(AUC) 0.840, 95% (CI) 0.735-0.916; p < 0.001] in the ROC curve analyses. GLS was found as independent predictors of cardiotoxicity. Our study demonstrates the potential of using systolic strain values obtained using 2D-STE in determining cardiotoxicity due to CO poisoning. Speckle tracking echocardiography has the potential of demonstrating subtle LV systolic dysfunction even in CO poisoning patients with preserved EF.