Background and objectives Hypertension is one of the most important risk factors for cardiovascular and cerebrovascular events. Inflammatory processes occupy an important place in the pathogenesis of hypertension. Many studies have studied inflammatory markers responsible for the onset of hypertension and organ damage. In this study, we investigated whether the systemic immune-inflammation index (SII) (platelet × neutrophil/lymphocyte), -one of the new inflammatory markers -can be used to predict cerebrovascular events in hypertensive patients.Methods Ambulatory blood pressure monitoring results between January 2019 and June 2020 of approximately 379 patients followed up with hypertension were retrospectively analyzed. These patients were divided into two groups as with or without a previous cerebrovascular event in the analyzed database. In all patients, complete blood count and biochemistry test results just before the cerebrovascular event were found from the database. SII, atherogenic index, neutrophil-lymphocyte ratio were calculated from the complete blood count. Fortynine patients with stroke (group 1: 12.9%; mean age: 64.3 ± 14.6) and 330 patients without stroke (group 2: 87.1%; mean age: 50.8 ± 14.4).Results Ambulatory blood pressure measurements were lower in group 1. Lipid parameters were also lower in this group. Receiver operating characteristic curve analysis showed that SII had a sensitivity of 85.7% and specificity of 84.8 % for stroke in individuals who participated in the study when the cutoff value of SII was 633.26 × 10 3 (P = 0.0001) area under curve (95%); 0.898 (0.856-0.941). In multivariate logistic regression analysis, age and SII were significantly associated with a higher risk of stroke. Age, (hazard ratio:1.067; 95% CI, 1.021-1.115), SII (hazard ratio:1.009; 95% CI, 1.000-1.009), respectively. ConclusionsIn conclusion, SII is a simple, useful new inflammatory parameter for predicting stroke from hypertension. We found that the high SII levels increase the risk of stroke in hypertensive patients.

Coronary artery disease (CAD) patients with concomitant peripheral artery disease (PAD) experience more extensive and calcified atherosclerosis, greater lesion progression and more common coronary events compared to patients with CAD only. To characterize the distinct features of this aggressive atherosclerotic disease, we studied novel cytokines that code different stages of atherogenesis. One hundred and eighty consecutive subjects (60 patients into each group of CAD+PAD, CAD and controls) were recruited among patients with stable angina pectoris scheduled for coronary angiography. An ankle-brachial index (ABI) ≤0.9 was determined as occlusive PAD. Fasting serum tumor necrosis factor (TNF)-like antigen 1A (TL1A) and its receptor death receptor 3 (DR3), NOGO-B (reticulon 4B) and its receptor NUS1, high-sensitivity C-reactive protein (hsCRP), A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) 1, 4, 5 and interleukin (IL) 6 levels were determined. Serum hsCRP and DR3/TL1A concentrations were similar and higher than controls in the CAD and CAD+PAD groups. Levels of NOGO-B and its receptor NUS1 were increased and ADAMTS-5 was decreased in patients with CAD+PAD. Independent predictors of ABI in multivariate analysis were smoking (B = -0.13, p = 0.04), NUS1 (B = -0.88, p < 0.001), ADAMTS-5 (B = 0.63, p < 0.001) and SYNTAX score (B = -0.26, p < 0.001). Similarly, smoking (OR = 5.5, p = 0.019), SYNTAX score (OR = 1.2, p < 0.001), NUS1 (OR = 14.4, p < 0.001), ADAMTS-5 (OR = 1.1, p < 0.001) and age (OR = 1.1, p = 0.042) independently predicted the involvement of peripheral vasculature in logistic regression. The diagnostic performance of these cytokines to discriminate CAD+PAD were AUC 0.79 ( p < 0.001) for NUS1 and 0.37 ( p = 0.013) for ADAMTS-5. We report herein that circulating cytokines can give clues to the ongoing atherosclerotic process and the extent of vascular involvement in which distinct features of ADAMTS-5 and NUS1 make them promising cytokines for future research.

Fundamento: O índice imunoinflamatório sistêmico (IIS), derivado das contagens de neutrófilos, plaquetas e linfócitos, representa o equilíbrio homeostático entre os estados inflamatório, imune e trombótico. O IIS é superior a índices como a relação neutrófilos-linfócitos no prognóstico de várias malignidades, além de ser um melhor preditor de futuros eventos cardíacos que os fatores de risco tradicionais após a intervenção coronariana. Objetivos: Este estudo objetivou avaliar a relação do IIS com a carga aterosclerótica e complicações hospitalares em pacientes com síndrome coronariana aguda. Métodos: Desfechos clínicos, como extensão do dano miocárdico, carga aterosclerótica, sangramento, insuficiência renal aguda, duração da internação e mortalidade hospitalar, foram avaliados em uma coorte retrospectiva de 309 pacientes consecutivos com síndrome coronariana aguda. O IIS foi calculado como (plaqueta x neutrófilos)/contagem de linfócitos na admissão. A população estudada foi categorizada em tercis de IIS. Valores de p<0,05 foram considerados estatisticamente significativos. Resultados: Os maiores valores de IIS foram encontrados em pacientes com infarto do miocárdio com supradesnivelamento do segmento ST (641,4 com angina pectoris instável, 843,0 com infarto do miocárdio sem supradesnivelamento do segmento ST e 996,0 com infarto do miocárdio com supradesnivelamento do segmento ST; p=0,004). Concentração máxima de troponina (0,94 versus 1,26 versus 3; p<0,001), número de vasos doentes (1 versus 2 versus 2; p<0,001), escore SYNTAX (The SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery -sinergia entre intervenção coronária percutânea com taxus e cirurgia cardíaca) (9 versus 14 versus 17,5; p<0,001) e duração da internação (2 versus 2 versus 3; p<0,001) também aumentaram de acordo com o tercil de IIS (tercil 1 versus tercil 2 versus tercil 3). O IIS foi um preditor independente de escore SYNTAX (ß: 0,232 [0,001 a 0,003]; p<0,001), extensão do dano miocárdico (ß: 0,152 [0 a 0,001]; p=0,005) e duração da internação (ß: 0,168 [0,0 a 0,001]; p=0,003). Conclusões: Este estudo demonstrou que o IIS, um índice hematológico simples, é um marcador melhor de carga aterosclerótica e internação mais longa do que fatores de risco bem conhecidos em pacientes com síndrome coronariana aguda de alto risco.

Our data show that sustained hypertensive patients have lower vitamin D levels than white coat hypertensive and normotensive individuals. White coat hypertensive patients without other cardiovascular risk factors have higher vitamin D levels than sustained hypertensive patients, suggesting that they have a lower cardiovascular risk.

Aim: Peripheral artery disease (PAD) is a manifestation of atherosclerosis with poor prognosis. It is generally complicated by vascular calcification, which is located either in the intima as patchy infiltrates; or circumferentially in the media, also known as medial arterial calcification (MAC). Obstructive PAD is reflected by low anklebrachial index (ABI ≤ 0.9), whereas MAC is revealed by high ABI (ABI > 1.4). Considering the increase in cardiovascular mortality at both ends of the ABI spectrum, this study aimed to explore the underlying pathology through cytokines with established prognostic significance; namely pentraxin-3(PTX3), high sensitivity C-reactive protein (hsCRP), copeptin, soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), NT-proBNP, and neopterin. Methods: We categorized 180 patients with previous multivessel coronary artery bypass grafting surgery into three groups based on their ABI measurements; 60 patients with ABI ≤ 0.9, 60 patients with ABI within 0.91 and 1.4 (normal ABI), and 60 patients with ABI > 1.4 constituted the “PAD,” “normal,” “MAC” groups, respectively. The circulating levels of the biochemical markers were determined. Results: In the PAD group, the cytokine levels with predominantly proatherogenic actions such as PTX3, hsCRP, copeptin, and sTREM-1 were increased and these cytokine levels declined as the ABI increased. In the MAC group, the cytokine concentrations with pleiotropic actions such as NT-proBNP and neopterin increased and; NT-proBNP and neopterin concentrations decreased as ABI decreased. The linear regression analysis revealed that neopterin ( β = 0.72), PTX3 ( β = −0.32), and copeptin ( β = −0.48) were independent predictors of ABI. Conclusions: These findings suggest that different inflammatory pathways influence the pathology at the opposing ends of the ABI spectrum. Consequently, we suggest that PTX3, copeptin, and neopterin are promising biomarkers for future research.

Objective:Galanin, a cotransmitter similar to neuropeptide Y (NPY), aggravates autonomic imbalance in systolic heart failure (HF) by attenuating vagal tonus after burst sympathetic activity. In animal HF models, galanin antagonists have improved cardiac function. To determine whether galanin is a promising therapeutic target in HF, we studied its concentrations in HF patients and evaluated its correlation with NPY, markers of humoral activity such as pro-BNP and copeptin, and echocardiographic parameters of HF severity.Methods:After recording demographic and echocardiographic characteristics of 87 individuals (57 HF patients and 30 control subjects), fasting serum concentrations of galanin, NPY, copeptin, and pro-BNP were determined.Results:Unlike pro-BNP, copeptin, and NPY, which were significantly elevated in HF patients (p<0.001, p<0.001, and p=0.001, respectively), galanin was similar in HF patients and control subjects (p=0.9). NPY correlated with the echocardiographic parameters of HF severity (r=–0.22, p=0.03 for EF; r=0.3, p=0.005 for Tei index of RV; r=–0.23, p=0.03 for TAPSE; and r=0.24, p=0.024 for E/e¢) and pro-BNP (r=0.22, p=0.046). NPY levels were also associated with beta blocker (BB) use, wherein BB significantly decreased NPY in both HF patients and control subjects. Galanin correlated with humoral biomarkers, pro-BNP and copeptin (r=0.39, p<0.001 and r=0.41, p<0.001, respectively). Although current smoking, BB therapy, pro-BNP, copeptin, and body mass index were associated with galanin in univariate analyses, the multiple linear regression model revealed that pro-BNP was the only significant determinant of galanin levels in HF patients.Conclusion:Our findings confirmed the role of NPY in autonomic balance and suggest that galanin is associated with the proadrenergic state, but its role in HF in humans remains unclear.

IntroductionEndothelial damage caused by high pressure applied for spasm relaxation during graft preparation is one of the most plausible theories explaining early graft failure.Aim of the studyWe aimed to demonstrate the extent of endothelial damage in saphenous vein grafts distended to different pressure levels by using immunohistochemical methods and in vitro tissue baths.Material and methodsSaphenous vein grafts (SVGs) of 25 patients who underwent isolated elective CABG surgery were used in this study. By using a specific mechanism, SVGs were distended to five different pressure levels for two minutes: 0 mmHg, 50 mmHg, 100 mmHg, 200 mmHg, 300 mmHg. In vitro tissue baths and immunohistochemical examinations were performed.ResultsNone of the grafts distended to 300 mmHg pressure were functional in the tissue bath system. The relaxation response to carbachol of SVGs distended to 0, 50, 100 and 200 mmHg was 97.87 ± 4.47%, 98.52 ± 3.95%, 93.78 ± 3.64%, and 30.87 ± 4.11%, respectively. There were no statistically significant differences in terms of relaxation responses between samples distended to 0, 50, and 100 mmHg (p = 0.490). The relaxation response of samples distended to 200 mmHg was significantly decreased (p = 0.021). The endothelia of samples distended to 0 mmHg were almost intact in CD31 staining. Endothelial cell loss occurred at all tested distension pressures at different degrees.Conclusion In vitro and immunohistochemical studies revealed that distending an SVG used for coronary artery bypass grafting with pressures of 100 mmHg or less results in less endothelial damage and increases graft patency.

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