Measurement of epicardial fatty tissue thickness has a diagnostic value in lichen planus patients and is associated with fibrinogen to albumin ratio and neutrophil to lymphocyte ratio.

OBJECTIVE: Lichen planus (LP) is one of the chronic inflammatory diseases. Epicardial fatty tissue (EFT) is the adipose tissue in which pro-inflammatory and pro-atherogenic hormones and cytokines are secreted. We planned to investigate the predictive value of EFT in LP patients by evaluating together with Fibrinogen to albumin ratio (FAR) other inflammation markers. MATERIALS AND METHODS: A total of 53 consecutive LP patients and 57 healthy controls were enrolled in this single-center, prospective, case-control study. Demographic data were recorded; blood tests were obtained from both groups. Then, EFT thickness was measured by echocardiography. RESULTS: Fibrinogen, FAR, neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio, and EFT thickness were higher in LP patients (p < 0.05, for all). EFT was positively correlated with FAR (r = 0.306, p = 0.001), NLR (r = 0.240, p = 0.011), and PLR (r = 0.297, p = 0.002). ROC analysis indicated that FAR could predict LP with a sensitivity of 83 % and a specificity of 44 %; NLR could predict LP with a sensitivity of 80 % and a specificity of 46 %; EFT could predict LP with a sensitivity of 79 % and a specificity of 54 %. In the binary logistic regression analysis NLR, FAR, and EFT were found to be independent predictors of LP. CONCLUSION: We found a relationship between LP and FAR together with other inflammation parameters NLR, and PLR. We demonstrated for the first time that FAR, NLR and EFT were independent predictors of LP. Also, there was a significant relationship between these parameters and EFT (Tab. 4, Fig. 1, Ref. 30). Text in PDF www.elis.sk Keywords: lichen planus, epicardial fatty tissue, fibrinogen, albumin, neutrophil, lymphocyte.

[The association between cardiac mr feature tracking strain and myocardial late gadolinium enhancement in patients with hypertrophic cardiomyopathy].

Aim    Hypertrophic cardiomyopathy (HCM) is a relatively common, heritable cardiomyopathy, and cardiac magnetic resonance (CMR) studies have been performed previously to evaluate different aspects of the disease. However, a comprehensive study, including all four cardiac chambers and analysis of left atrial (LA) function, is missing in the literature. The aim of this retrospective study was to analyze CMR-feature tracking (CMR-FT) strain parameters and atrial function of HCM patients and to investigate the association of these parameters with the amount of myocardial late gadolinium enhancement (LGE).Material and Methods    In this retrospective, cross-sectional study, we analyzed the CMR images (CMRI) of 58 consecutive patients, who from February 2020 to September 2022 were diagnosed with HCM at our tertiary cardiovascular center. Patients who were younger than 18 yrs or who had moderate or severe valvular heart disease, significant coronary artery disease, previous myocardial infarction, suboptimal image quality, or with contraindication to CMR were excluded. CMRI was performed at 1.5 T with a scanner, and all scans were assessed by an experienced cardiologist and then re-assessed by an experienced radiologist. SSFP 2-, 3- and 4­chamber, short axis views were obtained and left ventricular (LV) end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF), and mass were measured. LGE images were obtained using a PSIR sequence. Native T1 and T2 mapping and post-contrast T1 map sequences were performed and each patient's myocardial extracellular volume (ECV) was calculated. LA volume index (LAVI), LA ejection fraction (LAEF), LA coupling index (LACI) were calculated. The complete CMR analysis of each patient was performed with CVI 42 software (Circle CVi, Calgary, Canada), off-line.Results    The patients were divided into two groups, HCM with LGE (n=37, 64 %) and HCM without LGE (n=21, 36 %). The average patient age in the HCM patients with LGE was 50.8±14 yrs and 47±12.9 yrs in the HCM patients without LGE. Maximum LV wall thickness and basal antero-septum thickness were significantly higher in the HCM with LGE group compared to the HCM without LGE group (14.8±3.5 mm vs 20.3±6.5 mm (p<0.001), 14.2±3.2 mm vs 17.3±6.1 mm (p=0.015), respectively). LGE was 21.9±31.7 g and 15.7±13.4 % in the HCM with LGE group. LA area (22.2±6.1 vs 28.8±11.2 cm2; p=0.015) and LAVI (28.9±10.2 vs 45.6±23.1; p-0.004) were significantly higher in the HCM with LGE group. LACI was doubled in the HCM with LGE group (0.2±0.1 vs 0.4±0.2; p<0.001). LA strain (30.4±13.2 vs 21.3±16.2; p-0.04) and LV strain (15.2±3 vs 12.2±4.5; p=0.012) were significantly decreased in the HCM with LGE group.Conclusion    This study sheds light on the CMR-FT differences between HCM with and without LGE. We found a greater burden of LA volume but significantly lower LA and LV strain in the LGE patients. These findings highlight further the LA and LV remodeling in HCM. Impaired LA function appears to have physiological significance, being associated with greater LGE. While our CMR-FT findings support the progressive nature of HCM, beginning with sarcomere dysfunction to eventual fibrosis, further studies are needed to validate these results in larger cohorts and to evaluate their clinical relevance.

Evaluation of serum sST2 and sCD40L values in patients with microvascular angina.

OBJECTIVES: Coronary microvascular dysfunction plays a major role in the pathogenesis of microvascular angina (MVA). Along with endothelial dysfunction, microvascular atherosclerosis and inflammation seem to contribute to the development of coronary microvascular dysfunction. Serum soluble ST2 (sST2) and serum soluble CD40 ligand (sCD40L) are two biomarkers associated with inflammation and atherosclerosis. The aim of this study was to investigate the role of these biomarkers in the pathogenesis of MVA and determine their possible association with coronary microvascular dysfunction. METHODS: A total of 152 patients were included in the study. Ninety-one patients with MVA {median age 56 years (40-79), of which 55 are women} and sixty-one controls {median age 52 (38-76), of which 29 are women} were included in the study. Serum concentration of sST2 and sCD40L were measured with a commercially available ELISA kit. RESULTS: Serum sST2 (median 13.6 ng/ml; interquartile range (IQR), 3.5-63.8 ng/ml vs median 10.6 ng/ml; IQR, 2.9-34.2 ng/ml, p < 0.0005) and sCD40L (median 5.3 ng/ml; IQR, 0.5-20.6 ng/ml vs median 2.2 ng/ml; IQR, 0.7-10.8 ng/ml, p < 0.0005) were significantly higher in patients with MVA compared to controls. Analysis of the associations between these biomarkers and potential contributors of MVA revealed that serum sST2 showed a positive correlation with LDL-cholesterol (r = 0.19, p = 0.016) and serum sCD40L concentrations correlated positively with hs-CRP (r = 0.22, p = 0.005). In logistic regression analysis, sCD40L and hs-CRP but not sST2 were found to be significantly associated with MVA. CONCLUSION: Higher serum concentrations of sST2 and sCD40L in MVA patients may be associated with inflammatory activation and coronary microvascular dysfunction. Larger studies are required for understanding their role in the pathogenesis of inflammatory and possibly fibrotic process in MVA patients.

Presepsin (sCD14-ST): could it be a novel marker for the diagnosis of ST elevation myocardial infarction?

INTRODUCTION: Acute myocardial infarction (AMI) could be considered to be a state of inflammation. Many inflammatory markers have been evaluated in the AMI setting so far. Presepsin (PSP) is a novel biomarker for diagnosis and prognosis of systemic inflammation that has not been studied in the AMI setting to date. In this study, we aimed to examine serum PSP levels in patients with acute ST elevation myocardial infarction (STEMI). MATERIAL AND METHODS: Forty-eight patients with STEMI and fifty healthy controls without coronary artery disease, verified by coronary angiography, were included in the study. Together with routine laboratory tests needed for STEMI, plasma concentrations of PSP were measured in peripheral venous blood samples of the participants. RESULTS: Plasma PSP and troponin levels were significantly higher in patients with STEMI than controls (1988.89 ±3101.55 vs. 914.22 ±911.35 pg/ml, p = 0.001 and 3.46 ±3.39 vs. 0.08 ±0.43 ng/ml, p = 0.001, respectively). The cut-off value for PSP of 447 pg/ml was found to detect STEMI with 87.5% sensitivity, 44% specificity, 60% positive predictive value and 78.5% negative predictive value. CONCLUSIONS: In this study, PSP levels were found to be significantly elevated in patients with STEMI together with high-sensitivity troponins. The PSP may be a new marker for AMI detection. Large scale studies are needed to reveal the importance of PSP in the diagnosis and prognosis of AMI.

[Relationship between serum level of CD40 ligand and persistent lone atrial fibrillation]. / Serum CD40 ligand düzeyi ile tek basina israrci atriyum fibrilasyonu iliskisi.

OBJECTIVE: Inflammation is thought to play a role in the pathogenesis of atrial fibrillation. The relationship between CD40 ligand (CD40L), a prothrombotic and proinflammatory molecule, and lone atrial fibrillation was presently investigated for the first time. Levels of serum CD40L were also tested, regarding potential to distinguish patients with lone atrial fibrillation from healthy individuals. METHODS: Presently included were 35 patients with lone persistent atrial fibrillation and a control group of 30 healthy individuals. Serum levels of CD40L and high-sensitive C-reactive protein (hs-CRP) were measured, and transthoracic echocardiography was performed. RESULTS: Mean serum CD40L, hs-CRP, left ventricular end-diastolic diameter, and left atrial diameter values were significantly higher in the group with lone persistent atrial fibrillation than in the control group (7.4±3.5 ng/mL vs 4.3±1.2 ng/mL, p<0.0001; 3.7±1.6 mg/L vs 1.7±0.8 mg/L, p<0.0001; 53.0±4.2 mm vs 46.0±3.8, p<0.0001; 43.5±3.5 mm vs 33.7±3.5, p<0.0001, respectively). Serum CD40L levels were positively correlated with left atrial diameter (r=0.81, p<0.0001) and hs-CRP (r=0.72, p<0.0001). Receiver operating characteristic curve analysis revealed that serum CD40L at the optimal cut-off level of >4.5 ng/mL successfully discriminated patients with lone atrial fibrillation from controls (area under the curve: 0.847; 95% confidence interval: 0.759-0.934; p<0.0001). CONCLUSION: The present findings suggest that CD40L levels play a crucial role in the development of lone atrial fibrillation. In addition, results support that regular clinical follow-up of these patients is necessary, due to increased cardiovascular disease risk, determined by elevated CD40L levels.

Diagnostic significance of serum galectin-3 levels in heart failure with preserved ejection fraction.

OBJECTIVE: Galectin-3, reflecting cardiac fibrosis, is a promising biomarker in early detection of heart failure with preserved ejection fraction (HFpEF). We aimed to clarify the clinical utility of galectin-3 levels in the diagnosis of HFpEF and to compare galectin-3 with N-terminal pro-brain-type natriuretic peptide (NT-proBNP) levels. METHODS AND RESULTS: The study included 44 HFpEF patients (mean age 60 ± 6.78 years, 24 men) and 38 control subjects (mean age 57 ± 8.98 years, 20 men). Galectin-3 and NT-proBNP levels were assessed by the ELISA kits. The receiver operating characteristics (ROC) curve was used to examine the diagnostic performance of galectin-3 and NT-proBNP in HFpEF. Galectin-3 and NT-proBNP levels were significantly increased in patients with HFpEF compared to controls [5.35 ng/ml (0.86 ­ 14.90) vs 0.51 ng/ml (0.15 ­ 1.71) P < 0.0001, 617.75 ± 271.30 pg/ml vs 66.35 ± 54.01 pg/ml P < 0.0001, respectively]. Galectin-3 correlated with NT-proBNP, left atrial volume index, left ventricular mass index, and E/E' (r = 0.90, P < 0.0001; r = 0.75, P = 0.0001; r = 0.86, P = 0.0001; r = 0.80, P = 0.0001; respectively). The area under the ROC curve was 0.98 for galectin-3 and 1.0 for NT-proBNP. CONCLUSIONS: Our results support that, in addition to NT-proBNP, galectin-3 is also a valuable biomarker for the diagnosis of patients with HFpEF.

Does Inflammation Have a Role in the Pathogenesis of Cardiac Syndrome X? A Genetic-Based Clinical Study With Assessment of Multiple Cytokine Levels.

We compared Turkish patients with cardiac syndrome X (CSX) and controls with respect to serum pro- and anti-inflammatory cytokine levels, as well as the single-nucleotide polymorphisms located in the promoter regions of their related genes. This study included 111 consecutive patients angiographically diagnosed with CSX and 111 healthy controls with similar demographic characteristics. Serum interleukin (IL) 6, tumor necrosis factor α (TNF-α), and IL-10 levels were measured, and the genotypes of the patients and controls were determined using standard methods. Serum IL-6 and IL-10 levels were significantly higher in the CSX group than in the control group (P < .01, respectively). Serum TNF-α level was lower in the CSX group than in the control group (P < .001). On the other hand, participants with CSX and healthy controls were not significantly different with respect to the genotype distributions of IL-6, TNF-α, and IL-10 genes. As a result of our study, both pro-inflammatory and anti-inflammatory cytokines may play a role in the pathogenesis of CSX. In contrast, the studied gene polymorphisms did not influence CSX pathogenesis.

Low vitamin D status associated with dilated cardiomyopathy.

In recent years, a growing body of evidence supports that vitamin D plays a crucial role in various cardiovascular diseases. Cardiac muscle cells have vitamin D receptors as well as calcitriol-dependent Ca(2+) binding protein. Therefore, the vitamin D may have an effect on cardiac function. In this research, we investigated the association between vitamin D status and dilated cardiomyopathy (DCMP). We compared serum 25-hydroxy-vitamin D3 (25OHD3) concentrations in 39 patients (mean age 50.4 ± 11.7 years, 15 women) with DCMP and in 35 healthy controls (mean age 54.6 ± 13.2 years, 17 women). Parathyroid hormone (PTH), calcium (Ca++), phosphorus, lipid profile, albumin and echocardiographic parameters (left-ventricular (LV) ejection fraction, LV fractional shortening, LV-end-diastolic and end-systolic dimensions) were measured in all study participants. The mean serum 25OHD3 concentrations in patients with the DCMP were significantly lower in compared to healthy controls (24.1 ± 10.4 ng/mL versus 41.4 ± 20.9 ng/mL, P < 0.0001). PTH concentrations were significantly higher in patients with DCMP in comparison with healthy controls (90.6 ± 29.8 pg/mL versus 49.1 ± 18 pg/mL, P < 0.0001). Additionally, we observed a significant negative correlation between 25OHD3 concentrations and PTH concentrations, LV end-diastolic dimensions, LV end-systolic dimensions (r = -0.66; P < 0.0001, r = -0.49; P < 0.0001, r = -0.50; P < 0.0001, respectively). Moreover, 25OHD3 was positively correlated with LV ejection fraction, LV fractional shortening, stroke volume, cardiac output, cardiac index (r = 0.46; P < 0.001, r = 0.44; P < 0.001, r = 0.25; P = 0.03, r = 0.37; P < 0.001, r = 0.25; P = 0.03; respectively). Our findings support that vitamin D has a potential role both in the development of DCMP and LV remodeling.

Serum concentrations of galectin-3 in patients with cardiac syndrome X.

OBJECTIVE: Microvascular dysfunction has been reported in cardiac syndrome X (CSX), even though the underlying mechanisms still remain uncertain. Galectin-3 has been recently recognized as a biomarker of cardiovascular fibrosis and inflammation. We sought to investigate the role of galectin-3 in the CSX. METHODS: We studied 115 consecutive CSX patients (mean age 55.43 ± 8.71 years, 36 men) and 74 healthy controls (mean age 54.53 ± 10.07 years, 31 men). Serum concentrations of galectin-3 and high-sensitive C-reactive protein (hs-CRP) were measured on the blood samples. RESULTS: Galectin-3 concentrations were significantly higher in patients with CSX compared to controls (0.90 ng/ml; IQR, 0.40-1.70 ng/ml vs 0.40 ng/ml; IQR, 0.36-0.44 ng/ml, p < 0.0001). Although, the prevalence of diabetes mellitus, hypertension and family history of coronary artery disease (CAD) were significantly higher among patients with CSX, following adjustment for diabetes mellitus, hypertension, and family history of CAD, serum galectin-3 concentrations were still found significantly increased in patients with CSX. Galectin-3 concentrations correlated positively with hs-CRP (r = 0.16, p = 0.03). In addition, concentrations of galectin-3, hs-CRP, fasting glucose, uric acid and family history of CAD were determined as independent predictors of the CSX. CONCLUSION: It was found that galectin-3 serum concentrations are higher in patients with CSX compared to healthy controls. Further studies on larger population are needed to confirm the relation between the fibrosis and the CSX, as well as to explore the potential role of galectin-3 in the CSX.