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BACKGROUND: In this study, we aimed to examine the telomerase activity and hTERT gene expression in patients with acute coronary syndrome (ACS) and those with stable coronary artery disease (SCAD) and compare the results to controls. Additionally, we compared overall mortality rates relative to the telomerase activity. METHODS: A total of 211 patients (78 ACS and 71 SCAD patients) were included in the study. The telomerase concentration was measured by ELISA and used to determine telomerase activity. The hTERT gene expression was determined by real-time PCR. RESULTS: The serum telomerase enzyme concentration was lower in ACS (36.61 ± 1.54) and SCAD (36.79 ± 1.57) when compared to the control group (37.03 ± 2.25). However, this difference did not reach statistical significance (p = 0.890). The hTERT gene expression acting in telomerase enzyme synthesis was 2.7-fold lower in ACS group (p = 0.070) and 2.2-fold lower in the SCAD group (p = 0.101) compared to the control group. Patients were followed for a median of 32 months (minimum: 0.1, maximum: 46.8). The serum telomerase concentrations in patients who died and those survived in the SCAD group (35.98 ± 2.02 vs 36.86 ± 1.52 ng/ml, respectively; p = 0.529) were similar to those in the ACS group (36.39 ± 1.08 vs 36.63 ± 1.60 ng/ml, respectively p = 0.993). CONCLUSIONS: In the current study, telomerase activity or hTERT expression was similar in patients with ACS, SCAD, and controls. Moreover, telomerase activity was not associated with all-cause mortality during the 32-month follow-up. [ABSTRACT FROM AUTHOR]

BACKGROUND: In this study, we aimed to examine the telomerase activity and hTERT gene expression in patients with acute coronary syndrome (ACS) and those with stable coronary artery disease (SCAD) and compare the results to controls. Additionally, we compared overall mortality rates relative to the telomerase activity. METHODS: A total of 211 patients (78 ACS and 71 SCAD patients) were included in the study. The telomerase concentration was measured by ELISA and used to determine telomerase activity. The hTERT gene expression was determined by real-time PCR. RESULTS: The serum telomerase enzyme concentration was lower in ACS (36.61 ± 1.54) and SCAD (36.79 ± 1.57) when compared to the control group (37.03 ± 2.25). However, this difference did not reach statistical significance (p = 0.890). The hTERT gene expression acting in telomerase enzyme synthesis was 2.7-fold lower in ACS group (p = 0.070) and 2.2-fold lower in the SCAD group (p = 0.101) compared to the control group. Patients were followed for a median of 32 months (minimum: 0.1, maximum: 46.8). The serum telomerase concentrations in patients who died and those survived in the SCAD group (35.98 ± 2.02 vs 36.86 ± 1.52 ng/ml, respectively; p = 0.529) were similar to those in the ACS group (36.39 ± 1.08 vs 36.63 ± 1.60 ng/ml, respectively p = 0.993). CONCLUSIONS: In the current study, telomerase activity or hTERT expression was similar in patients with ACS, SCAD, and controls. Moreover, telomerase activity was not associated with all-cause mortality during the 32-month follow-up (Tab. 3, Fig. 1, Ref. 29). [ABSTRACT FROM AUTHOR]

BACKGROUND: The relationship between epicardial adipose tissue and inflammatory events has been shown in many studies. Because it is an inflammatory process in coronary progression, it is aimed to examine the relationship between coronary artery disease progression and epicardial adipose tissue thickness. MATERIALS AND METHODS: Our research was conducted with 50 patients (33 men, 17 women) who underwent planned or emergency coronary angiography, by evaluating the coronary artery disease progression from the coronary angiography images together with the echocardiographic epicardial adipose tissue thickness measurement. Patients were examined in two groups according to their tissue thickness, 17 patients with less than 0.55 cm were defined as group 1 and 33 patients with ≥ 0.55 were determined as group 2. RESULTS: There was no significant difference between the groups in terms of gender, diabetes, age, hypertension. In addition, a significant relationship was found with epicardial adipose tissue thickness (> 0.5 cm), ejection fraction and smoking in the group with coronary progression. Patients without stenotic changes were found to be statistically significantly lower p < 0.005. CONCLUSION: An independent relationship was found between epicardial adipose tissue and coronary artery progression. In the light of these findings, it can be concluded that epicardial adipose tissue residue is effective in the development of coronary artery stenosis and calcific-atherosclerotic changes in the coronary arteries. In the light of the information obtained, a positive correlation was determined between epicardial adipose tissue thickness and coronary artery disease [ABSTRACT FROM AUTHOR]

Inflammation plays a critical role in atherosclerosis. This study examines the effects of ticagrelor and clopidogrel on inflammatory parameters, obtained from complete blood count (CBC) and biochemical measurements, in patients with acute coronary syndrome. One hundred acute coronary syndrome (ACS) patients were included in the study and grouped according to clopidogrel (n = 50) or ticagrelor (n = 50) usage as an anti-aggregant (with acetylsalicylic acid). All patients underwent percutaneous coronary intervention. On admission, at third- and sixth-month after ACS, white blood cell (WBC) count, neutrophil-to-lymphocyte ratio (NLR), monocyte-to-high-density lipoprotein ratio (MHR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) were calculated from the CBC and biochemical measurements. NLR, PLR, and SII were significantly lower in the ticagrelor group (p < 0.001, at 3rd and 6th month). Also, MHR was lower in the ticagrelor group (p < 0.05). Conversely, WBC count was higher in the ticagrelor group (p < 0.001). NLR, MHR, PLR, and SII levels were lower in ACS patients treating with ticagrelor. Ticagrelor may improve these inflammatory parameters in percutaneous coronary intervention (PCI)-treated ACS patients compared to clopidogrel. [ABSTRACT FROM AUTHOR]

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Aim: The association of metabolic abnormalities and polycystic ovarian syndrome (PCOS) has been documented, but few studies have focused on cardiovascular risk in these women. The aim of this study was to compare arterial stiffness by using the cardio‐ankle vascular index (CAVI) in PCOS women with controls, and to evaluate whether any clinical or laboratory variables had independent associations with it. Methods: A group of 160 women, matched for age and body mass index were recruited. Diagnosis of PCOS was made according to the Rotterdam criteria. Arterial stiffness using CAVI was evaluated in non‐obese young woman, with and without PCOS. Results: In the PCOS group (n = 80), 60 cases (75%) had findings of hyperandrogenism, 59 (73.8%) had ovulatory dysfunction, and 70 (87.5%) had an ultrasonographic appearance of polycystic ovaries. Women with PCOS had significantly higher mean CAVI values when compared to subjects without PCOS (5.78 ± 0.64 vs 5.28 ± 0.77, P < 0.001). Multiple regression analysis revealed that androgen excess was associated with increased arterial stiffness, independent of ovulatory dysfunction, polycystic ovaries, body mass index and age. Conclusion: This data suggests that vascular compliance is decreased in young women with PCOS. Androgen excess is independently associated with increased arterial stiffness. [ABSTRACT FROM AUTHOR]

Pulmonary embolism is a common cardiovascular emergency. In case of delayed diagnosis and treatment morbidity and mortality is high. In this report, we presented a case of pulmonary embolism without apparent risk factors, which was initially misdiagnosed as peri/myocarditis. [ABSTRACT FROM AUTHOR]

Background: Pulmonary hypertension (PH) can complicate the course of myeloproliferative neoplasms (MPNs). Echocardiography is a useful noninvasive screening test for PH in populations at risk. We aimed to investigate the echocardiographic evidence of PH and clinical characteristics of patients with MPNs.Methods: This study included 197 patients with MPNs (mean age, 59 ± 14 years; females, 53%; mean disease duration, 3.4 ± 2.8 years). Clinical and laboratory characteristics, including JAK2V617F mutation status, were obtained. All participants underwent a comprehensive transthoracic echocardiographic examination. The echocardiographic evidence of PH was defined as systolic pulmonary artery pressure (SPAP) ≥40 mm Hg.Results: Overall, 11 patients (5.5%) with SPAP ≥40 mm Hg had echocardiographic evidence of PH. Patients with myelofibrosis had echocardiographic evidence of PH more often than patients with other MPNs (p < 0.001). Disease duration since the diagnosis of MPNs was 6.7 ± 4.6 years in the PH group and 3.1 ± 2.5 years in the non-PH group (p < 0.001). There was a weak positive correlation between SPAP values and time since diagnosis (r = 0.236, p =0.001). JAK2V617F mutation was not associated with PH. In multivariate logistic regression analysis, the presence of myelofibrosis (odds ratio [OR]: 22.177, 95% CI: 4.480-109.790, p < 0.001), long disease duration (OR: 1.217, 95% CI: 1.024-1.447, p = 0.026), and high uric acid levels (OR: 1.868, 95% CI: 1.049-3.328, p = 0.034) were found to be related with the echocardiographic evidence of PH. Survival was worse in the PH group (p = 0.0001).Conclusion: Our results suggest that patients with myelofibrosis are more likely to develop PH than other MPNs patients. Disease duration may predict the development of PH in MPN patients. [ABSTRACT FROM AUTHOR]

Background/Aim: This study aimed to measure the DNA methylation state of thousands of CpG islands in the blood of two monozygotic twins that were discordant for cardiovascular disease (CVD). Twin 1 had suffered myocardial infarction, while the other was healthy. Patients and Methods: Since the aim of this study was to identify differentially methylated regions which might act as potential markers, reduced-representation bisulfite libraries were used for whole-genome methylation analysis. Results: According to the analysis, 11 genes lipid droplet associated hydrolase (LDAH), apolipoprotein B (APOB), acyl-CoA synthetase medium chain family member 2A (ACSM2A), acyl-CoA synthetase medium chain family member 5(ACSM5), acyl-CoA synthetase family member 3 (ACSF3), carboxylesterase 1 (CES1), carboxylesterase 1 pseudogene 1 (CES1P1), AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), iron-sulfur cluster assembly enzyme (ISCU), SEC14 like lipid binding 2 (SEC14L2) and microsomal triglyceride transfer protein (MTTP) were all hypomethylated in DNA from twin 2, the unaffected twin. Methylation changes were observed at different multiple loci between the twins, suggesting loci that are affected by disease status in identical genetic backgrounds. Conclusion: This twin study may contribute significantly to the understanding of the genetic basis of CVD and resulting myocardial infarction. This approach may allow identification of possible target loci associated with aberrant epigenetic regulation in CVD. [ABSTRACT FROM AUTHOR]