Inflammatory bowel disease patients have an increased risk of early atherosclerosis as shown by greater values of cIMT, carotid artery stiffness, Hyc, hsCRP, and insulin resistance.
SUMMARYThe pathophysiology of cardiac syndrome X (CSX) is still unclear, but most patients with CSX have endothelial dysfunction. It has been shown that adropin uniquely effects the regulation of endothelial function. The purpose of the study was to evaluate the role of adropin in CSX. Eighty-six consecutive cardiac syndrome X-diagnosed patients and 86 age-sex matched healthy subjects were enrolled into the study. Serum adropin levels, nitrite/nitrate levels were measured in each subject. The adropin levels were significantly lower in patients with CSX than healthy subjects (1.7 AE 0.8 ng/mL and 3.4 AE 1.8 ng/mL, respectively; P < 0.001). The BMI values of patients with CSX were significantly higher than control subjects (28.1 AE 2.4 kg/m 2 and 26.0 AE 3.7 kg/m 2 , respectively; P < 0.001). Plasma nitrite/ nitrate levels were lower in patients with CSX than control subjects (15.9 AE 1.6 lmol/L vs. 25.4 AE 2.8 lmol/L, respectively; P < 0.001), and they have a significantly positive correlation with plasma adropin levels (r = 0.463, P < 0.001). In the multiple linear regression analysis, nitrite/nitrate levels, BMI, and adropin were found to be independent risk factors for CSX. A ROC curve is used to identify the ability of adropin levels to predict the cardiac syndrome X. The area under the ROC curve was 0.854 for adropin levels (P = 0.0001). The sensitivity and specificity values of adropin levels were 90.7 and 70.9%, respectively (cutoff value 2.73). In conclusion, lower serum adropin levels were associated with CSX. Adropin is an independent risk factor for CSX.Patients with a normal coronary angiogram, effort-induced angina pectoris, positive exercise stress test, and/or positive single-photon emission computed tomography study are considered to have cardiac syndrome X (CSX) [1]. The long-term prognosis of patients with CSX appears to be good, but these patients have recurrent chest pain attacks, a situation that does increase the rate of morbidity. The pathogenesis of CSX is still unclear. Although endothelial dysfunction is regarded as one of the main underlying reasons for CSX, the pathophysiology seems to be more complex. Motz et al. [2] first showed the impaired coronary endothelial function in patients with CSX. Patients with CSX have increased resistance in coronary flow which is attributed to endothelial dysfunction in microcirculation [3]. The endothelium has very important roles in the control of vascular tone, including regulation of both vasodilatory substances such as nitric oxide and prostacycline, and vasoconstrictive substances such as endothelin-1 and angiotensin II [4]. An adequate balance between these vasoconstrictors and vasodilators is essential for maintaining vascular homeostasis. Nitric oxide synthesized from the amino acid L-Arginine by the endothelial nitric oxide-synthetase (eNOS) enzyme plays a key role in the regulation of vascular tone and also inhibits the activation of plaque and leukocytes and has an antiproliferative effect on smooth vascular muscle [4]. L-arginine and tetra...
Objective:The awareness, time in therapeutic range (TTR), and safety of warfarin therapy were investigated in the adult Turkish population.Methods:This multicenter prospective study includes 4987 patients using warfarin and involved regular international normalized ratio (INR) monitoring between January 1, 2014 and December 31, 2014. TTR was calculated according to F.R. Roosendaal’s algorithm. Awareness was evaluated based on the patients’ knowledge of warfarin’s affect and food–drug interactions.Results:The mean TTR of patients was 49.52±22.93%. The patients with hypertension (55.3%), coronary artery disease (23.2%), congestive heart failure (24.5%), or smoking habit (20.8%) had significantly lower TTR levels than the others. Of the total number of patients, 42.6% had a mechanical valve, 38.4% had non-valvular atrial fibrillation (AF), and 19% had other indications for warfarin. Patients with other indications had lower TTR levels than those with mechanical valve and non-valvular AF (p=0.018). Warfarin awareness decreased in higher age groups. The knowledge of warfarin’s food–drug interactions was 55%. People with higher warfarin awareness had higher TTR levels. Patients with ≤8 INR monitoring/year had lower TTR levels (46.4±25.3 vs. 51.1±21.3, respectively, p<0.001) and lower awareness (44.6% vs. 60.6%, p<0.001) than patients with ≥8 INR monitoring/year. In this study, 20.1% of the patients had a bleeding event (major bleeding 15.8%, minor bleeding 84.2%) within a year.Conclusion:Both the mean TTR ratios and awareness of the Turkish population on warfarin therapy were found to be low. It was thought that low TTR levels of the Turkish population may be caused by the low awareness of warfarin, warfarin’s food–drug interactions, and high rates of concomitant diseases. (Anatol J Cardiol 2016; 16: 595-600)
BackgroundIt was speculated that fatty tissue originated adipocytokines may play role in pathogenesis of atherosclerosis. These adipocytokines may alter vascular homeostasis by effecting endothelial cells, arterial smooth muscle cells and macrophages. Vaspin is a newly described member of adipocytokines family. We aimed to investigate whether plasma vaspin level has any predictive value in coronary artery disease (CAD).MethodsForty patients who have at least single vessel ≥ 70 % stenosis demostrated angiographically and 40 subjects with normal coronary anatomy were included to the study. The vaspin levels were measured from serum that is obtained by centrifigation of blood and stored at -20 oC by ELISA method. The length, weight and body mass index of patients were measured. Biochemical parameters including total cholesterol, low density lipoprotein, high density lipoprotein, creatinine, sodium, potassium, hemoglobine, uric acid and fasting glucose were also measured.ResultsBiochemical markers levels were similar in both groups. Serum vaspin levels were significantly lower in CAD patients than control group (respectively; 256 ± 219 pg/ml vs. 472 ( 564 pg/ml, P < 0.02). Beside this serum vaspin level was lower in control group with high systolic blood pressure.ConclusionSerum vaspin levels were found significantly lower in patients with CAD than age-matched subjects with normal coronary anatomy. Vaspin may be used as a predictor of CAD.KeywordsCoronary artery disease; Vaspin; Adipokine
The aim of this experimental animal study was to evaluate the effects of systemic propranolol on new bone formation in peri-implant bone defects. Material and Methods: Implant slots were created 4 mm long and 2.5 mm wide. After the titanium implants were placed in the sockets, 2 mm defects were created in the neck of the implants. Bone grafts were placed in these defects. Then the rats were randomly divided into three equal groups: control (n = 8), propranolol dose-1 (PRP-1) (n = 8), and propranolol dose-2 (PRP-2) (n = 8) groups. In the control group, the rats received no further treatment during the eight-week experimental period after the surgery. The rats in the PRP-1 and PRP-2 groups were given 5 mg/kg and 10 mg/kg propranolol, respectively, every three days for the eight-week experimental period after the surgery. At the end of the experimental period, the rats were euthanized. Blood serum was collected for biochemical analysis, and the implants and surrounding bone tissues were used for the histological analysis. Results: There were no significant differences in the histological analysis results and the biochemical parameters (alkaline phosphatase, calcium, creatinine and phosphorus) of the groups (P > 0.05). Also, in the test groups, there was numerically but not statistically more new bone formation detected compared with the controls. Conclusions: Within the limitations of this study, propranolol did not affect the new bone formation in peri-implant defects.
Percutaneous coronary intervention-related periprocedural myocardial infarction (PCI-RPMI) has now been definitively linked in large data sets to long-term adverse outcomes. It is more likely that the relationship is caused by the underlying predisposing factors that led to the PCI-RPMI, such as plaque vulnerability. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved in multiple phases of vascular dysfunction, including atherosclerotic plaque formation and/or vulnerability. The purpose of this study was to determine whether soluble LOX-1 (sLOX-1) is associated with myocardial necrosis in elective native single-vessel PCI (NSV-PCI). From January 2010 to January 2012, 214 consecutive stable patients undergoing elective NSV-PCI were enrolled. Troponin T, CK and CK-MB were performed to screen for PCI-induced myocardial necrosis after the procedure, and PCI-RPMI was defined as three times the ULN of CK, which was confirmed by the elevation of the CK-MB and troponin T. According to the cardiac biomarkers result, patients were divided into two groups [PCI-RPMI(+) and PCI-RPMI(-)]. sLOX-1 levels were measured in serum by ELISA. Of the 214 patients who underwent NSV-PCI, 33 (15.4 %) patients developed PCI-RPMI. The results of this study showed that among patients undergoing elective NSV-PCI, those with PCI-RPMI had significantly higher circulating sLOX-1 levels than those without (167 ± 89 vs. 99 ± 68 pg/mL; p < 0 0.001). There were high correlations between sLOX-1 levels and CK and CK-MB values (r = 0.677 and r = 0.682, respectively; p < 0.001). Our study demonstrated that circulating sLOX-1 levels were associated with PCI-RPMI, which might predict periprocedural myocardial necrosis in elective NSV-PCI. Importantly, the study speculates that the level of sLOX-1 may help to identify patients at risk for PCI-RPMI before the procedure. sLOX-1 may provide new insights into not only risk stratification, but also therapeutic strategies for elective PCI.
Our study demonstrated that serum-soluble LOX-1 levels were associated with proximal/mid segment of the LAD lesions. Furthermore, this study suggested soluble LOX-1 might be a useful biomarker of coronary plaque vulnerability in patients with stable CAD. Soluble LOX-1, the novel biochemical marker, may provide new insights into not only risk stratification but also therapeutic strategy for CAD.
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