Oral apthous ulcers and skin lesions are the primary symptoms of Behcet's disease (BD). To date, there is no study to investigate possible associations between these lesions and endothelial functions. We have hypothesized that active BD period with oral and skin lesions might have more deteriorating effect on endothelial functions. Thirty-five patients with BD were registered for the study. Each subject was evaluated two times in both active and inactive disease periods. The subject with at least 30 days of lesion-free period was regarded in the inactive disease period, and the subject with any oral and/or skin lesions was regarded in the active disease period. For the control group, 35 healthy age- and sex-matched subjects were registered. In each subject, flow-mediated dilation (FMD) of the brachial artery after transient ischemia was evaluated in both active and inactive disease periods. High-sensitivity C-reactive protein (hsCRP) values (3.30 +/- 5.76 vs 14.19 +/- 13.55 vs 1.82 +/- 1.31, P < 0.001) and FMD values (13.89 +/- 5.57 vs 8.53 +/- 4.78 vs 15.83 +/- 5.29, P < 0.001) were significantly different among the BD patients in inactive and active disease periods and among control subjects. FMD values in inactive and active disease periods modestly correlated to hsCRP and low-density lipoprotein cholesterol values. Brachial FMD is more prominently impaired in BD patients within the active disease period. BD patients are possibly more vulnerable to cardiovascular manifestations when they are in the active disease period.
Objective: The aim of this study was to investigate the factors associated with coronary stent restenosis and if there is an association between plasma asymmetric dimethylarginine (ADMA) levels and stent restenosis. Methods: Ninety-one patients, who had a history of coronary bare metal stent implantation due to any cause in the last one year period, were admitted to this observational cross-sectional study. Coronary angiography was performed to all patients and quantitative angiography was used to determine the presence of stent restenosis. Laboratory parameters and angiographic features that contribute to stent restenosis were evaluated. Plasma ADMA levels were measured by using high performance liquid chromatography. Logistic regression analysis was used to determine the independent factors of stent restenosis. Results: Angiographic restenosis was found in 35 patients (38.5%). Stent diameter (p=0.038) and left ventricular ejection fraction (p=0.023) were lower and stent implantation history due to acute coronary syndrome (p=0.029), plasma ADMA level (5.0±1.8x10 -4 mmol/L vs. 3.9±1.0x10 -4 mmol/L, p=0.001), C-reactive protein concentration (p=0.016), white blood cell count (p=0.044) and stent length (p=0.005) were higher in patients with restenosis. Plasma ADMA level (β=0.536; OR: 1.710; CI: 1.022-2.861; p=0.041), C-reactive protein concentration (β=0.062; OR: 1.064; CI: 1.003-1.129; p=0.041), stent diameter (β=-3.047; OR: 0.048; CI: 0.007-0.313; p=0.002) and length (β=0.165; OR: 1.179; CI: 1.036-1.343; p=0.013) were found to be the independent predictors of stent restenosis in logistic regression analysis. Conclusion: We conclude that plasma ADMA levels may be used as a novel marker for stent restenosis beyond the classic stent restenosis markers. (Anadolu Kardiyol Derg 2014; 14: 491-7)
In this study, we aimed to assess the factors associated with laboratory-defined aspirin resistance and the relationship of this laboratory-defined aspirin resistance with thrombolysis in myocardial infarction risk score, markers of cardiac necrosis, and inflammatory and thrombotic risk factors in patients with unstable angina or non-ST elevation myocardial infarction. Ninety-seven patients who were under aspirin therapy and hospitalized with unstable angina/non-ST elevation myocardial infarction were included in the study. Laboratory-defined aspirin sensitive and resistant groups were determined by platelet function analyzer; aspirin resistance was defined as collagen/epinephrine closure time less than 165 s. Laboratory-defined aspirin resistance was noted in 29 patients (29.9%), and non-ST elevation myocardial infarction was observed in 46 patients (47.4%). Patients in the group with laboratory-defined aspirin resistance had significantly higher thrombolysis in myocardial infarction risk scores (P < 0.001). When the details of cardiac myonecrosis markers were compared, baseline and follow-up creatine kinase-myocardial band and troponin I values were higher in laboratory-defined aspirin-resistant group. Multivariate analyses revealed that laboratory-defined aspirin resistance was an independent predictor of non-ST elevation myocardial infarction (P = 0.022). Laboratory-defined aspirin resistance is associated with non-ST elevation myocardial infarction, higher markers of cardiac necrosis and thrombolysis in myocardial infarction risk score in patients hospitalized with unstable angina/non-ST elevation myocardial infarction.
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