ABSTRACT
@#【Objective】To observe the levels of CD11b expressions in the surface of neutrophils in serum，and its correlation with left atrial diameter ，and to study the inflammatory mechanisms in atrial fibrillation（AF） patients. 【Methods】Clinical characteristics and blood samples of AF group and sinal rhythm group were collected. CD11b levels in the surface of neutrophils were examined by flow cytometry. Left atrial diameter was examined by echocardiography. 【Results】The AF group included 85 patients ：36 with paroxysmal AF；26 with persistent AF；23 with permanent AF. The sinal rhythm group includes 57 patients. PMN- CD11b levels were significantly higher in Af group than in sinal rhythm group（P＜0.01）. The left atrial diameter was larger in AF group than in sinal rhythm group（P＜0.01）. Multivariate analysis revealed that PMN-CD11b，left atrial diameter and Valvular heart disease were independent predictors of atrial fibrillation.【Conclusions】PMN- CD11b levels were elevated in paroxysmal AF when AF was present and in persistent， permanent AF patients，implying atrial fibrillation was closely related to inflammation；PMN-CD11b were correlated with left atrial diameter，inflammation might participate in the atrial structural remodeling in AF patients ；PMN-CD11b levels were elevated in AF patients with high risk thrombosis，inflammation might have some value to embolic risk stratification according to CHA2DS2-VASc score.
ABSTRACT
<p><b>BACKGROUND</b>Some studies have shown that serum resistin levels increase in hypertensive patients. Whether the increase of resistin is related to inflammatory or vascular endothelial function is still unknown. We investigated the relationship of increased resistin levels to inflammatory factors and circulating biomarkers of vascular endothelial function in hypertensive patients.</p><p><b>METHODS</b>One hundred and forty-four nondiabetic patients with new onset, hypertension were recruited. Blood pressure, blood glucose, insulin, resistin, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), von Willebrand factor (vWF), endothelin-1 (ET-1) and nitric oxide (NO) were measured. The homeostasis model assessment, insulin resistance index (HOMA-IR) was calculated. Patients were divided into two groups according to the median level of resistin. Cytokine levels and indicators of vascular endothelial function were compared. Multiple linear regression was used to determine factors influencing resistin.</p><p><b>RESULTS</b>Serum resistin ranged from 2.57 ng/ml to 20.18 ng/ml in hypertensive patients. High resistin group (> 8.36 ng/ml) had higher levels of TNF-α, IL-6, vWF and ET-1 but lower level of NO compared with low resistin group (P < 0.01). Resistin was positively correlated with body mass index, systolic blood pressure, HOMA-IR, low-density lipoprotein cholesterol, TNF-α and ET-1 but negatively correlated with NO (all P < 0.05). Multiple linear regression analysis revealed that HOMA-IR, TNF-α, NO and ET-1 are independent predictors of resistin with standardized regression coefficients of 0.625, 0.368, -0.260 and 0.222, respectively (all P < 0.01).</p><p><b>CONCLUSIONS</b>We conclude that higher resistin levels are associated with inflammatory activation and endothelial dysfunction, because patients with essential hypertension have increased TNF-α, IL-6, vWF and ET-1 and decreased NO. Moreover, the statistical association of resistin with TNF-α, NO and ET-1 suggests involvement of resistin in the progression of hypertension by influencing inflammation and endothelial function.</p>
Subject(s)
Humans , Endothelin-1 , Blood , Enzyme-Linked Immunosorbent Assay , Hypertension , Blood , Inflammation , Blood , Interleukin-6 , Blood , Resistin , Blood , Tumor Necrosis Factor-alpha , BloodABSTRACT
<p><b>BACKGROUND</b>It has been reported that osteopontin has an important role in cardiac fibrosis and remodeling. However, its direct mechanisms remain unclear. The purpose of this study was to investigate the role of angiotensin and aldosterone blockades in cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted (MI) rats.</p><p><b>METHODS</b>Fifty SD rats that survived 24 hours after ligating left anterior descending coronary artery were randomly divided into three groups: MI-saline group (n = 15, 5 ml/d), MI-perindopril group (n = 18, perindopril 2 mgxkg(-1)d(-1)) and MI-spironolacton (n = 17, spironolacton 20 mgxkg(-1)xd(-1)). A sham operation group (n = 15) was selected as non-infarcted control. At 6 weeks after treatment, hemodynamic pararmeters and left ventricular function were measured with catheterization, interstitial fibrosis infiltration and cardiomyocyte diameters were evaluated histologically. Myocardium osteopontin protein expression level in the non-infarcted myocardium was detected by Western blotting.</p><p><b>RESULTS</b>No osteopontin protein was detected in the myocardium of sham-operation rats. High levels of osteopontin protein expression were detected in the MI-saline rats, but the levels were suppressed in the MI-perindopril and MI-spironolacton rats at 6 weeks following MI (P < 0.01, respectively). Compared with the sham operation group, all rats in the MI group showed marked interstitial fibrosis infiltration in the non-infarction area, higher ventricular weight/body weight ratio, significantly increased cardiomyocyte diameter (P < 0.01, respectively), and developed significant systolic and diastolic dysfunction as indicated by decreased left ventricular systolic pressure (LVSP) and +/-dp/dt, as well as increased left ventricular end-diastolic pressure (LVEDP) (P < 0.01, respectively). Angiotensin and aldosterone blockades partly prevented cardiac fibrosis and systolic and diastolic dysfunction (P < 0.01, respectively).</p><p><b>CONCLUSION</b>Treatment with angiotensin and aldosterone blockades inhibits expression of osteopontin in the non-infarcted myocardium and prevents cardiac remodeling following MI.</p>