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Thrombosed arteriovenous fistula for hemodialysis access is characterized by a marked inflammatory activity. Background. Thrombosis is the dominant cause of failure of arteriovenous fistulas for hemodialysis access. Vascular inflammation, an important pathologic change in various human vascular diseases, may be involved in the thrombotic process of arteriovenous fistulas. Methods. The inflammatory activities of 23 thrombosed and 13 nonthrombosed stenotic arteriovenous fistulas were compared by investigating the contents of macrophages and lymphocytes, and the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) using immunohistochemistry method. The expression of matrix metalloproteinase (MMP)-2 and MMP-9, which play important roles in thrombosis of human coronary artery, was also investigated. The immunoreaction results were characterized using a semiquantitative scoring system. Results. The macrophage and lymphocyte contents of the thrombosed group were abundant, and markedly greater than those of the nonthrombosed group ( P < 0.001 and P= 0.001, respectively). The infiltration of macrophages and neovasculature were spatially closely correlated. The expressions of VCAM-1, IL-6, and TNF-α, but not ICAM-1, were significantly higher in the thrombosed group ( P= 0.031, P= 0.010, P < 0.001, and P= 1.000, respectively). The expression of MMP-2 was not different in either groups ( P= 0. 344). Differential expression of MMP-9 by macrophages near the vascular lumen, but not those distant from the lumen, was observed in most thrombosed specimens. Conclusion. This study demonstrated that the thrombosed arteriovenous fistula was characterized by marked inflammation. We hypothesize that the preferential expression of MMP-9 at luminal edge may cause disruption of the anticoagulant endothelial barrier and contribute to luminal thrombosis of arteriovenous fistulas. [ABSTRACT FROM AUTHOR]

Objectives. Hyperuricaemia has been linked to atherosclerosis; however, there is limited evidence about its association with arterial stiffness and cardiac hypertrophy, which are associated with adverse cardiovascular outcomes. We studied the association of hyperuricaemia with an increased risk of arterial stiffness and cardiac hypertrophy in a population participating in a health-screening programme. [ABSTRACT FROM PUBLISHER]

Objective. The relation of gout and hyperuricaemia to cardiovascular diseases has been well documented. This study investigates the survival impact of both gout and hyperuricaemia. Methods. The subjects of this study comprised participants of a health screening programme conducted by the Chang Gung Memorial Hospital in Taiwan from 2000 to 2006. The status and causes of death were ascertained by the Taiwan National Death Registry 2000-07. Cox proportional hazard model was performed to examine the association. Results. Among 61 527 subjects, 1383 deaths (198 cardiovascular deaths) were identified, corresponding to a crude mortality rate of 4.86 deaths per 1000 person-years. Crude mortality rates were 4.50, 5.61 and 10.46 deaths per 1000 person-years for subjects with normouricaaemia, hyperuricaemia and gout, respectively. Compared with subjects with normouricaemia, the hazard ratios (HRs) of all-cause mortality were 1.46 (95% CI 1.12, 1.91) for individuals with gout and 1.07 (95% CI 0.94, 1.22) for those with hyperuricaemia, respectively, after adjustments were made for age, sex, component number of metabolic syndrome and proteinuria. The adjusted HRs of cardiovascular mortality were 1.97 (95% CI 1.08, 3.59) for individuals with gout and 1.08 (95% CI 0.78, 1.51) for those with hyperuricaemia. Moreover, the risk of all-cause or cardiovascular mortality for gout remained unchanged when limiting the data to those with an estimated glomerular filtration of >60 ml/min/1.73m2. Conclusion. This study demonstrates a link of gout, not hyperuricaemia, with a higher risk of death from all causes and cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Objective We studied the response of the superior vena cava (SVC) myocardial sleeve to atrial fibrillation (AF). Methods and results We examined adult male dogs without pacing (N=6) and after rapid atrial pacing (600 bpm) for 2 weeks (P2w; N=5) and 6-8 weeks (P6-8w; N=5). After pacing, the sleeve was increased in thickness (non-paced vs. either paced group, both P<0.05). This was associated with an increase in proliferative activity, which was higher in the P2w than the P6-8w animals (P < 0.05). In addition, collagen content increased, and the component cardiomyocytes become more unevenly oriented and shorter and narrower in shape (non-paced vs. either paced group, both P < 0.05). Pacing had different effects on connexin40 (Cx40) and Cx43 gap junctions. There was a 98% increase in Cx43 signal in P2w, and a 74% increase in P6-8w animals (non-paced vs. each paced group, both P < 0.05). In contrast, Cx40 signal decreased 47% in P2w but increased 44% in P6-8w animals (nonpaced vs. each paced group, both P < 0.05). Conclusions Rapid atrial pacing results in a specific pattern of remodeling of the canine SVC sleeve, including changes in size and shape, spatial orientation, and gap junction expression profile of the component cardiomyocytes. These changes may co-operatively affect the electrical properties and contribute to the formation and maintenance of the arrhythmogenic substrate of AF [ABSTRACT FROM AUTHOR]

We investigated the effect of nicotine on connexin43 (Cx43) expression and gap-junctional communication in human umbilical vein endothelial cells (HUVEC). We also evaluated whether the effect requires activation of acetyl choline receptors sensitive to nicotine (nAChRs) and is altered by statins. The results showed that expression of Cx43 protein is reduced by nicotine in a dose-dependent manner (6×10-4 M nicotine vs control, 33% reduction, p<0.01), though Cx43 mRNA is up-regulated (6×10-4 M nicotine vs control, 36% increase, p<0.01). Concomitantly, the communication function, determined by fluorescence recovery after photobleaching, is decreased (6×10-4 M nicotine vs control, 38% reduction, p<0.05). Such a down-regulation of Cx43 gap junctions by nicotine disappears in the presence of the nAChRs antagonist, dihydro-β-erythroidine, and protease inhibitors leupeptin plus N-acetyl-Leu-Leu-Norleu-al (ALLN). Similarly, the effect of nicotine is attenuated by statins, including fluvastatin, lovastatin, pravastatin, and simvastatin, even at the presence of mevalonate. We concluded that i) nicotine down-regulates Cx43 expression and gap-junctional communication in HUVEC via post-transcriptional modification, which involves enhancement of Cx43 proteolysis; ii) the effect of nicotine is mediated via activation of nAChRs; and iii) the effect of nicotine is attenuated by statins through mechanisms outside the hypolipidemic pathway. [ABSTRACT FROM AUTHOR]

Iliacus abscess is an extremely rare complication of percutaneous transfemoral artery catheterization. This is a report of a case of iliacus abscess and Acinetobacter baumanii sepsis following percutaneous transfemoral artery catheterization. After a 43-day course of intravenous antibiotics treatment and repeated drainage, clinical recovery was achieved, though without complete radiologic resolution. [ABSTRACT FROM AUTHOR]