PTA as the first choice revascularisation procedure is feasible, safe and effective for limb salvage in a high percentage of diabetic patients. Clinical restenosis was an infrequent event and PTA could successfully be repeated in most cases.
Our data show that the incidence of sudden death in haemodialysis patients is high and that atrial fibrillation, diabetes, hyperkalaemia, haemodialysis mode and C-reactive protein play an important role in developing fatal arrhythmia. Further studies will be necessary to define which interventions could be helpful in reducing this cause of mortality.
Lung Ultrasound Score (LUSS) is a useful tool for lung aeration assessment but presents two theoretical limitations. First, standard LUSS is based on longitudinal scan and detection of number/coalescence of B lines. In the longitudinal scan pleura visualization is limited by intercostal space width. Moreover, coalescence of B lines to define severe loss of aeration is not suitable for non-homogeneous lung pathologies where focal coalescence is possible. We therefore compared longitudinal vs. transversal scan and also cLUSS (standard coalescence-based LUSS) vs. qLUSS (quantitative LUSS based on % of involved pleura). 38 ICU patients were examined in 12 thoracic areas in longitudinal and transversal scan. B lines (number, coalescence), subpleural consolidations (SP), pleural length and pleural involvement (> or ≤ 50 %) were assessed. cLUSS and qLUSS were computed in longitudinal and transversal scan. Transversal scan visualized wider (3.9 [IQR 3.8 - 3.9] vs 2.0 [1.6 - 2.5] cm, p< 0.0001) and more constant (variance 0.02 vs 0.34 cm, p < 0.0001) pleural length, more B lines (70 vs 59 % of scans, p < 0.0001), coalescence (39 vs 28 %, p < 0.0001) and SP (22 vs 14 %, p < 0.0001) compared to longitudinal scan. Pleural involvement > 50 % was observed in 17 % and coalescence in 33 % of cases. Focal coalescence accounted for 52 % of cases of coalescence. qLUSS-transv generated a different distribution of aeration scores compared to cLUSS-long (p < 0.0001). In unselected ICU patients, variability of pleural length in longitudinal scans is high and focal coalescence is frequent. Transversal scan and quantification of pleural involvement are simple measures to overcome these limitations of LUSS.
MicroRNAs play an important role in myocardial diseases. MiR-133a regulates cardiac hypertrophy, while miR-29b is involved in cardiac fibrosis. The aim of this study was to evaluate whether miR-133a and miR-29b play a role in myocardial fibrosis caused by Angiotensin II (Ang II)-dependent hypertension. Sprague-Dawley rats were treated for 4 weeks with Ang II (200 ng/kg/min) or Ang II + irbesartan (50 mg/kg/day in drinking water), or saline by osmotic minipumps. At the end of the experimental period, cardiac miR-133a and miR-29b expression was measured by real-time PCR, and myocardial fibrosis was evaluated by morphometric analysis. A computer-based prediction algorithm led to the identification of collagen 1a1 (Col1A1) as a putative target of miR-133a. A reporter plasmid bearing the 3'-untranslated regions (UTRs) of Col1A1 mRNA was constructed and luciferase assay was performed. MiR-133a suppressed the activity of luciferase when the reporter gene was linked to a 3'-UTR segment of Col1A1 (P < 0.01). Mutation of miR-133a binding sites in the 3'-UTR of Col1A1 mRNA abolished miR-133a-mediated repression of reporter gene activity, showing that Col1A1 is a real target of miR-133a. In vivo, Ang II caused an increase in systolic blood pressure (P < 0.0001, tail cuff) and myocardial fibrosis in presence of a decrease in miR-133a (P < 0.01) and miR-29b (P < 0.01), and an increase in Col1A1 expression (P < 0.01). These effects were abolished by Ang II administration + irbesartan. These data demonstrate a relationship between miR-133a and Col1A1, suggesting that myocardial fibrosis occurring in Ang II-dependent hypertension is regulated by the down-regulation of miR-133a and miR-29b through the modulation of Col1A1 expression.
In our population of HD patients with AF, the mortality is very high. OAT is not associated with increased mortality, while antiplatelet drugs are. OAT seems, on the contrary, associated with a better survival; however, it does not decrease the incidence of ischaemic stroke, whereas it increases the incidence of bleeding. Bleeding risk is lower in subjects in whom the INR is kept within the therapeutic range.
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