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The clinical outcomes after DES (Xience; Abbott Vascular) for infrapopliteal lesions were somewhat satisfactory at 1year but inferior to the previously reported outcomes, especially at 3years. Further data with long-term follow-up are needed.

The clinical outcomes after DES (Xience; Abbott Vascular) for infrapopliteal lesions were somewhat satisfactory at 1 year but inferior to the previously reported outcomes, especially at 3 years. Further data with long-term follow-up are needed.

To report the early and mid-term outcomes following open surgical conversion (OSC) after failed endovascular aortic repair (EVAR) using data from a multicentric registry.

A retrospective study was carried out on consecutive patients undergoing OSC after failed EVAR at eight tertiary vascular units from the same geographic area in the North-East of Italy, from April 2005 to November 2019. Study endpoints included early and follow-up outcomes.

144 consecutive patients were included in the study. Endoleaks were the most common indication for OSC (50.7%), with endograft infection (24.6%) and occlusion (21.9%) being the second most prevalent causes. The overall rate of 30-day all-cause mortality was 13.9% (n=20); 32 patients (22.2%) experienced at least one major complication. Mean length of stay (LoS) was 13 ± 12.7 days. On multivariate logistic regression, age (OR 1.09, 95% CI 1.01-1-19, p= .02), renal clamping time (OR 1.07, 95% CI 1.02-1.13, p= .01), and suprarenal/celiac clamping (OR 6.66, 95% CI 1.81-2 those whose aortic-cross clamp site was infrarenal (76%, 95% CI 59-97; p= .041). Using multivariate Cox Proportional Hazard, older age and emergency setting were independently associate with higher risk for overall 5 years mortality.

OSC after failed EVAR was associated with relatively high rates of early morbidity and mortality, particularly for emergency setting surgery. Endoleaks with secondary sac expansion were the main indication for OSC and suprarenal aortic cross-clamping was frequently required. Endograft infection and emergent treatment remained associated with poorer short-term and long-term survival.

OSC after failed EVAR was associated with relatively high rates of early morbidity and mortality, particularly for emergency setting surgery. Endoleaks with secondary sac expansion were the main indication for OSC and suprarenal aortic cross-clamping was frequently required. Endograft infection and emergent treatment remained associated with poorer short-term and long-term survival.

In women, preeclampsia has a known association with increased long-term cardiovascular morbidity and mortality. However, it is unknown whether it is associated with increased post-operative cardiovascular morbidity and mortality in women. We aimed to determine if preeclampsia is an independent risk factor for myocardial injury after non-cardiac surgery (MINS) and post-operative 30-day mortality.

This study was a large international multicentre cohort study of a representative sample of 40,004 patients recruited between August 2007 and November 2013. Participants were ≥45 years of age and underwent inpatient non-cardiac surgery. Within this cohort, our study examined women with a history of pregnancy. Using multivariable models, we explored the association between a history of pregnancy affected by preeclampsia and our primary outcome of MINS and secondary outcome of post-operative mortality within 30-days. MINS was defined as prognostically relevant myocardial injury due to ischemia that occurred during or within 30 days after non-cardiac surgery.

Analyses were restricted to the 13,902 participants with a history of pregnancy. Among these women, 976 (7.0%) had a history of preeclampsia. A history of preeclampsia was associated with an increased risk of MINS, with an adjusted hazard ratio of 1.26 (95% CI, 1.03-1.53; p=0.02). Preeclampsia was not significantly associated with 30-day mortality.

Preeclampsia is a risk factor for MINS and should be considered in the pre-operative cardiovascular risk assessment of women.

Preeclampsia is a risk factor for MINS and should be considered in the pre-operative cardiovascular risk assessment of women.Non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) are frequently used to treat pain, fever, and inflammation. selleck kinase inhibitor Historically, NSAIDs have been categorized as traditional NSAIDs and newer cyclooxygenase (COX)-2 inhibitors (coxibs). However, traditional NSAIDs also inhibit the COX-1 and COX-2 enzyme isoforms to a varying degree. This diversity of COX-1 and COX-2 selectivity within the class of traditional NSAIDs has proven clinically important with evidence accumulating on the cardiovascular risks associated with selective COX-2 inhibition. Thus, the relative COX-2 selectivity of traditional NSAIDs correlates with their cardiovascular risk profile, being more favorable for non-selective NSAIDs, such as naproxen and low-dose ibuprofen, and less favorable for more COX-2 selective agents, such as diclofenac. To enhance clinically relevant terminology, we advocate categorizing all non-aspirin NSAIDs- including traditional NSAIDs-according to their relative COX-1 and COX-2 selectivity as either (1) COX-1 inhibitors, (2) non-selective NSAIDs, or (3) COX-2 inhibitors. We further recommend subcategorizing COX-2 inhibitors as newer COX-2 inhibitors (coxibs) or older COX-2 inhibitors. Finally, we recommend also to examine the effects of the individual NSAIDs included in each of the proposed categories. Adhering to these recommendations will align future studies, advance interpretation of COX-specific adverse cardiovascular effects, and provide better guidance to clinicians prescribing NSAIDs.Fructose consumption has been linked with metabolic syndrome and obesity. Fructose-based sweeteners like high fructose corn syrup taste sweeter, improve food palatability, and are increasingly prevalent in our diet. The increase in fructose consumption precedes the rise in obesity and is a contributing driver to the obesity epidemic worldwide. The role of dietary fructose in obesity can be multifactorial by promoting visceral adiposity, hypertension, and insulin resistance. Interestingly, one emergent finding from human and animal studies is that dietary fructose promotes overfeeding. As the brain is a critical regulator of food intake, we reviewed the evidence that fructose can act in the brain and elucidated the major brain systems underlying fructose-induced overfeeding. We found that fructose acts on multiple interdependent brain systems to increase orexigenic drive and the incentive salience of food while decreasing the latency between food bouts and reducing cognitive control to disinhibit feeding. We concluded that the collective actions of fructose may promote feeding behavior by producing a hunger-like state in the brain.