A series of 113 osteochondromas were treated in our institution with a long-term follow-up. A retrospective study of the cases of solitary osteochondroma diagnosed and treated in our center from 1970 to 2002 was done. A diagnosis for clinical findings in 73% of the patients was made. The most frequent location was the distal femur. Six patients had a recurrence and in two patients the lesions became malignant and chondrosarcoma developed. Relapse of the exostosis is rare, occurring in an estimated 2% of the resections. The growth of an osteochondroma and/or the presence of pain in older patients suggest possible malignancy.

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was: is patient-prosthesis mismatch an independent risk factor for 30-day and mid-term overall mortality in adult patients undergoing aortic valve replacement (AVR)? Altogether, almost 400 papers were found using the reported search, of which 22 represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. The majority of the selected articles have focused their analysis on moderate mismatch defined mostly by the presence of an indexed effective orifice area (IEOA)0.65 cm(2)/m(2)) is an independent risk factor for 30-day or mid-term overall mortality for adult patients undergoing AVR. An exception could be represented by patients with poor ejection fraction, a condition that can make moderate mismatch a predictor of overall mortality after AVR. On the other hand, severe mismatch is a predictor of overall 30-day or mid-term mortality for patients undergoing AVR independently from the presence of poor ejection fraction. In conclusion, our review suggests that the condition of severe PPM should be always avoided, while the presence of moderate mismatch could be tolerated in patients with normal ejection fraction without any impact on overall survival.

Experimental evidence suggests a causal link between inflammation and VC that would change the clinical approach to prevention and treatment of VC. However, the molecular basis remains unclear and little is known about VC in humans treated with drugs targeting inflammatory cytokines. The effect of biologicals targeting TNF-α, RANKL, IL-6, and other inflammatory mediators on VC, in addition to the impact of dietary phosphate in patients with chronic systemic inflammation, requires study.

Vascular calcification (VC) is associated with increased cardiovascular mortality in aging, chronic kidney disease (CKD), type 2 diabetes mellitus (T2DM) and atherosclerosis. TNF-like weak inducer of apoptosis (TWEAK) recently emerged as a new biomarker for the diagnosis and prognosis of cardiovascular diseases. TWEAK binding to its functional receptor Fn14 was reported to promote several steps of atherosclerotic plaque progression. However, no information is currently available on the role of TWEAK/Fn14 on the development of medial calcification, which is highly prevalent in aging, CKD and T2DM. This study explored the involvement of TWEAK in human vascular smooth muscle cells (h-VSMCs) calcification in vitro. We report that TWEAK binding to Fn14 promotes inorganic phosphate-induced h-VSMCs calcification, favors h-VSMCs osteogenic transition, decreasing acta2 and myh11 and increasing bmp2 mRNA and tissue non-specific alkaline phosphatase (TNAP), and increases MMP9 activity. Blockade of the canonical NFκB pathway reduced by 80% TWEAK pro-calcific properties and decreased osteogenic transition, TNAP and MMP9 activity. Blockade of non-canonical NFκB signaling by a siRNA targeting RelB reduced by 20% TWEAK pro-calcific effects and decreased TWEAK-induced loss of h-VSMCs contractile phenotype and MMP9 activity, without modulating bmp2 mRNA or TNAP activity. Inhibition of ERK1/2 activation by a MAPK kinase inhibitor did not influence TWEAK pro-calcific properties. Our results suggest that TWEAK/Fn14 directly favors inorganic phosphate-induced h-VSMCs calcification by activation of both canonical and non-canonical NFκB pathways. Given the availability of neutralizing anti-TWEAK strategies, our study sheds light on the TWEAK/Fn14 axis as a novel therapeutic target in the prevention of VC.

A specific molecular marker panel composed by PKM, valine and pyruvate is shown here linked to cardiovascular risk.

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Patients suffering from mismatch were twice as likely to undergo reoperation for aortic bioprosthesis replacement for SVD than those without mismatch.