Search

BackgroundSeveral clinical and laboratory variables have an impact on the prognosis of STEMI patients undergoing PPCI; however, little is known about the role of ongoing DAPT at the time of the event and the smoking status as prognostic factors affecting the outcome of these patients.Methods and ResultsSeven-hundred and thirteen consecutive STEMI patients undergoing PPCI, admitted to the S. Anna and S. Sebastiano Hospital (Caserta, Italy) and to the OLV Clinic (Aalst, Belgium), between March 2009 and December 2011, were retrospectively enrolled. Rescue PCI was the only exclusion criterion. Primary end-point was the combination of death for all causes, re-infarction, stroke, and target lesion revascularization (TLR). Patients already on DAPT at admission (26.4%) showed a significant increase in the event rate at univariate analysis (HR 2.34, CI 1.62-3.75, P1 were more frequently present than in patients not on DAPT), Cox regression analysis confirmed that both DAPT (HR 1.74, 95%CI 1.20-2.53, P

Background: Proximal optimization technique (POT) has been proposed to adapt the conventional drug-eluting stent (DES) with the fractal anatomy of the bifurcation. However, only few DES are labeled for post-expansion beyond 5.0 mm. Furthermore, recrossing in the side branch (SB) through the main vessel (MV) stent cells may be challenging. Objectives: To compare the sirolimus-eluting, balloon-expandable dedicated bifurcation stent BiOSS LIM DES versus the second generation DES in the treatment of distal unprotected left main coronary arteries (ULMCAs) lesions. Methods: Forty-two consecutive patients with distal ULMCA lesions were treated with the BiOSS LIM (BiOSS LIM group) in our center. A matched-group of patients treated with second-generation DES was selected from our database (Control group). The primary endpoint was the procedural complication rate, including (a) SB occlusion, defined as intraprocedural TIMI flow grade

During the past few years, a new and attractive approach--transcatheter aortic valve implantation (TAVI)--has been developed for patients who are symptomatic of aortic stenosis and, due to the high expected operative risk, would not be otherwise treated. Unfortunately, TAVI can result in endocarditis of the percutaneously implanted valve that may present atypically and cause delays in diagnosis and treatment. Herein, the case is described of a 79-year-old female affected by endocarditis on aortic valve percutaneously implanted caused by Enterococcus faecium, complicated by iatrogenic pancytopenia and subacute disseminated intravascular coagulation, that proved fatal at six months after TAVI. During the past few years, a new and attractive approach--transcatheter aortic valve implantation (TAVI)--has been developed for patients who are symptomatic of aortic stenosis and, due to the high expected operative risk, would not be otherwise treated. Unfortunately, TAVI can result in endocarditis of the percutaneously implanted valve that may present atypically and cause delays in diagnosis and treatment. Herein, the case is described of a 79-year-old female affected by endocarditis on aortic valve percutaneously implanted caused by Enterococcus faecium, complicated by iatrogenic pancytopenia and subacute disseminated intravascular coagulation, that proved fatal at six months after TAVI.

Cholesterol deposition plays a central role in atherogenesis. The accumulation of lipid material is the result of an imbalance between the influx and efflux of cholesterol within the arterial wall. High levels of plasma low-density lipoprotein-cholesterol are considered the major mechanism responsible for the influx and accumulation of cholesterol in the arterial wall, while high-density lipoprotein (HDL)- cholesterol seems responsible for its efflux. The mechanism by which cholesterol is removed from extra-hepatic organs and delivered to the liver for its catabolism and excretion is called reverse cholesterol transport (RCT). Epidemiological evidence has associated high levels of HDL-cholesterol/ApoA-I with protection against atherosclerotic disease, but the ultimate mechanism(s) responsible for the beneficial effect is not well established. HDLs are synthesized by the liver and small intestine and released to the circulation as a lipid-poor HDL (nascent HDL), mostly formed by ApoA-I and phospholipids. Through their metabolic maturation, HDLs interact with the ABCA1 receptor in the macrophage surface increasing their lipid content by taking phospholipids and cholesterol from macrophages becoming mature HDL. The cholesterol of the HDLs is transported to the liver, via the scavenger receptor class B, type I, for further metabolization and excretion to the intestines in the form of bile acids and cholesterol, completing the process of RCT. It is clear that an inherited mutation or acquired abnormality in any of the key players in RCT mat affect the atherosclerotic process.