Compared with the extensive data on left‐sided infective endocarditis ( IE ), there is much less published information on the features and management of right‐sided IE . Right‐sided IE accounts for 5% to 10% of all IE cases, and compared with left‐sided IE , it is more often associated with intravenous drug use, intracardiac devices, and central venous catheters, all of which has become more prevalent over the past 20 years. In this manuscript on right‐sided IE we provide an up‐to‐date overview on the epidemiology, etiology, microbiology, potential locations of infection in the right heart, diagnosis, imaging, common complications, management, and prognosis. We present updated information on the treatment of pacemaker and device infections, infected fibrin sheaths that appear to be an easily missed source of infection after central line as well as pacemaker removal. We review current data on the AngioVac percutaneous aspiration device, which can obviate the need for surgery in patients with infected pacemaker leads and fibrin sheaths. We also focused on advanced diagnostic modalities, such as positron emission tomography/computed tomography. All of these are supported by specific case examples with detailed echocardiographic imaging from our experience.

Background Endothelial dysfunction contributes to cardiovascular disease in diabetes mellitus. Autophagy is a multistep mechanism for removal of damaged proteins and organelles from the cell. Under diabetic conditions, inadequate autophagy promotes cellular dysfunction and insulin resistance in non-vascular tissue. We hypothesized that impaired autophagy contributes to endothelial dysfunction in diabetes mellitus. Methods and Results We measured autophagy markers and endothelial nitric oxide synthase (eNOS) activation in freshly isolated endothelial cells from diabetic subjects (n=45) and non-diabetic controls (n=41). p62 levels were higher in cells from diabetics (34.2±3.6 vs. 20.0±1.6, P=0.001), indicating reduced autophagic flux. Bafilomycin inhibited insulin-induced activation of eNOS (−21±5% vs. 64±22%, P=0.003) in cells from controls, confirming that intact autophagy is necessary for eNOS signaling. In endothelial cells from diabetics, activation of autophagy with spermidine restored eNOS activation, suggesting that impaired autophagy contributes to endothelial dysfunction (P=0.01). Indicators of autophagy initiation including the number of LC3-bound puncta and beclin 1 expression were similar in diabetics and controls, whereas an autophagy terminal phase indicator, the lysosomal protein Lamp2a, was higher in diabetics. In endothelial cells under diabetic conditions, the beneficial effect of spermidine on eNOS activation was blocked by autophagy inhibitors bafilomycin or 3-methyladenine. Blocking the terminal stage of autophagy with bafilomycin increased p62 (P=0.01) in cells from diabetics to a lesser extent than in cells from controls (P=0.04), suggesting ongoing, but inadequate autophagic clearance. Conclusion Inadequate autophagy contributes to endothelial dysfunction in patients with diabetes and may be a target for therapy of diabetic vascular disease.