Background Untreated HIV infection is associated with changes in blood lipids, inflammation, thrombotic activity, and increased risk for CVD. Methods We studied high-density lipoprotein particle (HDLp) concentrations and inflammatory (hsCRP, IL-6), endothelial activation (E-selectin, sICAM-1) and thrombotic (fibrinogen and D-dimer) biomarkers in 32 untreated HIV-infected and 29 uninfected persons. Differences in blood lipids and biomarkers by HIV status were examined before and after adjustment for: age, gender, race/ethnicity, smoking status, BMI, and hepatitis C. Results HIV-infected, versus uninfected, participants had lower HDLc (−26%) and total (−21%), large (−50%)and small HDLp (−20%; p≤0.01 for all), but not medium HDLp. A trend was present for higher total cholesterol (p=0.15) and triglycerides (p=0.11) with HIV infection. Levels of IL-6, sICAM-1 and D-dimer were 65–70% higher in HIV-infected participants (p≤0.02 for all). Covariate adjustment did not diminish these associations. For HIV-infected participants, total and small HDLp (respectively) tended to correlate inversely with levels of IL-6 (p=0.08 and p=0.02), sICAM-1 (p<0.01 for both) and D-dimer (p=0.03 and p<0.01). Conclusions Persons with untreated HIV infection have lower HDLp, primarily large and small HDLp, and higher IL-6, sICAM-1, and D-dimer levels, and the relationship of these markers with risk for HIV-mediated atherosclerotic risk requires further study.

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Membrane diffusion potentials induced by amphotericin B (AmB), amphotericin B methyl ester (AmE), N-fructosyl AmB (N FruAmB) and vacidin, an aromatic polyene antibiotic, in ergosterol- or cholesterol-containing egg yolk phosphatidylcholine large unilamellar vesicles (LUV), were measured in various media, in order to determine the relative selectivity of Na+, K+, Cl- and other ions in these environments. Changes in the membrane potential were followed by fluorescence changes of 3,3'-dipropylthiadicarbocyanine (diS-C3-(5)). Subtle changes in intercationic selectivity were monitored by measuring biionic potentials, using the fluorescent pH sensitive probe pyranine. In all the cases studied, the intercationic selectivity of the permeability pathways induced by the four antibiotics was weak compared to that of specific biological channels, though distinct differences were noted. With AmB the selectivity appeared to be concentration dependent. Above 5 x 10(-7) M, the sequence determined for sterol-free small unilamellar vesicles (SUV) and cholesterol-containing SUV and LUV, Na+ > K+ > Rb+ > or = Cs+ > Li+ (sulfate salts), corresponded closely to Eisenman selectivity sequence number VII. At 5 x 10(-7) M and below the selectivity switched from Na+ > K+ to K+ > Na+. In contrast, Li+ was the most permeant ion for AmB channels in the presence of ergosterol. The selectivity between Na+ or K+ vs. Cl- varied with the antibiotic. It was very strong with vacidin at concentrations below 5 x 10(-7) M, smaller with AmB, nil with AmE and N FruAmB. The selectivities observed were antibiotic, concentration and time dependent, which confirms the existence of different types of channels.

We describe a case of Staphylococcus lugdunensis pulmonary valve endocarditis in a 65-year-old woman on chronic hemodialysis and provide a review of previously reported cases. The patient presented with fever and altered mental status, but had no other localizing symptoms or signs; coagulase-negative staphylococcus (subsequently identified as S. lugdunensis) was isolated from two sets of blood cultures. Transthoracic and transesophageal echocardiograms showed a large (2.3 × 3.1 cm) vegetation on the pulmonary valve with moderate valvular insufficiency. The patient was treated with 6 weeks of antibiotic therapy and is stable 4 months following the completion of therapy; no surgical intervention was performed. Of the 28 previously reported cases of S. lugdunensis endocarditis, only 1 had previously survived with medical therapy alone. This is the 3rd case report of S. lugdunensis endocarditis in a patient on hemodialysis; the presumed portal of entry in this and previously reported cases was the vascular access device. Endocarditis due to this organism is characterized by a high mortality, rapid tissue destruction, and a predilection for native valves. Because the clinical outcome is much more favorable with valvular replacement, speciation of the organism assumes great importance in defining the therapeutic approach.

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Background Metabolic syndrome (MS) is a well-known risk factor for the development of cardiovascular (CV) disease, yet controversy persists whether it adds incremental prognostic value in patients with established CV disease. Objectives This study was performed to determine if MS is associated with worse CV outcomes in patients with established CV disease treated intensively with statins. Methods We performed a post hoc analysis of the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes) trial, in which patients with established CV disease and atherogenic dyslipidemia (n=3,414) were randomly assigned to receive extended-release niacin (ERN) or placebo during a mean 36 month follow-up, to assess whether the presence of MS or the number of MS components contributed to CV outcomes. Results The composite primary endpoint of CV events occurred in 15.1% of patients without MS versus 13.8%, 16.9% and 16.8 of patients with MS in the subsets with 3, 4 and 5 MS components respectively (corresponding adjusted hazard ratios 0.9, 1.1 and 1.1 relative to patients without MS), P=0.55. Comparing subgroups with 3 versus 4 or 5 MS components, there was no significant difference in either the composite primary endpoint or secondary endpoints. Patients with diabetes mellitus had higher event rates, with or without presence of MS. Conclusions The presence of MS was not associated with worse CV outcomes in the AIM-HIGH population. The rate of CV events in statin-treated AIM-HIGH patients with MS was not significantly influenced by the number of MS components.

Background Approximately 400,000 people who smoke cigarettes survive Acute Coronary Syndrome (ACS; unstable angina, ST and non-ST elevation myocardial infarction) each year in the US. Continued smoking following ACS is an independent predictor of mortality. Depressed mood post-ACS is also predictive of mortality, and smokers with depressed mood are less likely to abstain from smoking following an ACS. A single, integrated treatment targeting depressed mood and smoking could be effective in reducing post-ACS mortality. Method/design The overall aim of the current study is to conduct a fully powered efficacy trial enrolling 324 smokers with ACS and randomizing them to 12 weeks of an integrated smoking cessation and mood management treatment [Behavioral Activation Treatment for Cardiac Smokers (BAT-CS)] or control (smoking cessation and general health education). Both groups will be offered 8 weeks of the nicotine patch if medically cleared. Counseling in both arms will be provided by tobacco treatment specialists. Follow-up assessments will be conducted at end-of-treatment (12-weeks) and 6, 9, and 12 months after hospital discharge. We will track major adverse cardiac events and all-cause mortality for 36 months post-discharge. Primary outcomes are depressed mood and biochemically validated 7-day point prevalence abstinence from smoking over 12 months. Discussion Results of this study will inform smoking cessation treatments post-ACS and provide unique data on the impact of depressed mood on success of post-ACS health behavior change attempts. Trial registration ClinicalTrials.gov, NCT03413423. Registered 29 January 2018. https://beta.clinicaltrials.gov/study/NCT03413423.

Mini‐Abstract Aorto‐right atrial fistula (A‐RAF) is a rare condition that has been reported as a postsurgical complication following cardiac surgery. Diagnosing A‐RAF can be challenging, and requires a high index of suspicion. In our patient, following surgical myectomy for hypertrophic cardiomyopathy, aortic dissection occurred at the aortotomy site that was then contained by postsurgical adhesions, leading to formation of A‐RAF.