Introduction HIV infection and certain antiretroviral therapy (ART) medications increase atherosclerotic cardiovascular disease risk, mediated, in part, through traditional cardiovascular disease risk factors.Methods and ResultsWe studied cardiovascular disease risk factor changes in the START (Strategic Timing of Antiretroviral Treatment) trial, a randomized study of immediate versus deferred ART initiation among HIV‐positive persons with CD4+ cell counts >500 cells/mm3. Mean change from baseline in risk factors and the incidence of comorbid conditions were compared between groups. The characteristics among 4685 HIV‐positive START trial participants include a median age of 36 years, a CD4 cell count of 651 cells/mm3, an HIV viral load of 12 759 copies/mL, a current smoking status of 32%, a median systolic/diastolic blood pressure of 120/76 mm Hg, and median levels of total cholesterol of 168 mg/dL, low‐density lipoprotein cholesterol of 102 mg/dL, and high‐density lipoprotein cholesterol of 41 mg/dL. Mean follow‐up was 3.0 years. The immediate and deferred ART groups spent 94% and 28% of follow‐up time taking ART, respectively. Compared with patients in the deferral group, patients in the immediate ART group had increased total cholesterol and low‐density lipoprotein cholesterol and higher use of lipid‐lowering therapy (1.2%; 95% CI, 0.1–2.2). Concurrent increases in high‐density lipoprotein cholesterol with immediate ART resulted in a 0.1 lower total cholesterol to high‐density lipoprotein cholesterol ratio (95% CI, 0.1–0.2). Immediate ART resulted in 2.3% less BP‐lowering therapy use (95% CI, 0.9–3.6), but there were no differences in new‐onset hypertension or diabetes mellitus.ConclusionsAmong HIV‐positive persons with preserved immunity, immediate ART led to increases in total cholesterol and low‐density lipoprotein cholesterol but also concurrent increases in high‐density lipoprotein cholesterol and decreased use of blood pressure medications. These opposing effects suggest that, in the short term, the net effect of early ART on traditional cardiovascular disease risk factors may be clinically insignificant."Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00867048.

Background: Adverse cardiovascular events after liver transplantation (LT) are relatively common and are a significant source of early mortality. Although new-onset systolic dysfunction after LT is a reported phenomenon, there is little data regarding its incidence, risk factors, and outcomes. Methods and Results: This single-center retrospective study included all adult patients from January 2002 to March 2015 with deceased-donor LT and available preoperative transthoracic echocardiograms (TTEs). In total, 1,760 patients were included in the study, 602 (34.2%) of whom had a postoperative TTE. The primary end point was development of new-onset cardiomyopathy, defined as a new left ventricular ejection fraction (LVEF) of <40% within 180 days of transplant. Sixty-nine (11.4%) of the patients who received post-LT TTE had a reduction in LVEF to <40% within 6 months. Clinical parameters of donor and recipient did not show significant impact on development of post-LT LV systolic dysfunction (LVSD). Presence of wall motion abnormalities (P = .004) on preoperative TTE was predictive of development of post-LT LVSD. These patients did not have longer hospitalizations, but they had worse survival. Conclusions: Post-LT LV systolic dysfunction occurs at higher rates than previously suspected and may develop more frequently in patients with underlying cardiac structural abnormalities, which appear to adversely affect post-LT survival.

Aims This study sought to evaluate the feasibility of a rapid deflation technique (RDT) after transradial catheterisation to achieve patent haemostasis and to assess whether this could reduce radial artery occlusion (RAO). Ensuring patent haemostasis is the most important factor in reducing RAO. The use of larger sheath sizes and antiplatelet and antithrombotic agents limits achieving patent haemostasis immediately after transradial intervention. Methods and results A feasibility assessment was first performed in 105 patients to assess whether RDT could be performed safely and consistently achieve patent haemostasis after transradial catheterisation. Prospective data were then collected on 201 patients who underwent either rapid or standard deflation technique and had RAO assessment at 24 hours. Acute coronary syndrome was the indication for transradial catheterisation in 62.7% of patients. Baseline patent haemostasis increased from 40% to 95% after RDT. RAO at 24 hours was seen in two (2.0%) patients in the RDT group and 15 (14.9%) in the standard deflation group (OR 0.117; 95% CI: 0.026 to 0.526, p=0.005). Other independent predictors of RAO included body surface area (OR 0.022; 95% CI: 0.002 to 0.273, p=0.003) and male sex (OR 0.298; 95% CI: 0.108 to 0.824, p=0.020). No significant difference was found in safety outcomes: need to re-inflate compression band (2% versus 1.8%) or haematoma (0% versus 0.9%). Conclusions Rapid deflation of the compression band after transradial catheterisation is a safe and effective method of achieving patent haemostasis that reduces RAO.

Heart failure is common and results in substantial morbidity and mortality. Current guidelinebased therapies for heart failure with reduced ejection fraction, including beta-blockers, angiotensin converting enzyme (ACE) inhibitors, and aldosterone antagonists aim to interrupt deleterious neurohormonal pathways and have shown significant success in reducing morbidity and mortality associated with heart failure. Continued efforts to further improve outcomes in patients with heart failure with reduced ejection fraction have led to the first new-in-class medications approved for heart failure since 2005, ivabradine and sacubitril/valsartan. Ivabradine targets the I f channels in the sinoatrial node of the heart, decreasing heart rate. Sacubitril/valsartan combines a neprilysin inhibitor that increases levels of beneficial vasodilatory peptides with an angiotensin receptor antagonist. On a background of previously approved, guideline-directed medical therapies for heart failure, these medications have shown improved clinical outcomes ranging from decreased hospitalizations in a select group of patients to a reduction in all-cause mortality across all pre-specified subgroups. In this review, we will discuss the previously established guideline-directed medical therapies for heart failure with reduced ejection fraction, the translational research that led to the development of these new therapies, and the results from the major clinical trials of ivabradine and sacubitril/valsartan.

Severe coronary artery calcification (CAC) increases the complexity of percutaneous coronary intervention (PCI) by inhibiting optimal stent expansion, leading to an increased risk of death, myocardial infarction, repeat revascularization, and stent thrombosis. Coronary atherectomy modifies and debulks calcified plaque to facilitate PCI. Although there is no clear consensus, and further studies are needed, the decision to perform atherectomy should be based upon the presence of fluoroscopic CAC or with the use of intravascular imaging. The management of CAC in the modern era relies on rotational and orbital atherectomy to prepare the lesion to facilitate stent delivery and optimal expansion. While the two technologies differ in equipment, technique, and mechanism of action, the available literature suggests similar efficacy and safety of the two systems, although head-to-head comparisons are limited. While rotational and orbital atherectomy have been shown to have excellent procedural success in terms of facilitating stent delivery, no system has been shown to reduce long-term major adverse cardiovascular events, although the definitive trial for orbital atherectomy has not been completed. Additional trials are needed to find the population who would derive the most benefit of atherectomy and to compare the two systems in a prospective manner.