Despite significant advances in the management of heart failure (HF), further improvement in the outcome of this chronic and progressive disease is still considered a major unmet need. Recurrent hospitalizations due to decompensated HF frequently occur, resulting in increased morbidity and mortality rates. Past attempts at early detection of clinical deterioration were mainly based on monitoring of signs and symptoms of HF exacerbation, which have mostly given disappointing results. Extensive research of the pathophysiology of HF decompensation has indicated that hemodynamic alterations start days prior to clinical manifestation. Novel technologies aim to monitor these minute hemodynamic changes, allowing time for therapeutic interventions to prevent hemodynamic derangement and HF exacerbation. The latest noticeable advancements include assessment of lung fluid volume, wearable devices with integrated sensors, and microelectromechanical systems-based implantable devices for continuous measurement of cardiac filling pressures. This manuscript will review the rationale for monitoring HF patients and discuss previous and ongoing attempts to develop clinically meaningful monitoring devices to improve daily HF health care, with particular emphasis on the recent advances and clinical trials relevant to this evolving field.

Anticoagulants are a cornerstone of treatment in atrial fibrillation. Nowadays, direct oral anticoagulants (DOACs) are extensively used for this condition in developed countries. However, DOAC treatment may be inappropriate in certain patient populations, such as: patients with chronic kidney disease in whom DOAC concentrations may be dangerously elevated; frail elderly patients with an increased risk of falls; patients with significant drug–drug interactions (DDI) affecting either DOAC concentration or effect; patients at the extremes of body mass in whom an “abnormal” volume of distribution may result in inappropriate drug concentrations; patients with recurrent stroke reflecting an unusually high thromboembolic tendency; and, lastly, patients who experience major hemorrhage on an anticoagulant and in whom continued anticoagulation is deemed necessary. Herein we provide a fictional case-based approach to review the recommendations for the use of DOACs in these special patient populations.

Background/Objectives: Retinal vascular occlusions are a significant cause of visual impairment in older adults, resulting in ischemic retinal damage and sudden vision loss. This study evaluates the retinal, optic nerve head (ONH), and choroidal capillary networks in chronic and acute-on-chronic hypoxia compared to normal controls using optical coherence tomography angiography (OCT-A). Methods: We evaluated a prospective study including twenty patients in the hypoxic group (mean age 61.2 ± 10.2) in two phases, chronic hypoxia and acute-on-chronic hypoxia, and 21 control subjects (mean age 59 ± 9.4 years). All patients underwent a comprehensive eye examination, OCT, and OCT-A imaging. The data were analyzed using OCT-A analysis software (Zeiss OCT-A software 2.1.0.55513) and Fiji software (1.51a). Vascular density of the retina and ONH, choriocapillaries, and foveal avascular zone (FAZ) size were measured. Results: The superficial peripapillary vascular density was higher for the control group (0.387 ± 0.03) compared to the hypoxic patients with (0.383 ± 0.03) and without O2 supplementation (0.383 ± 0.03; p = 0.018). No retinal angiographic differences were identified between the two study groups. The ganglion cell layer (GCL) was thinner in the hypoxic group. Both hypoxic subgroups demonstrated denser choriocapillaries (mean 13,073 ± 1812 and 12,689 ± 1815, with and without O2 supplementation, respectively) compared to the control group (mean 9749 ± 2881, p < 0.001 for both groups). Hypoxic patients demonstrated increased area size of choriocapillaries (+O2 supplementation—mean 44,347 ± 10,563; −O2 supplementation—mean 46,984 ± 12,822) compared to the control group (mean 30,979 ± 9635; p < 0.01 and p < 0.001, respectively). Conclusions: Chronic and acute-on-chronic hypoxia did not affect the retinal vascular network, most probably due to the strong autoregulation of vascular function of the retina. However, compared to the control group, GCL, ONH vasculature density, and most choriocapillaries indices were significantly altered among hypoxic patients.

We present a case of bacterial endocarditis with both methicillin-sensitive and methicillin-resistant Staphylococcus aureus, which based on typing, originated from two distinct clones. Such a case may be misinterpreted by microbiology lab automation to be a monoclonal multi-drug resistant Staphylococcus aureus, while simple microbiology techniques will instantly reveal distinct clonality.