Beta-blockers are a class of drugs with important benefits in cardiovascular pathology. In this paper, we aim to highlight their adverse and therapeutic effects in the neuropsychiatric field. With respect to permeability, we would like to mention that most beta-blockers are lipophilic and can cross the blood–brain barrier. Observational studies show the presence of neuropsychiatric side effects when taking beta-blockers, and is the reason for which caution is recommended in their use in patients with depressive syndrome. From a therapeutic point of view, most current evidence is for the use of beta-blockers in migraine attacks, essential tremor, and akathisia. Beta-blockers appear to be effective in the treatment of aggressive behavior, beneficial in the prevention of posttraumatic stress syndrome and may play a role in the adjuvant treatment of obsessive–compulsive disorder, which is refractory to standard therapy. In conclusion, the relationship between beta-blockers and the central nervous system appears as a two-sided coin. Summarizing the neuropsychiatric side effects of beta-blockers, we suggest that clinicians pay special attention to the pharmacological properties of different beta-blockers.

The overweight status or obesity can be confirmed through classical methods such as the body mass index (BMI) and the waist-to-hip ratio (WHR). Apart from metabolic issues such as atherosclerosis, liver steatosis, or diabetes mellitus, long-term obesity or overweight status can pose a risk for cardiovascular and neurovascular complications. While some acute adverse events like coronary syndromes of strokes are well-documented to be linked to an increased body mass, there are also chronic processes that, due to their silent onset and evolution, are underdiagnosed and not as thoroughly studied. Through this review, we aimed to collect all relevant data with regard to the long-term impact of obesity on cognitive function in all ages and its correlation with an earlier onset of dementia such as Alzheimer’s disease (AD). The exact mechanisms through which a decline in cognitive functions occurs in overweight or obese persons are still being discussed. A combination of factors has been acknowledged as potential triggers, such as a sedentary lifestyle and stress, as well as a genetic predisposition, for example, the apolipoprotein E (ApoE) alleles in AD. Most research highlights the impact of vascular dysfunction and systemic inflammation on the nervous system in patients with obesity and the subsequent neurological changes. Obesity during the early to mid-ages leads to an earlier onset of cognitive dysfunction in various forms. Also, lifestyle intervention can reverse cognitive dysfunction, especially dieting, to encourage weight loss.

Obstructive sleep apnea (OSA) causes recurrent apneas due to upper respiratory tract collapse, leading to sympathetic nervous system hyperactivation and increased cardiovascular risk. Moderate and severe forms of obstructive sleep apnea are associated with increased atrial volumes and affect left ventricular diastolic and then systolic function. Right ventricular ejection fraction can be accurately assessed via three-dimensional echocardiography, while bidimensional imaging can only provide a set of surrogate parameters to characterize systolic function (tricuspid annulus plane systolic excursion, right ventricular fractional area change, and lateral S’). Tissue Doppler imaging is a more sensitive tool in detecting functional ventricular impairment, but its use is limited by angle dependence and the unwanted influence of tethering forces. Two-dimensional speckle tracking echocardiography is considered more suitable for the assessment of ventricular function, as it is able to distinguish between active and passive wall motion. Abnormal strain values, a marker of subclinical myocardial dysfunction, can be detected even in patients with normal ejection fraction and chamber volumes. The left ventricular longitudinal strain is more affected by the presence of obstructive sleep apnea than circumferential strain values. Although the observed OSA-induced changes are subtle, the benefit of a detailed echocardiographic screening for subclinical heart failure in OSA patients on therapy adherence and outcome should be addressed by further studies.

(1) Background: There has been a growing interest in understanding the causes of obesity and developing effective prevention strategies. Lifestyle change programs are often considered the gold standard for weight reduction, and they can help individuals with obesity achieve an annual weight loss of around 8–10%. The aim of this review was to evaluate the effect of food during the winter holidays. This knowledge will serve as a valuable foundation for the development of targeted interventions and prevention programs. (2) Methods: We conducted a systematic search of the literature via one database (PubMed). The search was limited to studies published in English in the last 10 years, with adult participants, but without specifying limits regarding the study design. We excluded articles that addressed intermittent fasting diets or weight loss intervention methods during the holidays through various diets. (3) In separate sections, we analyzed the psychological causes of gaining weight during the winter holidays, behavioral patterns, prevention strategies and the nutritional composition of the different types of food served during the festive period. Results: Using the combination of the terms “holiday and obesity”, “holiday and weight gain”, “festive season and obesity”, and “festive season and weight gain” we obtained 216 results involving the addressed topic. Thus, only ten articles remained after screening, with a total of 4627 participants. Most participants experienced weight fluctuations during the study period, particularly during holidays. One concerning observation was that most of the weight gained during these periods was maintained even after the end of the studies, especially in those with obesity. A supervised exercise program and a controlled diet at work over the Christmas period are effective strategies for avoiding weight gain and its deleterious effects in people with metabolic syndrome or weight problems. (4) In addition, attention must be focused on the psycho-social factors during the holidays because for some people it is a stressful period and can cause a much higher caloric consumption. The simplest method to approach during the holidays is to implement small tips and tricks during this period that will prevent individuals from gaining extra pounds. Conclusions: It is essential to acknowledge that obesity is a multifaceted condition that requires a comprehensive and multidisciplinary approach to address its underlying factors and provide ongoing assistance to individuals in their weight-management endeavors. Even the most effective short-term interventions are likely to produce continued positive outcomes with persistent intervention and support.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global coronavirus (COVID-19) pandemic. Although initially viewed as an acute respiratory illness, COVID-19 is clearly a complex multisystemic disease with extensive cardiovascular involvement. Emerging evidence shows that the endothelium plays multiple roles in COVID-19 physiopathology, as both a target organ that can be directly infected by SARS-CoV-2 and a mediator in the subsequent inflammatory and thrombotic cascades. Arterial stiffness is an established marker of cardiovascular disease. The scope of this review is to summarize available data on the acute and long-term consequences of COVID-19 on vascular function. COVID-19 causes early vascular aging and arterial stiffness. Fast, noninvasive bedside assessment of arterial stiffness could optimize risk stratification in acute COVID-19, allowing for early escalation of treatment. Vascular physiology remains impaired at least 12 months after infection with SARS-CoV-2, even in otherwise healthy adults. This raises concerns regarding the extent of arterial remodeling in patients with preexisting vascular disease and the potential development of a persistent, chronic COVID-19 vasculopathy. Long-term follow up on larger cohorts is required to investigate the reversibility of COVID-19-induced vascular changes and their associated prognostic implications.