The deleterious consequences of alcohol consumption are extensively documented across various dimensions of human health, encompassing somatic disorders such as nervous system impairments, digestive system abnormalities, and circulatory dysfunctions, in addition to socio-psychological aspects. Within the domain of cardiology, a substantial portion of the ongoing scientific discourse centers on elucidating the toxic dose of alcohol. Presented herewith are the findings from a comprehensive review of the latest publications pertinent to this crucial issue.

Atherosclerosis is a chronic disease, characterized by chronic inflammation, endothelial dysfunction, and lipid deposition in the vessel. Although many major, well-identified risk factors for atherosclerosis [e.g., hyperlipidemia, hypertension, type 2 diabetes (T2D), smoking habit, and obesity] explain a lot about the risk, there is a considerable number of patients who develop atherosclerotic damage and undergo adverse events without presenting any of these established modifiable risk factors. This observation has stimulated an urgent need to expand knowledge towards the identification of additional, less established risk factors that may help in the assessment of risk and fill the gap of knowledge in the cardiovascular (CV) setting. Among them, the hypothesis of a possible relationship between viral infectious agents and atherosclerosis has risen since the early 1900s. However, there is still a great deal of debate regarding the onset and progression of CV disease in relation to the roles of the pathogens (as active inducers or bystanders), host genomic counterparts, and environmental triggers, affecting both virus abundance and the composition of viral communities. Accordingly, the aim of this review is to discuss the current state of knowledge on infectious agents in the atherosclerotic process, with particular focus on two environmental-related viruses, as examples of familiar (influenza) and unfamiliar [severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)] disease triggers.

While authorship practices can vary across different disciplines, authorship should reflect the individuals who have made a substantial contribution to the research project, take public responsibility for the paper’s content, and agree to its submission for publication. In real life, the article is usually authored by at least one truly genuine author and some parasitic authors. The first author and the last author are especially important. The middle authors are less important, and their participation is often wrongly seen as an inconsequential decorative favor. The honorary author, a gift or guest author, is added as a bonus to please someone higher in the hierarchy than the submitting author. This practice is believed to enhance the chances of publication, but usually, the excess of honorary authors will make reviewers more critical. A ghost author contributed substantially but it does not appear in the list of authors to avoid declaring an overt conflict of interest. The gold author is someone paid by a third party in direct or indirect forms, and capable of writing and signing everything asked by the payer, including overstating the merits of a new drug or ignoring its drawbacks. A fake author does not exist, and while it may seem humorous it is a breach of scientific integrity and can lead to serious consequences for the individuals involved. With Chat-generative pre-trained transformer (Chat-GPT), artificial intelligence may contribute decisively to the article content and presentation. Overall, it is important to maintain high standards of integrity and transparency in authorship practices to ensure that research findings are trustworthy and reliable. The reputation of your work is in the hands of your coauthors, so choose them carefully and make sure they share your commitment to scientific integrity.

Left ventricular (LV) function is typically evaluated through LV ejection fraction (EF), a robust indicator of risk, showing a nonlinear increase in mortality rates below 40%. Conversely, excessively high EF values (> 65%) also correlate with elevated mortality, following a U-shaped curve, with its nadir observed between 50% and 65%. This underscores the necessity for improved identification of the hypercontractile phenotype. However, EF is not synonymous with LV contraction function, as it can fluctuate independently of contractility due to variations in afterload, preload, heart rate, and ventricular-arterial coupling. Assessing the contractile status of the LV requires more specific metrics, such as LV elastance (or contractile force) and global longitudinal strain. Current guidelines outline various parameters for a more precise characterization of LV contractility, yet further research is warranted for validation. The true hypercontractile phenotype is evident in cardiac pathologies such as hypertrophic cardiomyopathy, ischemia with angiographically normal coronary arteries, Tako-tsubo syndrome, heart failure with preserved EF, and may also stem from systemic disorders including anemia, hyperthyroidism, liver, kidney, or pulmonary diseases. The hypercontractile phenotype constitutes a distinctive hemodynamic substrate underlying clinical manifestations such as angina, dyspnea, or arrhythmias, presenting a target for intervention through beta-blockers or specific cardiac myosin inhibitors. While EF remains pivotal for clinical classification, risk stratification, and therapeutic decision-making, integrating it with other indices of LV function can enhance the characterization of the hypercontractile phenotype.