Factores de riesgo cardiovascular: desde los clásicos hasta los emergentes a la luz de las nuevas evidencias

Cardiovascular diseases (CVD) are the main cause of morbidity and mortality worldwide, especially affecting the population over 60 years of age, they can manifest depending on their origin in coronary disease (acute myocardial infarction, angina pectoris, sudden cardiac arrest, heart failure and sudden death) and cerebrovascular disease (strokes and transient ischemic events). Several risk factors associated with the development of CVD have been described, the classic factors (modifiable and non-modifiable), and others that have been added to the list as a result of new evidence, such as inflammation, thrombosis, stress, alterations in the levels of natriuretic peptides, heavy metals/environmental pollutants, renal insufficiency, and some infectious agents. The objective of this article is to present the state of the art associated with classic cardiovascular risk factors (CRFs) and the evidence that supports emerging CRFs.  Las enfermedades cardiovasculares (ECV) son la causa principal de morbimortalidad a nivel mundial, afectando especialmente a la población mayor de 60 años, pueden manifestarse según su origen en enfermedad coronaria (infarto agudo de miocardio, angina pectoris, insuficiencia cardiaca, y muerte súbita) y enfermedad cerebrovascular (accidentes cerebrovasculares y eventos isquémicos transitorios). Varios factores de riesgo asociados al desarrollo de las ECV han sido descritos; los factores clásicos (modificables y no modificables), y otros que se han añadido a la lista como producto de las nuevas evidencias como es el caso de la inflamación, trombosis, estrés, alteraciones en los niveles de péptidos natriuréticos, metales pesados/contaminantes ambientales, insuficiencia renal y algunos agentes infecciosos. El objetivo de este artículo es presentar el estado del arte asociado con los factores de riesgo cardiovasculares (FRC) clásicos y las evidencias que soportan los FRC emergentes. &nbsp

COVID-19 Transmission in Children: Implications for Schools

The COVID-19 pandemic poses multiple issues of importance to child health including threats to physical health and disruption of in-school learning. This chapter reviews what is currently known about COVID-19 epidemiology, presentation, pathophysiology, case definitions, therapies, and in-school transmission in children. COVID-19 has some unique characteristics in children including the rare yet severe Multisystem Inflammatory Syndrome in Children (MIS-C) that may be related to acquired immune responses. There are limited studies to date to define therapeutic guidelines in children, however consensus recommendations from multiple organizations are summarized including the use of immunomodulatory therapies (intravenous immunoglobulin, steroids, anakinra and tocilizumab), antiplatelet (aspirin) and anti-coagulant (low molecular weight heparin) therapies. Finally, considerations for safe return to the classroom are discussed including strategies for optimized student to teacher ratios, hand washing, social distancing, sibling pairing and staged re-opening strategies

Novel Effects of Statins on Cancer via Autophagy

Cancer is one of the main causes of death globally. Most of the molecular mechanisms underlying cancer are marked by complex aberrations that activate the critical cell-signaling pathways that play a pivotal role in cell metabolism, tumor development, cytoskeletal reorganization, and metastasis. The phosphatidylinositol 3-kinase/protein kinase-B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway is one of the main signaling pathways involved in carcinogenesis and metastasis. Autophagy, a cellular pathway that delivers cytoplasmic components to lysosomes for degradation, plays a dual role in cancer, as either a tumor promoter or a tumor suppressor, depending on the stage of the carcinogenesis. Statins are the group of drugs of choice to lower the level of low-density lipoprotein (LDL) cholesterol in the blood. Experimental and clinical data suggest the potential of statins in the treatment of cancer. In vitro and in vivo studies have demonstrated the molecular mechanisms through which statins inhibit the proliferation and metastasis of cancer cells in different types of cancer. The anticancer properties of statins have been shown to result in the suppression of tumor growth, the induction of apoptosis, and autophagy. This literature review shows the dual role of the autophagic process in cancer and the latest scientific evidence related to the inducing effect exerted by statins on autophagy, which could explain their anticancer potential

Novel Insights into the Cardioprotective Effects of the Peptides of the Counter-Regulatory Renin–Angiotensin System

Currently, cardiovascular diseases are a major contributor to morbidity and mortality worldwide, having a significant negative impact on both the economy and public health. The renin–angiotensin system contributes to a high spectrum of cardiovascular disorders and is essential for maintaining normal cardiovascular homeostasis. Overactivation of the classical renin–angiotensin system is one of the most important pathophysiological mechanisms in the progression of cardiovascular diseases. The counter-regulatory renin–angiotensin system is an alternate pathway which favors the synthesis of different peptides, including Angiotensin-(1-7), Angiotensin-(1-9), and Alamandine. These peptides, via the angiotensin type 2 receptor (AT2R), MasR, and MrgD, initiate multiple downstream signaling pathways that culminate in the activation of various cardioprotective mechanisms, such as decreased cardiac fibrosis, decreased myocardial hypertrophy, vasodilation, decreased blood pressure, natriuresis, and nitric oxide synthesis. These cardioprotective effects position them as therapeutic alternatives for reducing the progression of cardiovascular diseases. This review aims to show the latest findings on the cardioprotective effects of the main peptides of the counter-regulatory renin–angiotensin system

Effects of Metformin on Ischemia/Reperfusion Injury: New Evidence and Mechanisms

The search for new drugs with the potential to ensure therapeutic success in the treatment of cardiovascular diseases has become an essential pathway to follow for health organizations and committees around the world. In June 2021, the World Health Organization listed cardiovascular diseases as one of the main causes of death worldwide, representing 32% of them. The most common is coronary artery disease, which causes the death of cardiomyocytes, the cells responsible for cardiac contractility, through ischemia and subsequent reperfusion, which leads to heart failure in the medium and short term. Metformin is one of the most-used drugs for the control of diabetes, which has shown effects beyond the control of hyperglycemia. Some of these effects are mediated by the regulation of cellular energy metabolism, inhibiting apoptosis, reduction of cell death through regulation of autophagy and reduction of mitochondrial dysfunction with further reduction of oxidative stress. This suggests that metformin may attenuate left ventricular dysfunction induced by myocardial ischemia; preclinical and clinical trials have shown promising results, particularly in the setting of acute myocardial infarction. This is a review of the molecular and pharmacological mechanisms of the cardioprotective effects of metformin during myocardial ischemia-reperfusion injury

Regulatory T-cells and GARP expression are decreased in exercise-associated chikungunya viral arthritis flares

Objective: Chikungunya virus (CHIKV) causes persistent arthritis, and our prior study showed that approximately one third of CHIKV arthritis patients had exacerbated arthritis associated with exercise. The underlying mechanism of exercise-associated chikungunya arthritis flare (EACAF) is unknown, and this analysis aimed to examine the regulatory T-cell immune response related to CHIKV arthritis flares. Methods: In our study, 124 Colombian patients with a history of CHIKV infection four years prior were enrolled and 113 cases with serologically confirmed CHIKV IgG were used in this analysis. Patient information was gathered questionnaires, and blood samples were taken to identify total live peripheral blood mononuclear cells, CD4+ cells, T regulatory cells, and their immune markers. We compared outcomes in CHIKV patients with (n = 38) vs. without (n = 75) EACAF using t-tests to assess means and the Fisher\u27s exact test, chi-squared to evaluate categorical variables, and Kruskal-Wallis tests in the setting of skewed distributions (SAS 9.3). Results: 33.6% of CHIKV cases reported worsening arthritis with exercise. EACAF patients reported higher global assessments of arthritis disease ranging from 0-100 (71.2 ± 19.7 vs. 59.9 ± 28.0, p=0.03). EACAF patients had lower ratios of T regulatory (Treg)/CD4+ T-cells (1.95 ± 0.73 vs. 2.4 ± 1.29, p = 0.04) and lower percentage of GARP (glycoprotein-A repetitions predominant) expression per Treg (0.13 ± 0.0.33 vs. 0.16 ± 0.24 p= 0.020). Conclusion: These findings suggest relative decreases in GARP expression may indicate a decreased level of immune suppression. Treg populations in patients with CHIKV arthritis may contribute to arthritis flares during exercise, though current research is conflicting