Analysis of the Influence of Abdominal Obesity on Systemic Arterial Hypertension and on the Lipid Profile on Cardiometabolic Risk Stratification in Adult Women

Abstract Background: Obesity is a public health problem and has been associated with the development of metabolic disorders that have a strong relationship with the onset of cardiovascular diseases (CVD). Objective: The objective was to analyze the influence of abdominal obesity (AO) on systemic arterial hypertension (SAH) and on the lipid profile in cardiovascular risk stratification in adult women. Methods: Altogether, 91 women participated in the research. Lifestyle information was collected, in addition to the analysis of clinical measures of cardiovascular risk and biochemical parameters. Unpaired Student's t-test, logistic regression, and Pearson's correlation were performed for data analysis, with a value of p <0.05 considered significant. Results: The prevalence of AO was 62.6%. Logistic regression showed that AO increased the chance of developing SAH by 2.9-fold. The same behavior was observed in the TG/HDL-c lipid ratio (3.93 ± 0.3 vs. 2.16 ± 0.2), representing an 82% increase in obese women. The present study also demonstrated that the best anthropometric parameter to analyze cardiovascular risk in the studied population was the waist/height ratio (AUC = 0.707). Conclusions: It can therefore be concluded that AO plays a significant role in the development of SAH and changes in lipid values that predict increased cardiovascular risk, configuring a strong influence factor for CVD.

Quais são os mecanismos celulares relacionados aos eventos tromboembólicos em pacientes com COVID-19? / What cellular mechanisms are related to thromboembolic events in patients with COVID-19?

Resumo O SARS-CoV-2 é o vírus responsável pela pandemia da COVID-19. Essa doença começou a ser melhor entendida devido a outras manifestações clínicas além das respiratórias. Ao longo dos meses de atendimento aos pacientes infectados pelo vírus, foram identificadas alterações clínicas e laboratoriais que incitaram os pesquisadores a discutir sobre o potencial do SARS-CoV-2 no desencadeamento de uma resposta imunológica exacerbada capaz de alterar a homeostase endotelial, através de mecanismos diretos e indiretos. Com esse intuito, foram revisados os possíveis mecanismos que desencadeiam este fenômeno em pacientes portadores de COVID-19. Dessa forma, torna-se importante o entendimento fisiopatológico dos mecanismos imunológicos relacionados à doença para a compreensão do potencial de dano endotelial que a COVID-19 pode promover.

Abstract SARS-CoV-2 is the virus responsible for the COVID-19 pandemic. This disease is beginning to be better understood in terms of its other, non-respiratory, clinical manifestations. Over the course of months caring for patients infected by the virus, clinical and laboratory changes have been identified that have prompted researchers to debate the potential that SARS-CoV-2 has to trigger an exacerbated immune response that is capable of changing endothelial homeostasis through both direct and indirect mechanisms. With the intention of contributing to this debate, a review was conducted of the possible mechanisms that could trigger these phenomena in patients with COVID-19. It is important to understand the pathophysiology of the immunological mechanisms related to this disease in order to understand the potential endothelial damage that COVID-19 can provoke.

Cardiovascular damage due to COVID-19: what do we need to know?

SUMMARY Severe Acute Respiratory Syndrome Coronavirus 2 is part of the Cononaviridae family and is the causative agent of the 2019 (Covid-19) Coronavirus pandemic declared by the World Health Organization in March, 2020. This virus has a high rate of transmission, affecting several individuals, and has caused thousands of deaths. The clinical manifestations of Severe Acute Respiratory Syndrome Coronavirus 2 infection are not restricted only to the respiratory tract, and there is an express involvement of the cardiovascular system with a higher risk of death in this group. In such patients there is an overactivation of renin-angiotensin-aldosterone system, which promotes an increase in the expression of angiotensin-converting enzyme - 2 that acts as a receptor for the SPIKE protein expressed by the virus and enables the interaction between the host cell and Severe Acute Respiratory Syndrome Coronavirus 2. This process of infection causes a hyperinflammatory state that increases the inflammatory markers of cardiac injury. Hence, an adequate understanding and clinical guidance regarding the monitoring, and controlling the damage in these patients is essential to avoid worsening of their clinical condition and to prevent death.