RESUMEN
Cardiovascular disease is the leading cause of mortality and morbidity worldwide. One of the main risk factors for cardiovascular events is hypertension. The use of antihypertensive drugs can protect against these events. It occurs directly through the control of hypertension and indirectly through other cardiovascular effects. This meta-analysis and systematic review aimed to assess the impact of various antihypertensive medications (ACE inhibitors, beta-blockers, calcium channel blockers, diuretics, etc.) on blood pressure and various cardiovascular outcomes. A thorough search was conducted using several online databases and search engines, including PubMed, Google Scholar, ScienceDirect, Medline, Embase, and others. RCTs evaluating the impact of antihypertensive medications on BP and other cardiovascular events like coronary heart disease and stroke were included in this study. Included were studies detailing the use of antihypertensive medication in monotherapy. The meta-analysis was done using RevMan version 5.4 software (Cochrane Collaboration, London, UK). Means and standard deviations were extracted for the continuous variables and events, and the total sample number was extracted for the dichotomous variables. This analysis encompassed a total of 18 RCTs of the elderly population. The data for each variable was extracted independently, and analysis was performed. Overall, systolic blood pressure (SBP) revealed an impact of -11.88, CI=95% (-20.56, -3.19). The diastolic blood pressure (DBP) showed -5.41, CI=95% (-9.62, -1.20), myocardial infarction 0.92, CI=95% (0.82, 1.04), stroke 0.83, CI=95% (0.74, 0.94), and cardiovascular mortality 0.93, CI=95% (0.86, 1.00). Heterogeneity was present due to the variable sample size of the studies and other unidentified biases. In conclusion, there was a significant reduction in the elderly population's risk of stroke, myocardial infarction, and cardiovascular death when antihypertensive medications were taken.
RESUMEN
BACKGROUND: Given the sparse data on the renin-angiotensin system (RAS) and its biological effector molecules ACE1 and ACE2 in pediatric COVID-19 cases, we investigated whether the ACE1 insertion/deletion (I/D) polymorphism could be a genetic marker for susceptibility to COVID-19 in Egyptian children and adolescents. METHODS: This was a case-control study included four hundred sixty patients diagnosed with COVID-19, and 460 well-matched healthy control children and adolescents. The I/D polymorphism (rs1799752) in the ACE1 gene was genotyped by polymerase chain reaction (PCR), meanwhile the ACE serum concentrations were assessed by ELISA. RESULTS: The ACE1 D/D genotype and Deletion allele were significantly more represented in patients with COVID-19 compared to the control group (55% vs. 28%; OR = 2.4; [95% CI: 1.46-3.95]; for the DD genotype; P = 0.002) and (68% vs. 52.5%; OR: 1.93; [95% CI: 1.49-2.5] for the D allele; P = 0.032). The presence of ACE1 D/D genotype was an independent risk factor for severe COVID-19 among studied patients (adjusted OR: 2.6; [95% CI: 1.6-9.7]; P < 0.001. CONCLUSIONS: The ACE1 insertion/deletion polymorphism may confer susceptibility to SARS-CoV-2 infection in Egyptian children and adolescents. IMPACT: Recent studies suggested a crucial role of renin-angiotensin system and its biological effector molecules ACE1 and ACE2 in the pathogenesis and progression of COVID-19. To our knowledge, ours is the first study to investigate the association of ACE1 I/D polymorphism and susceptibility to COVID-19 in Caucasian children and adolescents. The presence of the ACE1 D/D genotype or ACE1 Deletion allele may confer susceptibility to SARS-CoV-2 infection and being associated with higher ACE serum levels; may constitute independent risk factors for severe COVID-19. The ACE1 I/D genotyping help design further clinical trials reconsidering RAS-pathway antagonists to achieve more efficient targeted therapies.
RESUMEN
Patients diagnosed with coronavirus disease (CVD) who experience cardiovascular complications or have pre-existing cardiovascular disease are at an increased risk of death. The primary heart-related consequences associated with COVID-19 encompass venous thromboembolism, shock, heart failure, arrhythmias, myocarditis, acute myocardial infarction, and acute cardiac damage. The coronavirus has the potential to induce cardiovascular complications or exacerbate pre-existing CVD through various mechanisms. These mechanisms include dysregulation of the renin-angiotensin-aldosterone system; direct viral toxicity; damage to endothelial cells; formation of blood clots and subsequent inflammation, a phenomenon known as thromboinflammation; an excessive immune response known as cytokine storm; and an imbalance between the demand and supply of oxygen in the body. In this study, we comprehensively analyze the cardiovascular symptoms, histology, and underlying mechanisms associated with COVID-19. Our aim is to contribute to the identification of future research objectives and aid in the advancement of therapeutic management approaches.