Frontiers in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Dec. 9, 2024

The current COVID-19 pandemic is a worldwide emergency because of its rapid spread and high mortality rate, resulting in considerable disruptions. virus responsible for COVID-19, brought the world to halt, presenting 2020 with coronavirus still on rise around [1] . Individuals afflicted have potential get pneumonia, Severe manifestations acute respiratory distress syndrome (ARDS) collapse numerous organs [2][3][4] [5] High fatality rate due had impact lives people, substantial stresses daily life [6] Despite extensive reports mental health during pandemic, there lack research individuals moderate cardiac psychological issues. World Health Organisation (2020) states that chronic conditions those who fail follow protection protocols are at higher risk infection. characterized by unpredictability implementation lockdowns physical distancing, may heighten issues exacerbate existing problems [7] relentless evolution this variants remains formidable challenge global public health, thus prompting significant concern among authorities emergent strains [8] .Recently has included new strain JN.1, database "Variant Of Interest," which was initially identified September, 2023 12 countries, largest occurrences observed Canada, France, Singapore, Sweden, UK, US [9] This Interest" (VOI) recently as distinct sub-lineage stemming from BA.2.86 variant. Noteworthy mutations include R3821K ORF1a, L455S spike protein, F19L ORF7b, characterize prevalence steadily surging worldwide, signalling remarkable competitive advantage. While differing parent variant, BA.2.86, terms infectivity immune evasion, evidence does not support heightened pathogenicity associated it however, augmented evasion capabilities raise concerns about waves infections, particularly previously exposed earlier [10] And JN.1 also genetic variation belongs lineage characterised particular alterations. Based data obtained website cov-spectrum (https://cov-spectrum.org), detection variant (including all descendant variants) reached total 16,604 sequences 26 December 2023. accounts proportion (47.9%) demonstrates consistent upward trend [11] .So, main aim examine JN. 1 infection development progression cardiac-related clinical disorders, including possible influence heart disease. seeks elucidate molecular physiological pathways connecting cardiovascular so improving comprehension role concerns, facilitating early diagnosis, guiding treatment approaches reduce risks problems.The emergence significantly individual increase stress reminiscent previous pandemic. Research shows arterial hypertension linked greater susceptibility SARS-CoV-2 infection, worsened disease severity, rates [12][13] Moreover, experimental indicated critical pathophysiological hypertension, such stimulation renin-angiotensin system (RAS), contribute [14][15] prior analysis overlooked link between pandemic-induced problems, leading number deaths Vascular dysfunction key contributor various diseases, diabetes, obesity, COVID-19-related mortality.A comprehensive literature conducted locate scholarly articles caused severe 2 (SARS-CoV-2). search performed using databases (WHO) American Heart Association, covering period March August 2022. A prominent academic New York City, retrospective observational design reported 45,398 be diagnosed During 6-month follow-up period, shown 20.6% patients were hospitalised ongoing blood pressure [16] history fulfilled least one three criteria before pandemic: (1) Patients an average above 140 mm Hg systolic or 90 diastolic two weeks being COVID-19. Please refer sensitivity cutoffs 130/80 Hg. ( material four crucial structural proteins: (S), envelope (E), matrix/membrane (M), nucleocapsid (N), addition group supplementary proteins [17] [18] Among them play entry coronaviruses into cells causing functional receptor been angiotensin-converting enzyme (ACE2) [19] primary purpose ACE2 metalloprotease activity, controlling processing Renin-Angiotensin (RAS) circulating peptides. acts counter regulatory mechanism counteract effects angiotensin II (Ang II) produced ACE [20] In order infect hosts, uses receptor, ACE2. As RAS series receptors, enzymes, peptides essential maintaining fluid electrolyte balance well regulating through pathways: pressor pathway depressor [21] last decades, heptapeptide product Ang 1-7 increasingly acknowledged counterregulatory modulators classical activation Mas (MasR) [22] primarily transforms 1-7, subsequently activating MasR pathway, exerts protective downstream microcirculatory environment. functions type-1 (AT1R) elicit vasoconstriction, stimulate inflammatory cytokine production, promote extracellular matrix creation. further promotes adrenal aldosterone synthesis, salt retention elevation pressure. Conversely, MasR, vasodilation suppresses synthesis proinflammatory cytokines, counteracting [23] .Therefore, viral invasion leads decrease presence cell membrane simultaneous reduction enzymatic function RAS. Thus, cause decline (1-7) levels, tilting equilibrium towards vasoconstrictor aspect RAS, potentially loss stability [24] Another can lead complications storm [Fig 01(a)]. Cytokine (CSS) advanced cases causes attributed several pathways. hyperinflammatory response, release excessive cytokines system. response like (ARDS), organ failure, increased [25] human ACE2, transmembrane glycoprotein part reninangiotensin-aldosterone (RAAS). cleaves I II, produces RAAS-antagonistic properties. binds internalization cleavage cellular proteases, tissue downregulation ACE2-mediated anti-inflammatory, antithrombotic, anti-fibrotic effects, along upregulation II-AT1 axis, thromboinflammatory state [26] .And initial involves elevated level conversion Ang-(1-7). Therefore, unregulated ACE/Ang II/AT1R levels IL-1, IL-6, TNF-α, enhanced both innate adaptive immunological responses [27] augment DNA-binding capability nuclear factors, NF-KB, mRNA transcription interleukins.Therefore, indicates factor disease, especially failure. It present cells, epithelial myocytes, vascular smooth muscle, endothelial brain tissues [28] Prolonged inhibition left ventricular wall thicknesses, interstitial collagen fraction area, cardiomyocyte hypertrophy 01 .(b)]. suggests [29] .Confounding Variables : Confounding lifestyle, predisposition, pre-existing conditions, sufficiently controlled, thereby affecting outcomes. Geographical Ethnic Limitations: If study localized certain place, results applicable other populations varying environmental characteristics.Global Collaborative Studies: Conducting studies multiple countries regions would help determine if across different populations, regional factors (like diet, healthcare access) role. Public Strategies: study's should inform programs focused monitoring managing symptoms 1. entail screening communities impacted 1.COVID-19 become major symptoms, posing complex dilemma. Understanding processes behind developing effective therapies preventative methods. surge infections likely unavoidable. advised stay alert lineages Omicron, arise invasion, reactions, drug use. vaccinations, remain concern. closely monitor epidemiology newly variations detect any illness Assessing vaccine antibody-based against these crucial, next-generation vaccines, improved monoclonal antibodies prevent evolving lineages.

Language: Английский