Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 179
Filter
1.
Front Immunol ; 13: 776861, 2022.
Article in English | MEDLINE | ID: covidwho-1701723

ABSTRACT

Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2-induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2-driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.


Subject(s)
Blood Platelets/metabolism , COVID-19/pathology , Cardiovascular Diseases/pathology , Endothelium, Vascular/metabolism , Platelet Activation/immunology , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/mortality , Cardiovascular Diseases/virology , Coronavirus Nucleocapsid Proteins/immunology , Endothelial Cells/metabolism , Humans , Myocardium/pathology , Phosphoproteins/immunology , SARS-CoV-2/immunology , Spike Glycoprotein, Coronavirus/immunology , Spike Glycoprotein, Coronavirus/metabolism
2.
Life Sci ; 294: 120392, 2022 Apr 01.
Article in English | MEDLINE | ID: covidwho-1670857

ABSTRACT

The SARS coronavirus 2 (SARS CoV-2) causes Coronavirus Disease (COVID-19), is an emerging viral infection. SARS CoV-2 infects target cells by attaching to Angiotensin-Converting Enzyme (ACE2). SARS CoV-2 could cause cardiac damage in patients with severe COVID-19, as ACE2 is expressed in cardiac cells, including cardiomyocytes, pericytes, and fibroblasts, and coronavirus could directly infect these cells. Cardiovascular disorders are the most frequent comorbidity found in COVID-19 patients. Immune cells such as monocytes, macrophages, and T cells may produce inflammatory cytokines and chemokines that contribute to COVID-19 pathogenesis if their functions are uncontrolled. This causes a cytokine storm in COVID-19 patients, which has been associated with cardiac damage. Tregs are a subset of immune cells that regulate immune and inflammatory responses. Tregs suppress inflammation and improve cardiovascular function through a variety of mechanisms. This is an exciting research area to explore the cellular, molecular, and immunological mechanisms related to reducing risks of cardiovascular complications in severe COVID-19. This review evaluated whether Tregs can affect COVID-19-related cardiovascular complications, as well as the mechanisms through which Tregs act.


Subject(s)
COVID-19/immunology , Cardiovascular Diseases/immunology , Cardiovascular Diseases/prevention & control , SARS-CoV-2 , T-Lymphocytes, Regulatory/physiology , Adoptive Transfer , Animals , Cardiovascular Diseases/virology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/prevention & control , Humans , Inflammation/immunology , T-Lymphocytes, Regulatory/immunology
3.
Bull Exp Biol Med ; 172(3): 283-287, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1611428

ABSTRACT

We studied laboratory parameters of patients with COVID-19 against the background of chronic pathologies (cardiovascular pathologies, obesity, type 2 diabetes melitus, and cardiovascular pathologies with allergy to statins). A decrease in pH and a shift in the electrolyte balance of blood plasma were revealed in all studied groups and were most pronounced in patients with cardiovascular pathologies with allergy to statin. It was found that low pH promotes destruction of lipid components of the erythrocyte membranes in patients with chronic pathologies, which was seen from a decrease in Na+/K+-ATPase activity and significant hyponatrenemia. In patients with cardiovascular pathologies and allergy to statins, erythrocyte membranes were most sensitive to a decrease in pH, while erythrocyte membranes of obese patients showed the greatest resistance to low pH and oxidative stress.


Subject(s)
COVID-19/complications , Hyponatremia/etiology , Hypoxia/complications , Sodium-Potassium-Exchanging ATPase/physiology , Aged , COVID-19/metabolism , Cardiovascular Diseases/complications , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/virology , Case-Control Studies , Chronic Disease , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/virology , Drug Hypersensitivity/complications , Drug Hypersensitivity/metabolism , Drug Hypersensitivity/virology , Erythrocyte Membrane/metabolism , Erythrocytes/metabolism , Female , Fluid Shifts/physiology , Humans , Hydrogen-Ion Concentration , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Hyponatremia/metabolism , Hyponatremia/virology , Hypoxia/metabolism , Lipid Peroxidation/physiology , Male , Middle Aged , Obesity/complications , Obesity/metabolism , Obesity/virology , Oxidative Stress/physiology , SARS-CoV-2/physiology , Sodium/metabolism , Stress, Physiological/physiology
4.
Arch Cardiol Mex ; 91(Suplemento COVID): 074-078, 2021 Dec 20.
Article in Spanish | MEDLINE | ID: covidwho-1609014

ABSTRACT

The COVID-19 pandemic has had an important impact on older adults, conferring a worse prognosis. Older adults may have atypical presentations, which can delay the diagnosis of the disease, making its evolution more unfavorable. In addition to the cardiovascular damage mechanisms conferred by SARS-CoV-2 infection, the changes inherent in the aging cardiovascular and immune system favor the appearance of cardiovascular complications in a more relevant way in this population. The objective of this article will be to summarize the knowledge about cardiovascular involvement in older adults and explain its pathophysiological mechanisms, to alert about the early recognition and timely treatment of these complications.


La pandemia por COVID-19 ha impactado de forma importante en los adultos mayores, confiriéndoles un peor pronóstico. Los adultos mayores pueden tener presentaciones atípicas, las cuales pueden retrasar el diagnóstico de la enfermedad, haciendo su evolución más desfavorable. Además de los mecanismos de daño cardiovascular conferidos por la infección por SARS-CoV-2, los cambios inherentes al sistema cardiovascular e inmune ya envejecido, favorecen la aparición de complicaciones cardiovasculares de forma más relevante en esta población. El objetivo de este artículo será resumir los conocimientos sobre el involucro cardiovascular en adultos mayores y explicar los mecanismos fisiopatológicos de este, para alertar sobre el reconocimiento temprano y tratamiento oportuno de estas complicaciones.


Subject(s)
COVID-19 , Cardiovascular Diseases/virology , Cardiovascular System , Aged , COVID-19/complications , Humans , Pandemics
5.
Glob Heart ; 16(1): 22, 2021 04 19.
Article in English | MEDLINE | ID: covidwho-1557646

ABSTRACT

Background: The emergence of novel coronavirus disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2), has presented an unprecedented global challenge for the healthcare community. The ability of SARS-CoV-2 to get transmitted during the asymptomatic phase, and its high infectivity have led to the rapid transmission of COVID-19 beyond geographic regions facilitated by international travel, leading to a pandemic. To guide effective control and interventions, primary data is required urgently, globally, including from low- and middle-income countries where documentation of cardiovascular manifestations and risk factors in people hospitalized with COVID-19 is limited. Objectives: This study aims to describe the cardiovascular manifestations and cardiovascular risk factors in patients hospitalized with COVID-19. Methods: We propose to conduct an observational cohort study involving 5000 patients recruited from hospitals in low-, middle- and high-income countries. Eligible adult COVID-19 patients will be recruited from the participating hospitals and followed-up until 30 days post admission. The outcomes will be reported at discharge and includes the need of ICU admission, need of ventilator, death (with cause), major adverse cardiovascular events, neurological outcomes, acute renal failure, and pulmonary outcomes. Conclusion: Given the enormous burden posed by COVID-19 and the associated severe prognostic implication of CVD involvement, this study will provide useful insights on the risk factors for severe disease, clinical presentation, and outcomes of various cardiovascular manifestations in COVID-19 patients particularly from low and middle income countries from where the data remain scant.


Subject(s)
COVID-19/epidemiology , Cardiovascular Diseases/virology , Global Health , Observational Studies as Topic/methods , Cohort Studies , Hospitalization , Humans , Multicenter Studies as Topic , Pandemics , Prognosis , Risk Factors
6.
Curr Drug Targets ; 22(16): 1832-1843, 2021.
Article in English | MEDLINE | ID: covidwho-1511929

ABSTRACT

ACE2 has long been known as an injury protective protein, which can protect against a variety of organ damage such as the heart, liver, kidney, and lung. Especially in cardiovascular diseases, as a negative regulator of RAAS, ACE2 is an extremely important protective factor that mainly plays a role by converting Ang II to Ang-(1-7). Nevertheless, with the recent outbreak of COVID-19, it is exposed that another identity of ACE2 is the entry receptor for SARS-CoV-2, which previously serves as the entry receptor for SARS. With the in-depth clinical research, it is found that the severity and susceptibility of COVID-19 are related to cardiovascular diseases, and SARS-CoV-2 binding to ACE2 receptor is also potentially associated with heart injury symptoms. Therefore, in this article, we mainly summarize the relationship between ACE2, COVID-19, and cardiovascular diseases/heart injury.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19 , Cardiovascular Diseases , Heart Injuries , COVID-19/pathology , Cardiovascular Diseases/virology , Heart Injuries/virology , Humans
7.
Mol Cell Biochem ; 477(1): 225-240, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1469743

ABSTRACT

Severe acute respiratory syndrome-coronavirus-2 (COVID-19) virus uses Angiotensin-Converting Enzyme 2 (ACE2) as a gateway for their entry into the human body. The ACE2 with cleaved products have emerged as major contributing factors to multiple physiological functions and pathogenic complications leading to the clinical consequences of the COVID-19 infection Decreased ACE2 expression restricts the viral entry into the human cells and reduces the viral load. COVID-19 infection reduces the ACE2 expression and induces post-COVID-19 complications like pneumonia and lung injury. The modulation of the ACE2-Ang (1-7)-Mas (AAM) axis is also being explored as a modality to treat post-COVID-19 complications. Evidence indicates that specific food components may modulate the AAM axis. The variations in the susceptibility to COVID-19 infection and the post-COVID its complications are being correlated with varied dietary habits. Some of the food substances have emerged to have supportive roles in treating post-COVID-19 complications and are being considered as adjuvants to the COVID-19 therapy. It is possible that some of their active ingredients may emerge as the direct treatment for the COVID-19.


Subject(s)
Angiotensin I/metabolism , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/complications , COVID-19/diet therapy , Peptide Fragments/metabolism , /metabolism , Cardiovascular Diseases/pathology , Cardiovascular Diseases/virology , Dietary Proteins/pharmacology , Flavonoids/pharmacology , Humans , Lung/pathology , Lung/virology , Plant Oils/pharmacology , Polyphenols/pharmacology , Terpenes/pharmacology , Virus Internalization , Vitamins/pharmacology
8.
Front Immunol ; 12: 711741, 2021.
Article in English | MEDLINE | ID: covidwho-1430696

ABSTRACT

COVID-19 is widespread worldwide and seriously affects the daily life and health of humans. Countries around the world are taking necessary measures to curb the spread. However, COVID-19 patients often have at least one organ complication and sequelae in addition to respiratory symptoms. Controlling the epidemic is only a phased victory, and the complication and sequelae of COVID-19 will need more attention in the post-epidemic era. We collected general information from over 1000 articles published in 2020 after the COVID-19 outbreak and systematically analyzed the complication and sequelae associated with eight major systems in COVID-19 patients caused by ACE2 intervention in the RAS regulatory axis. The autoimmune response induced by 2019-nCoV attacks and damages the normal tissues and organs of the body. Our research will help medical workers worldwide address COVID-19 complication and sequelae.


Subject(s)
COVID-19/pathology , Cardiovascular Diseases/pathology , Endocrine System Diseases/pathology , Gastrointestinal Diseases/pathology , Nervous System Diseases/pathology , Urologic Diseases/pathology , COVID-19/complications , Cardiovascular Diseases/virology , Disease Outbreaks , Disease Progression , Endocrine System Diseases/virology , Gastrointestinal Diseases/virology , Humans , Nervous System Diseases/virology , SARS-CoV-2 , Urologic Diseases/virology
9.
Cardiovasc Res ; 117(14): 2705-2729, 2021 12 17.
Article in English | MEDLINE | ID: covidwho-1411978

ABSTRACT

The cardiovascular system is significantly affected in coronavirus disease-19 (COVID-19). Microvascular injury, endothelial dysfunction, and thrombosis resulting from viral infection or indirectly related to the intense systemic inflammatory and immune responses are characteristic features of severe COVID-19. Pre-existing cardiovascular disease and viral load are linked to myocardial injury and worse outcomes. The vascular response to cytokine production and the interaction between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and angiotensin-converting enzyme 2 receptor may lead to a significant reduction in cardiac contractility and subsequent myocardial dysfunction. In addition, a considerable proportion of patients who have been infected with SARS-CoV-2 do not fully recover and continue to experience a large number of symptoms and post-acute complications in the absence of a detectable viral infection. This conditions often referred to as 'post-acute COVID-19' may have multiple causes. Viral reservoirs or lingering fragments of viral RNA or proteins contribute to the condition. Systemic inflammatory response to COVID-19 has the potential to increase myocardial fibrosis which in turn may impair cardiac remodelling. Here, we summarize the current knowledge of cardiovascular injury and post-acute sequelae of COVID-19. As the pandemic continues and new variants emerge, we can advance our knowledge of the underlying mechanisms only by integrating our understanding of the pathophysiology with the corresponding clinical findings. Identification of new biomarkers of cardiovascular complications, and development of effective treatments for COVID-19 infection are of crucial importance.


Subject(s)
COVID-19/complications , Cardiovascular Diseases/virology , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/enzymology , COVID-19/etiology , COVID-19/physiopathology , COVID-19/therapy , Cardiometabolic Risk Factors , Cardiovascular Diseases/enzymology , Cardiovascular Diseases/physiopathology , Clinical Trials as Topic , Humans , Inflammation/complications , Inflammation/virology , Microcirculation , Sex Characteristics
10.
Int J Mol Sci ; 22(18)2021 Sep 13.
Article in English | MEDLINE | ID: covidwho-1409702

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic with high infectivity and mortality has caused severe social and economic impacts worldwide. Growing reports of COVID-19 patients with multi-organ damage indicated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) may also disturb the cardiovascular system. Herein, we used human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (iCMs) as the in vitro platform to examine the consequence of SARS-CoV2 infection on iCMs. Differentiated iCMs expressed the primary SARS-CoV2 receptor angiotensin-converting enzyme-II (ACE2) and the transmembrane protease serine type 2 (TMPRSS2) receptor suggesting the susceptibility of iCMs to SARS-CoV2. Following the infection of iCMs with SARS-CoV2, the viral nucleocapsid (N) protein was detected in the host cells, demonstrating the successful infection. Bioinformatics analysis revealed that the SARS-CoV2 infection upregulates several inflammation-related genes, including the proinflammatory cytokine tumor necrosis factor-α (TNF-α). The pretreatment of iCMs with TNF-α for 24 h, significantly increased the expression of ACE2 and TMPRSS2, SASR-CoV2 entry receptors. The TNF-α pretreatment enhanced the entry of GFP-expressing SARS-CoV2 pseudovirus into iCMs, and the neutralization of TNF-α ameliorated the TNF-α-enhanced viral entry. Collectively, SARS-CoV2 elevated TNF-α expression, which in turn enhanced the SARS-CoV2 viral entry. Our findings suggest that, TNF-α may participate in the cytokine storm and aggravate the myocardial damage in COVID-19 patients.


Subject(s)
COVID-19/complications , Cardiovascular Diseases/immunology , Cytokine Release Syndrome/immunology , SARS-CoV-2/immunology , Tumor Necrosis Factor-alpha/metabolism , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/immunology , COVID-19/pathology , COVID-19/virology , Cardiovascular Diseases/virology , Cell Differentiation , Cell Line , Computational Biology , Coronavirus Nucleocapsid Proteins/metabolism , Cytokine Release Syndrome/pathology , Cytokine Release Syndrome/virology , Humans , Induced Pluripotent Stem Cells , Myocardium/cytology , Myocardium/immunology , Myocardium/pathology , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/virology , Phosphoproteins/metabolism , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Serine Endopeptidases/metabolism , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Up-Regulation/immunology , Virus Internalization/drug effects
11.
PLoS One ; 16(9): e0256988, 2021.
Article in English | MEDLINE | ID: covidwho-1394552

ABSTRACT

Epidemiological studies suggest that individuals with comorbid conditions including diabetes, chronic lung, inflammatory and vascular disease, are at higher risk of adverse COVID-19 outcomes. Genome-wide association studies have identified several loci associated with increased susceptibility and severity for COVID-19. However, it is not clear whether these associations are genetically determined or not. We used a Phenome-Wide Association (PheWAS) approach to investigate the role of genetically determined COVID-19 susceptibility on disease related outcomes. PheWAS analyses were performed in order to identify traits and diseases related to COVID-19 susceptibility and severity, evaluated through a predictive COVID-19 risk score. We utilised phenotypic data in up to 400,000 individuals from the UK Biobank, including Hospital Episode Statistics and General Practice data. We identified a spectrum of associations between both genetically determined COVID-19 susceptibility and severity with a number of traits. COVID-19 risk was associated with increased risk for phlebitis and thrombophlebitis (OR = 1.11, p = 5.36e-08). We also identified significant signals between COVID-19 susceptibility with blood clots in the leg (OR = 1.1, p = 1.66e-16) and with increased risk for blood clots in the lung (OR = 1.12, p = 1.45 e-10). Our study identifies significant association of genetically determined COVID-19 with increased blood clot events in leg and lungs. The reported associations between both COVID-19 susceptibility and severity and other diseases adds to the identification and stratification of individuals at increased risk, adverse outcomes and long-term effects.


Subject(s)
COVID-19/genetics , Obesity/genetics , Thrombophlebitis/genetics , Thrombosis/genetics , COVID-19/epidemiology , COVID-19/virology , Cardiovascular Diseases/genetics , Cardiovascular Diseases/pathology , Cardiovascular Diseases/virology , Female , Genetic Predisposition to Disease , Humans , Male , Mendelian Randomization Analysis , Obesity/epidemiology , Obesity/virology , Phenomics , Phenotype , Polymorphism, Single Nucleotide/genetics , SARS-CoV-2/pathogenicity , Thrombophlebitis/epidemiology , Thrombophlebitis/virology , Thrombosis/epidemiology , Thrombosis/virology
12.
Stem Cell Rev Rep ; 17(6): 2107-2119, 2021 12.
Article in English | MEDLINE | ID: covidwho-1345193

ABSTRACT

The virus responsible for coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected over 190 million people to date, causing a global pandemic. SARS-CoV-2 relies on binding of its spike glycoprotein to angiotensin-converting enzyme 2 (ACE2) for infection. In addition to fever, cough, and shortness of breath, severe cases of SARS-CoV-2 infection may result in the rapid overproduction of pro-inflammatory cytokines. This overactive immune response is known as a cytokine storm, which leads to several serious clinical manifestations such as acute respiratory distress syndrome and myocardial injury. Cardiovascular disorders such as acute coronary syndrome (ACS) and heart failure not only enhance disease progression at the onset of infection, but also arise in hospitalized patients with COVID-19. Tissue-specific differentiated cells and organoids derived from human pluripotent stem cells (hPSCs) serve as an excellent model to address how SARS-CoV-2 damages the lungs and the heart. In this review, we summarize the molecular basis of SARS-CoV-2 infection and the current clinical perspectives of the bidirectional relationship between the cardiovascular system and viral progression. Furthermore, we also address the utility of hPSCs as a dynamic model for SARS-CoV-2 research and clinical translation.


Subject(s)
COVID-19/virology , Cardiovascular System/virology , Pluripotent Stem Cells/virology , COVID-19/immunology , Cardiovascular Diseases/immunology , Cardiovascular Diseases/virology , Cardiovascular System/immunology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/virology , Humans , Lung/immunology , Lung/virology , Pandemics/prevention & control , Pluripotent Stem Cells/immunology , SARS-CoV-2/pathogenicity
13.
Int J Mol Sci ; 21(21)2020 Nov 03.
Article in English | MEDLINE | ID: covidwho-1344351

ABSTRACT

Progressive respiratory failure is seen as a major cause of death in severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection. Relatively little is known about the associated morphologic and molecular changes in the circulation of these patients. In particular, platelet and erythrocyte pathology might result in severe vascular issues, and the manifestations may include thrombotic complications. These thrombotic pathologies may be both extrapulmonary and intrapulmonary and may be central to respiratory failure. Previously, we reported the presence of amyloid microclots in the circulation of patients with coronavirus disease 2019 (COVID-19). Here, we investigate the presence of related circulating biomarkers, including C-reactive protein (CRP), serum ferritin, and P-selectin. These biomarkers are well-known to interact with, and cause pathology to, platelets and erythrocytes. We also study the structure of platelets and erythrocytes using fluorescence microscopy (using the markers PAC-1 and CD62PE) and scanning electron microscopy. Thromboelastography and viscometry were also used to study coagulation parameters and plasma viscosity. We conclude that structural pathologies found in platelets and erythrocytes, together with spontaneously formed amyloid microclots, may be central to vascular changes observed during COVID-19 progression, including thrombotic microangiopathy, diffuse intravascular coagulation, and large-vessel thrombosis, as well as ground-glass opacities in the lungs. Consequently, this clinical snapshot of COVID-19 strongly suggests that it is also a true vascular disease and considering it as such should form an essential part of a clinical treatment regime.


Subject(s)
Blood Platelets/pathology , Cardiovascular Diseases/virology , Coronavirus Infections/blood , Coronavirus Infections/pathology , Erythrocytes/pathology , Ferritins/blood , P-Selectin/blood , Pneumonia, Viral/blood , Pneumonia, Viral/pathology , Betacoronavirus/isolation & purification , Blood Coagulation/physiology , Blood Platelets/virology , COVID-19 , Cardiovascular Diseases/blood , Cardiovascular Diseases/pathology , Coronavirus Infections/virology , Erythrocytes/virology , Female , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/virology , SARS-CoV-2 , Thrombosis/pathology , Thrombosis/virology
14.
Am J Infect Control ; 49(2): 238-246, 2021 02.
Article in English | MEDLINE | ID: covidwho-1336188

ABSTRACT

INTRODUCTION: On February 11, 2020 WHO designated the name "COVID-19" for the disease caused by "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2), a novel virus that quickly turned into a global pandemic. Risks associated with acquiring the virus have been found to most significantly vary by age and presence of underlying comorbidity. In this rapid literature review we explore the prevalence of comorbidities and associated adverse outcomes among individuals with COVID-19 and summarize our findings based on information available as of May 15, 2020. METHODS: A comprehensive systematic search was performed on PubMed, Medline, Scopus, Embase, and Google Scholar to find articles published until May 15, 2020. All relevant articles providing information on PCR tested COVID-19 positive patient population with clinical characteristics and epidemiological information were selected for review and analysis. RESULTS: A total of 27 articles consisting of 22,753 patient cases from major epicenters worldwide were included in the study. Major comorbidities seen in overall population were CVD (8.9%), HTN (27.4%), Diabetes (17.4%), COPD (7.5%), Cancer (3.5%), CKD (2.6%), and other (15.5%). Major comorbidity specific to countries included in the study were China (HTN 39.5%), South Korea (CVD 25.6%), Italy (HTN 35.9%), USA (HTN 38.9%), Mexico, (Other 42.3%), UK (HTN 27.8%), Iran (Diabetes 35.0%). Within fatal cases, an estimated 84.1% had presence of one or more comorbidity. Subgroup analysis of fatality association with having comorbidity had an estimated OR 0.83, CI [0.60-0.99], p<0.05. CONCLUSIONS: Based on our findings, hypertension followed by diabetes and cardiovascular diseases were the most common comorbidity seen in COVID-19 positive patients across major epicenters world-wide. Although having one or more comorbidity is linked to increased disease severity, no clear association was found between having these risk factors and increased risk of fatality.


Subject(s)
COVID-19/epidemiology , Comorbidity , Global Health/statistics & numerical data , Hypertension/epidemiology , SARS-CoV-2 , Adult , Aged , Aged, 80 and over , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/virology , Diabetes Mellitus/epidemiology , Diabetes Mellitus/virology , Female , Humans , Hypertension/virology , Male , Middle Aged , Neoplasms/epidemiology , Neoplasms/virology , Prevalence , Pulmonary Disease, Chronic Obstructive/epidemiology , Pulmonary Disease, Chronic Obstructive/virology , Renal Insufficiency, Chronic/epidemiology , Renal Insufficiency, Chronic/virology , Young Adult
15.
Vascul Pharmacol ; 141: 106899, 2021 12.
Article in English | MEDLINE | ID: covidwho-1322386

ABSTRACT

A new virus strain detected in late 2019 and not previously described in humans is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes corona virus disease (COVID-19). While potential therapeutic approaches for COVID-19 are being investigated, significant initiatives are being made to create protective drugs and study various antiviral agents to cure the infection. However, an effective treatment strategy against COVID-19 is worrisome inadequate. The objective of the present manuscript is to discuss the potential role of thymoquinone (TQ) in preventing the cardiovascular complications of COVID-19, focusing on viral inhibition, antioxidant potential, vascular effect, and cardiac protection. The multifunctional properties of TQ could potentially synergize with the activity of current therapeutic interventions and offer a basis for managing COVID-19 disease more effectively. Even though the experimental evidence is positive, a translational application of TQ in COVID-19 is timely warranted.


Subject(s)
Benzoquinones/pharmacology , COVID-19/complications , Cardiovascular Diseases/prevention & control , Animals , Antiviral Agents/administration & dosage , Antiviral Agents/pharmacology , Benzoquinones/administration & dosage , COVID-19/drug therapy , Cardiotonic Agents/administration & dosage , Cardiotonic Agents/pharmacology , Cardiovascular Diseases/virology , Humans , SARS-CoV-2/isolation & purification
16.
Rev Cardiovasc Med ; 22(2): 343-351, 2021 06 30.
Article in English | MEDLINE | ID: covidwho-1310350

ABSTRACT

Coronavirus disease 2019 (COVID-19), a mystified cryptic virus has challenged the mankind that has brought life to a standstill. Catastrophic loss of life, perplexed healthcare system and the downfall of global economy are some of the outcomes of this pandemic. Humans are raging a war with an unknown enemy. Infections, irrespective of age and gender, and more so in comorbidities are escalating at an alarming rate. Cardiovascular diseases, are the leading cause of death globally with an estimate of 31% of deaths worldwide out of which nearly 85% are due to heart attacks and stroke. Theoretically and practically, researchers have observed that persons with pre-existing cardiovascular conditions are comparatively more vulnerable to the COVID-19 infection. Moreover, they have studied the data between less severe and more severe cases, survivors and non survivors, intensive care unit (ICU) patients and non ICU patients, to analyse the relationship and the influence of COVID-19 on cardiovascular health of an individual, further the risk of susceptibility to submit to the virus. This review aims to provide a comprehensive particular on the possible effects, either direct or indirect, of COVID-19 on the cardiovascular heath of an individual.


Subject(s)
COVID-19/virology , Cardiovascular Diseases/virology , Cardiovascular System/virology , SARS-CoV-2/pathogenicity , Antiviral Agents/therapeutic use , COVID-19/drug therapy , COVID-19/mortality , COVID-19/physiopathology , COVID-19/therapy , Cardiovascular Agents/therapeutic use , Cardiovascular Diseases/mortality , Cardiovascular Diseases/physiopathology , Cardiovascular Diseases/therapy , Cardiovascular System/drug effects , Cardiovascular System/physiopathology , Comorbidity , Host-Pathogen Interactions , Humans , Prognosis , Risk Assessment , Risk Factors , SARS-CoV-2/drug effects
17.
Curr Oncol Rep ; 23(8): 99, 2021 07 14.
Article in English | MEDLINE | ID: covidwho-1309080

ABSTRACT

PURPOSE OF REVIEW: To give an overview of the role of social media (SoMe) in cardio-oncology during the COVID-19 pandemic. RECENT FINDINGS: SoMe has been critical in fostering education, outreach, awareness, collaboration, dissemination of information, and advocacy in cardio-oncology. This has become increasingly evident during the COVID-19 pandemic, during which SoMe has helped share best practices, community, and research focused on the impact of COVID-19 in cardiology and hematology/oncology, with cardio-oncology at the interface of these two subspecialty fields. A strength of SoMe is the ability to amplify a message in real-time, globally, with minimal investment of resources. This has been particularly beneficial for the emerging field of cardio-hematology/cardio-oncology, a field focused on the interplay of cancer and cardiovascular disease. SoMe field especially during the COVID-19 pandemic. We illustrate how social media has supported innovation (including telemedicine), amplification of healthcare workers' voice, and illumination of pre-existing and continued health disparities within the field of cardio-oncology during the pandemic.


Subject(s)
COVID-19/complications , Cardiovascular Diseases/therapy , Neoplasms/therapy , SARS-CoV-2/isolation & purification , Social Media/statistics & numerical data , Telemedicine , COVID-19/transmission , COVID-19/virology , Cardiovascular Diseases/virology , Humans , Information Dissemination , Neoplasms/virology
18.
Viruses ; 13(7)2021 07 12.
Article in English | MEDLINE | ID: covidwho-1308454

ABSTRACT

The SARS-CoV-2 virus causing COVID-19 disease has emerged expeditiously in the world and has been declared pandemic since March 2020, by World Health Organization (WHO). The destructive effects of SARS-CoV-2 infection are increased among the patients with pre-existing chronic conditions and, in particular, this review focuses on patients with underlying cardiovascular complications. The expression pattern and potential functions of SARS-CoV-2 binding receptors and the attributes of SARS-CoV-2 virus tropism in a physio-pathological state of heart and blood vessel are precisely described. Of note, the atheroprotective role of ACE2 receptors is reviewed. A detailed description of the possible detrimental role of SARS-CoV-2 infection in terms of vascular leakage, including endothelial glycocalyx dysfunction and bradykinin 1 receptor stimulation is concisely stated. Furthermore, the potential molecular mechanisms underlying SARS-CoV-2 induced clot formation in association with host defense components, including activation of FXIIa, complements and platelets, endothelial dysfunction, immune cell responses with cytokine-mediated action are well elaborated. Moreover, a brief clinical update on patient with COVID-19 disease with underlying cardiovascular complications and those who had new onset of cardiovascular complications post-COVID-19 disease was also discussed. Taken together, this review provides an overview of the mechanistic aspects of SARS-CoV-2 induced devastating effects, in vital organs such as the heart and vessels.


Subject(s)
COVID-19/immunology , COVID-19/metabolism , Cardiovascular Diseases/virology , SARS-CoV-2/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Blood Vessels/metabolism , Blood Vessels/pathology , Blood Vessels/virology , Cardiovascular Diseases/metabolism , Heart/virology , Humans , Pandemics
19.
Diabetes Metab Syndr ; 15(4): 102148, 2021.
Article in English | MEDLINE | ID: covidwho-1284040

ABSTRACT

BACKGROUND: Socio-demographics and comorbidities are involved in determining the severity and fatality in patients with COVID-19 suggested by studies in various countries, but study in Bangladesh is insufficient. AIMS: We designed the study to evaluate the association of sociodemographic and comorbidities with the prognosis of adverse health outcomes in patients with COVID-19 in Bangladesh. METHODS: A multivariate retrospective cohort study was conducted on data from 966 RT-PCR positive patients from eight divisions during December 13, 2020, to February 13, 2021. Variables included sociodemographic, comorbidities, symptoms, Charlson comorbidity index (CCI) and access to health facilities. Major outcome was fatality. Secondary outcomes included hospitalization, duration of hospital stay, requirement of mechanical ventilation and severity. RESULTS: Male (65.8%, 636 of 966) was predominant and mean age was 39.8 ± 12.6 years. Fever (79%), dry cough (55%), and loss of test/smell (51%) were frequent and 74% patients had >3 symptoms. Fatality was recorded in 10.5% patients. Comorbidities were found in 44% patients. Hypertension (21.5%) diabetes (14.6%), and cardiovascular diseases (11.3%) were most prevalent. Age >60 years (OR: 4.83, 95% CI: 2.45-6.49), and CCI >3 (OR: 5.48, 95% CI: 3.95-7.24) were predictors of hospitalizations. CCI >4 (aOR: 3.41, 95% CI: 2.57-6.09) was predictor of severity. Age >60 years (aOR: 3.77, 95% CI: 1.07-6.34), >3 symptoms (aOR: 2.14, 95% CI: 0.97-4.91) and CCI >3 vs. CCI <3 (aOR: 5.23, 95% CI: 3.77-8.09) were independently associated with fatality. CONCLUSIONS: Increased age, >3 symptoms, increasing comorbidities, higher CCI were associated with increased hospitalization, severity and fatality in patients with COVID-19.


Subject(s)
COVID-19/complications , Cardiovascular Diseases/mortality , Diabetes Mellitus/mortality , Hospitalization/statistics & numerical data , Hypertension/mortality , SARS-CoV-2/isolation & purification , Adolescent , Adult , Age Factors , Aged , Bangladesh/epidemiology , COVID-19/transmission , COVID-19/virology , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/pathology , Cardiovascular Diseases/virology , Child , Child, Preschool , Comorbidity , Diabetes Mellitus/epidemiology , Diabetes Mellitus/pathology , Diabetes Mellitus/virology , Female , Humans , Hypertension/epidemiology , Hypertension/pathology , Hypertension/virology , Infant , Infant, Newborn , Male , Middle Aged , Prognosis , Retrospective Studies , Risk Assessment , Risk Factors , Survival Rate , Young Adult
20.
Viruses ; 13(6)2021 06 18.
Article in English | MEDLINE | ID: covidwho-1282641

ABSTRACT

This article reviews the current knowledge on how viruses may utilize Extracellular Vesicle Assisted Inflammatory Load (EVAIL) to exert pathologic activities. Viruses are classically considered to exert their pathologic actions through acute or chronic infection followed by the host response. This host response causes the release of cytokines leading to vascular endothelial cell dysfunction and cardiovascular complications. However, viruses may employ an alternative pathway to soluble cytokine-induced pathologies-by initiating the release of extracellular vesicles (EVs), including exosomes. The best-understood example of this alternative pathway is human immunodeficiency virus (HIV)-elicited EVs and their propensity to harm vascular endothelial cells. Specifically, an HIV-encoded accessory protein called the "negative factor" (Nef) was demonstrated in EVs from the body fluids of HIV patients on successful combined antiretroviral therapy (ART); it was also demonstrated to be sufficient in inducing endothelial and cardiovascular dysfunction. This review will highlight HIV-Nef as an example of how HIV can produce EVs loaded with proinflammatory cargo to disseminate cardiovascular pathologies. It will further discuss whether EV production can explain SARS-CoV-2-mediated pulmonary and cardiovascular pathologies.


Subject(s)
Extracellular Vesicles/immunology , Extracellular Vesicles/virology , Inflammation/virology , COVID-19/complications , COVID-19/immunology , COVID-19/physiopathology , Cardiovascular Diseases/virology , Endothelial Cells/pathology , Endothelial Cells/virology , Exosomes/metabolism , HIV Infections/complications , HIV Infections/immunology , HIV Infections/physiopathology , HIV-1/pathogenicity , Humans , SARS-CoV-2/pathogenicity
SELECTION OF CITATIONS
SEARCH DETAIL