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1.
Turk Kardiyol Dern Ars ; 49(4): 334-338, 2021 06.
Article in English | MEDLINE | ID: covidwho-1262653

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the global coronavirus disease 2019 (COVID-19) pandemic. Although the virus predominantly causes respiratory system infection, recent reports have shown that it is also associated with many cardiovascular complications. It has been reported that COVID-19 may cause myocarditis, type 1 and 2 acute myocardial infarction, and thrombotic complications.[1] Spontaneous coronary artery dissection (SCAD) is a rare form of coronary artery disease that has recently been associated with COVID-19 in a few case reports. The case reported here is of COVID-19 associated SCAD in a patient with no history of cardiovascular disease.


Subject(s)
COVID-19/complications , Coronary Artery Disease , Coronary Vessel Anomalies , Vascular Diseases/congenital , Coronary Artery Disease/physiopathology , Coronary Artery Disease/therapy , Coronary Artery Disease/virology , Coronary Vessel Anomalies/physiopathology , Coronary Vessel Anomalies/therapy , Coronary Vessel Anomalies/virology , Electrocardiography , Humans , Male , Middle Aged , Vascular Diseases/physiopathology , Vascular Diseases/therapy , Vascular Diseases/virology
2.
Rev Recent Clin Trials ; 16(3): 262-271, 2021.
Article in English | MEDLINE | ID: covidwho-1171287

ABSTRACT

BACKGROUND: Infectious agents may be involved in the pathogenesis of vascular disease and related complications. The aim of this review is to analyze the most relevant information on the common infections related to vascular disease, discussing the main pathophysiological mechanisms. METHODS: In the current review, the most important evidence on the issue of infections and vascular disease is searched on Medline, Scopus, and ScienceDirect database. RESULTS: Among infectious agents, herpesviruses, parvovirus B19, hepatitis viruses, human immunodeficiency virus, severe acute respiratory syndrome coronavirus 2, treponema pallidum, mycobacterium tuberculosis, pseudomonas aeruginosa, staphylococcus aureus, and candida albicans seem to particularly related to vascular disease. CONCLUSION: Infectious agents may affect vessel's homeostasis and functionality, both on the arterial and venous side, by means of several pathophysiological mechanisms such as dysregulation in vasomotor function, thromboembolic complications, initiation and progression of atherosclerosis, alteration of perivascular adipose tissue, recruiting inflammatory cells and molecules.


Subject(s)
Infections/physiopathology , Vascular Diseases/physiopathology , Disease Progression , Homeostasis/physiology , Humans
3.
Stroke ; 52(5): 1885-1894, 2021 05.
Article in English | MEDLINE | ID: covidwho-1166635

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 or coronavirus disease 2019 (COVID-19) pandemic has raised concerns about the correlation with this viral illness and increased risk of stroke. Although it is too early in the pandemic to know the strength of the association between COVID-19 and stroke, it is an opportune time to review the relationship between acute viral illnesses and stroke. Here, we summarize pathophysiological principles and available literature to guide understanding of how viruses may contribute to ischemic stroke. After a review of inflammatory mechanisms, we summarize relevant pathophysiological principles of vasculopathy, hypercoagulability, and hemodynamic instability. We will end by discussing mechanisms by which several well-known viruses may cause stroke in an effort to inform our understanding of the relationship between COVID-19 and stroke.


Subject(s)
Brain Ischemia/complications , Brain Ischemia/physiopathology , COVID-19/complications , COVID-19/epidemiology , Ischemic Stroke/complications , Ischemic Stroke/physiopathology , Acute Disease , Blood Coagulation , Brain Ischemia/virology , Hemodynamics , Herpesvirus 3, Human , Humans , Inflammation/physiopathology , Ischemic Stroke/virology , Pandemics , Plaque, Atherosclerotic/physiopathology , Risk , Thrombophilia/physiopathology , Thrombosis/physiopathology , Vascular Diseases/physiopathology , Virus Diseases/physiopathology
5.
Ann Diagn Pathol ; 50: 151645, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1064802

ABSTRACT

The objective of this study was to elucidate the pathophysiology that underlies severe COVID-19 by assessing the histopathology and the in situ detection of infectious SARS-CoV-2 and viral capsid proteins along with the cellular target(s) and host response from twelve autopsies. There were three key findings: 1) high copy infectious virus was limited mostly to the alveolar macrophages and endothelial cells of the septal capillaries; 2) viral spike protein without viral RNA localized to ACE2+ endothelial cells in microvessels that were most abundant in the subcutaneous fat and brain; 3) although both infectious virus and docked viral spike protein was associated with complement activation, only the endocytosed pseudovirions induced a marked up-regulation of the key COVID-19 associated proteins IL6, TNF alpha, IL1 beta, p38, IL8, and caspase 3. Importantly, this microvasculitis was associated with characteristic findings on hematoxylin and eosin examination that included endothelial degeneration and resultant basement membrane zone disruption and reduplication. It is concluded that serious COVID-19 infection has two distinct mechanisms: 1) a microangiopathy of pulmonary capillaries associated with a high infectious viral load where endothelial cell death releases pseudovirions into the circulation, and 2) the pseudovirions dock on ACE2+ endothelial cells most prevalent in the skin/subcutaneous fat and brain that activates the complement pathway/coagulation cascade resulting in a systemic procoagulant state as well as the expression of cytokines that produce the cytokine storm. The data predicts a favorable response to therapies based on either removal of circulating viral proteins and/or blunting of the endothelial-induced response.


Subject(s)
COVID-19/physiopathology , Capsid Proteins/metabolism , SARS-CoV-2/pathogenicity , Spike Glycoprotein, Coronavirus/metabolism , Thrombotic Microangiopathies/physiopathology , Vascular Diseases/physiopathology , Adult , Aged , Aged, 80 and over , Angiotensin-Converting Enzyme 2/metabolism , Autopsy , COVID-19/virology , Capsid Proteins/genetics , Endothelial Cells/enzymology , Endothelial Cells/virology , Female , Humans , Lung/physiopathology , Lung/virology , Male , Microvessels/physiopathology , Microvessels/virology , Middle Aged , RNA, Viral/genetics , SARS-CoV-2/genetics , Spike Glycoprotein, Coronavirus/genetics , Thrombotic Microangiopathies/virology , Vascular Diseases/virology , Virion
6.
Radiat Res ; 195(1): 1-24, 2021 01 01.
Article in English | MEDLINE | ID: covidwho-1021760

ABSTRACT

As the multi-systemic components of COVID-19 emerge, parallel etiologies can be drawn between SARS-CoV-2 infection and radiation injuries. While some SARS-CoV-2-infected individuals present as asymptomatic, others exhibit mild symptoms that may include fever, cough, chills, and unusual symptoms like loss of taste and smell and reddening in the extremities (e.g., "COVID toes," suggestive of microvessel damage). Still others alarm healthcare providers with extreme and rapid onset of high-risk indicators of mortality that include acute respiratory distress syndrome (ARDS), multi-organ hypercoagulation, hypoxia and cardiovascular damage. Researchers are quickly refocusing their science to address this enigmatic virus that seems to unveil itself in new ways without discrimination. As investigators begin to identify early markers of disease, identification of common threads with other pathologies may provide some clues. Interestingly, years of research in the field of radiation biology documents the complex multiorgan nature of another disease state that occurs after exposure to high doses of radiation: the acute radiation syndrome (ARS). Inflammation is a key common player in COVID-19 and ARS, and drives the multi-system damage that dramatically alters biological homeostasis. Both conditions initiate a cytokine storm, with similar pro-inflammatory molecules increased and other anti-inflammatory molecules decreased. These changes manifest in a variety of ways, with a demonstrably higher health impact in patients having underlying medical conditions. The potentially dramatic human impact of ARS has guided the science that has identified many biomarkers of radiation exposure, established medical management strategies for ARS, and led to the development of medical countermeasures for use in the event of a radiation public health emergency. These efforts can now be leveraged to help elucidate mechanisms of action of COVID-19 injuries. Furthermore, this intersection between COVID-19 and ARS may point to approaches that could accelerate the discovery of treatments for both.


Subject(s)
COVID-19/physiopathology , Pandemics , Radiation Injuries/physiopathology , SARS-CoV-2/pathogenicity , Acute Lung Injury/etiology , Acute Lung Injury/physiopathology , Angiotensin-Converting Enzyme 2/deficiency , Angiotensin-Converting Enzyme 2/physiology , Animals , Anti-Bacterial Agents/therapeutic use , Anti-Inflammatory Agents/therapeutic use , Antioxidants/therapeutic use , Biomarkers/blood , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/physiopathology , COVID-19/drug therapy , COVID-19/epidemiology , COVID-19/immunology , Clinical Trials as Topic , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Hematologic Diseases/etiology , Hematologic Diseases/physiopathology , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Inflammation/etiology , Inflammation/physiopathology , Intercellular Signaling Peptides and Proteins/therapeutic use , Mesenchymal Stem Cell Transplantation , Mice , Organ Specificity , Pyroptosis , Radiation Injuries/blood , Radiation Injuries/drug therapy , Radiation Injuries/immunology , Receptors, Virus/physiology , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiology , SARS-CoV-2/isolation & purification , Vascular Diseases/drug therapy , Vascular Diseases/etiology , Vascular Diseases/physiopathology
7.
Arterioscler Thromb Vasc Biol ; 40(10): 2404-2407, 2020 10.
Article in English | MEDLINE | ID: covidwho-1015733

ABSTRACT

OBJECTIVE: Alveolar-capillary endothelial cells can be activated by severe acute respiratory syndrome coronavirus 2 infection leading to cytokine release. This could trigger endothelial dysfunction, pyroptosis, and thrombosis, which are the vascular changes, commonly referred to as coronavirus disease 2019 (COVID-19) endotheliopathy. Thus, this study aimed to identify tissue biomarkers associated with endothelial activation/dysfunction and the pyroptosis pathway in the lung samples of patients with COVID-19 and to compare them to pandemic influenza A virus H1N1 subtype 2009 and control cases. Approach and Results: Postmortem lung samples (COVID-19 group =6 cases; H1N1 group =10 cases, and control group =11 cases) were analyzed using immunohistochemistry and the following monoclonal primary antibodies: anti-IL (interleukin)-6, anti-TNF (tumor necrosis factor)-α, anti-ICAM-1 (intercellular adhesion molecule 1), and anticaspase-1. From the result, IL-6, TNF-α, ICAM-1, and caspase-1 showed higher tissue expression in the COVID-19 group than in the H1N1 and control groups. CONCLUSIONS: Our results demonstrated endothelial dysfunction and suggested the participation of the pyroptosis pathway in the pulmonary samples. These conditions might lead to systemic thrombotic events that could impair the clinical staff's efforts to avoid fatal outcomes. One of the health professionals' goals should be to identify the high risk of thrombosis patients early to block endotheliopathy and its consequences.


Subject(s)
Coronavirus Infections/pathology , Endothelial Cells/cytology , Endothelium, Vascular/pathology , Pneumonia, Viral/pathology , Thrombosis/pathology , Vascular Diseases/pathology , Autopsy , Biopsy, Needle , COVID-19 , Cause of Death , Coronavirus Infections/mortality , Endothelial Cells/pathology , Endothelium, Vascular/physiopathology , Female , Humans , Immunohistochemistry , Male , Pandemics , Pneumonia, Viral/mortality , Risk Assessment , Thrombosis/etiology , Thrombosis/mortality , Vascular Diseases/mortality , Vascular Diseases/physiopathology
8.
Nat Rev Cardiol ; 18(3): 194-209, 2021 03.
Article in English | MEDLINE | ID: covidwho-936141

ABSTRACT

The core pathology of coronavirus disease 2019 (COVID-19) is infection of airway cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that results in excessive inflammation and respiratory disease, with cytokine storm and acute respiratory distress syndrome implicated in the most severe cases. Thrombotic complications are a major cause of morbidity and mortality in patients with COVID-19. Patients with pre-existing cardiovascular disease and/or traditional cardiovascular risk factors, including obesity, diabetes mellitus, hypertension and advanced age, are at the highest risk of death from COVID-19. In this Review, we summarize new lines of evidence that point to both platelet and endothelial dysfunction as essential components of COVID-19 pathology and describe the mechanisms that might account for the contribution of cardiovascular risk factors to the most severe outcomes in COVID-19. We highlight the distinct contributions of coagulopathy, thrombocytopathy and endotheliopathy to the pathogenesis of COVID-19 and discuss potential therapeutic strategies in the management of patients with COVD-19. Harnessing the expertise of the biomedical and clinical communities is imperative to expand the available therapeutics beyond anticoagulants and to target both thrombocytopathy and endotheliopathy. Only with such collaborative efforts can we better prepare for further waves and for future coronavirus-related pandemics.


Subject(s)
Blood Coagulation Disorders/blood , Blood Platelet Disorders/blood , COVID-19/blood , Endothelium, Vascular/physiopathology , Inflammation/blood , Thrombosis/blood , Administration, Inhalation , Anticoagulants/therapeutic use , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/physiopathology , Blood Platelet Disorders/drug therapy , Blood Platelet Disorders/etiology , Blood Platelet Disorders/physiopathology , COVID-19/complications , COVID-19/drug therapy , COVID-19/physiopathology , Endothelium-Dependent Relaxing Factors/therapeutic use , Epoprostenol/therapeutic use , Heart Disease Risk Factors , Humans , Iloprost/therapeutic use , Inflammation/etiology , Inflammation/physiopathology , Nitric Oxide/therapeutic use , Platelet Aggregation Inhibitors/therapeutic use , SARS-CoV-2 , Systemic Inflammatory Response Syndrome/blood , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/physiopathology , Thrombosis/etiology , Thrombosis/immunology , Thrombotic Microangiopathies/blood , Thrombotic Microangiopathies/drug therapy , Thrombotic Microangiopathies/etiology , Thrombotic Microangiopathies/physiopathology , Vascular Diseases/blood , Vascular Diseases/drug therapy , Vascular Diseases/etiology , Vascular Diseases/physiopathology , Vasodilator Agents/therapeutic use , Venous Thromboembolism/blood , Venous Thromboembolism/drug therapy , Venous Thromboembolism/etiology , Venous Thromboembolism/physiopathology
9.
Rev Cardiovasc Med ; 21(3): 315-319, 2020 09 30.
Article in English | MEDLINE | ID: covidwho-875132

ABSTRACT

Great attention has been paid to endothelial dysfunction (ED) in coronavirus disease 2019 (COVID-19). There is growing evidence to suggest that the angiotensin converting enzyme 2 receptor (ACE2 receptor) is expressed on endothelial cells (ECs) in the lung, heart, kidney, and intestine, particularly in systemic vessels (small and large arteries, veins, venules, and capillaries). Upon viral infection of ECs by severe acute respiratory syndrome coronarvirus 2 (SARS-CoV-2), ECs become activated and dysfunctional. As a result of endothelial activation and ED, the levels of pro-inflammatory cytokines (interleukin -1, interleukin-6 (IL-6), and tumor necrosis factor-α), chemokines (monocyte chemoattractant protein-1), von Willebrand factor (vWF) antigen, vWF activity, and factor VIII are elevated. Higher levels of acute phase reactants (IL-6, C-reactive protein, and D-dimer) are also associated with SARS-CoV-2 infection. Therefore, it is reasonable to assume that ED contributes to COVID-19-associated vascular inflammation, particularly endotheliitis, in the lung, heart, and kidney, as well as COVID-19-associated coagulopathy, particularly pulmonary fibrinous microthrombi in the alveolar capillaries. Here we present an update on ED-relevant vasculopathy in COVID-19. Further research for ED in COVID-19 patients is warranted to understand therapeutic opportunities.


Subject(s)
Betacoronavirus , Blood Coagulation Disorders/etiology , Coronavirus Infections/complications , Endothelium, Vascular/physiopathology , Pneumonia, Viral/complications , Vascular Diseases/etiology , Vasodilation/physiology , Blood Coagulation Disorders/physiopathology , COVID-19 , Coronavirus Infections/epidemiology , Humans , Inflammation/etiology , Inflammation/physiopathology , Pandemics , Pneumonia, Viral/epidemiology , SARS-CoV-2 , Vascular Diseases/physiopathology
10.
Am J Respir Crit Care Med ; 202(5): 690-699, 2020 09 01.
Article in English | MEDLINE | ID: covidwho-646801

ABSTRACT

Rationale: Clinical and epidemiologic data in coronavirus disease (COVID-19) have accrued rapidly since the outbreak, but few address the underlying pathophysiology.Objectives: To ascertain the physiologic, hematologic, and imaging basis of lung injury in severe COVID-19 pneumonia.Methods: Clinical, physiologic, and laboratory data were collated. Radiologic (computed tomography (CT) pulmonary angiography [n = 39] and dual-energy CT [DECT, n = 20]) studies were evaluated: observers quantified CT patterns (including the extent of abnormal lung and the presence and extent of dilated peripheral vessels) and perfusion defects on DECT. Coagulation status was assessed using thromboelastography.Measurements and Results: In 39 consecutive patients (male:female, 32:7; mean age, 53 ± 10 yr [range, 29-79 yr]; Black and minority ethnic, n = 25 [64%]), there was a significant vascular perfusion abnormality and increased physiologic dead space (dynamic compliance, 33.7 ± 14.7 ml/cm H2O; Murray lung injury score, 3.14 ± 0.53; mean ventilatory ratios, 2.6 ± 0.8) with evidence of hypercoagulability and fibrinolytic "shutdown". The mean CT extent (±SD) of normally aerated lung, ground-glass opacification, and dense parenchymal opacification were 23.5 ± 16.7%, 36.3 ± 24.7%, and 42.7 ± 27.1%, respectively. Dilated peripheral vessels were present in 21/33 (63.6%) patients with at least two assessable lobes (including 10/21 [47.6%] with no evidence of acute pulmonary emboli). Perfusion defects on DECT (assessable in 18/20 [90%]) were present in all patients (wedge-shaped, n = 3; mottled, n = 9; mixed pattern, n = 6).Conclusions: Physiologic, hematologic, and imaging data show not only the presence of a hypercoagulable phenotype in severe COVID-19 pneumonia but also markedly impaired pulmonary perfusion likely caused by pulmonary angiopathy and thrombosis.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Lung/blood supply , Pneumonia, Viral/complications , Pulmonary Circulation/physiology , Vascular Diseases/etiology , Adult , Aged , COVID-19 , Coronavirus Infections/epidemiology , Female , Humans , Lung/diagnostic imaging , Male , Middle Aged , Pandemics , Pneumonia, Viral/epidemiology , SARS-CoV-2 , Tomography, X-Ray Computed , Vascular Diseases/diagnosis , Vascular Diseases/physiopathology
11.
J Thromb Thrombolysis ; 50(3): 567-579, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-630015

ABSTRACT

After the emergence of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV) in the last two decades, the world is facing its new challenge in Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) pandemic with unprecedented global response. With the expanding domain of presentations in COVID-19 patients, the full range of manifestations is yet to unfold. The classical clinical symptoms for SARS-CoV-2 affected patients are dry cough, high fever, dyspnoea, lethal pneumonia whereas many patients have also been found to be associated with a few additional signs and clinical manifestations of isolated vasculopathy. Albeit a deep and profound knowledge has been gained on the clinical features and management of COVID-19, less clear association has been provided on SARS-CoV-2 mediated direct or indirect vasculopathy and its possible correlation with disease prognosis. The accumulative evidences suggest that novel coronavirus, apart from its primary respiratory confinement, may also invade vascular endothelial cells of several systems including cerebral, cardio-pulmonary as well as renal microvasculature, modulating multiple visceral perfusion indices. Here we analyse the phylogenetic perspective of SARS-CoV-2 along with other strains of ß-coronaviridae from a standpoint of vasculopathic derangements. Based on the existing case reports, literature and open data bases, we also analyse the differential pattern of vasculopathy related changes in COVID-19 positive patients. Besides, we debate the need of modulation in clinical approach from a hemodynamical point of view, as a measure towards reducing disease transmission, morbidity and mortality in SARS-CoV-2 affected patients.


Subject(s)
Betacoronavirus/pathogenicity , Blood Vessels/virology , Coronavirus Infections/virology , Pneumonia, Viral/virology , Vascular Diseases/virology , Animals , Betacoronavirus/genetics , Betacoronavirus/immunology , Blood Coagulation , Blood Vessels/immunology , Blood Vessels/metabolism , Blood Vessels/physiopathology , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/metabolism , Coronavirus Infections/physiopathology , Cytokines/metabolism , Hemodynamics , Host-Pathogen Interactions , Humans , Inflammation Mediators/metabolism , Pandemics , Phylogeny , Pneumonia, Viral/immunology , Pneumonia, Viral/metabolism , Pneumonia, Viral/physiopathology , Prognosis , Risk Assessment , Risk Factors , SARS-CoV-2 , Vascular Diseases/immunology , Vascular Diseases/metabolism , Vascular Diseases/physiopathology
12.
Med Hypotheses ; 144: 110015, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-608986

ABSTRACT

Several risk factors are associated with a worse outcome for COVID-19 patients; the most recognized are demographic characteristics such as older age and male gender, and pre-existing cardiovascular conditions. About the latter, hypertension and coronary heart disease are among the most common comorbidities recorded in infected patients, together with type 2 diabetes mellitus (T2DM). Data from Istituto Superiore di Sanità (ISS, Italy) show that more than 68.3% of patients had hypertension, 28.2% ischemic heart disease, 22.5% atrial fibrillation, while 30.1% T2DM. Several authors suggested that cardiovascular diseases and diabetes mellitus are linked to endothelial dysfunction, and all of them are strictly related to aging. Considering the impact of the gender on the COVID-19 epidemic, even if confirmed cases from each nation are changing every day, epidemiological data clearly evidence that in men the infection causes worse outcomes compared to women. In Italy, up to 21 May, in the age range of 60-89 years, male deaths were 63.9% of total cases. The reason behind this difference between genders appears not clear; however, the diversity in sex-hormones and styles of life are believed to play a role in the patient's susceptibility to severe SARS-CoV-2 outcomes. It is known that the activation of endothelial estrogen receptors increases NO and decreases ROS, protecting the vascular system from angiotensin II-mediated vasoconstriction, inflammation, and ROS production. During the pandemic, joining forces is vital; thus, as people help doctors by limiting their displacements out of their houses avoiding hence the spread of the infection, doctors help patients to overcome severe SARS-CoV-2 infections by using multiple pharmacological approaches. In this context, the preservation of endothelial function and the mitigation of vascular inflammation are prominent targets, essential to reduce severe outcomes also in male older patients.


Subject(s)
Age Factors , COVID-19/physiopathology , Endothelium, Vascular/physiopathology , Sex Factors , Vascular Diseases/physiopathology , Aged , Aged, 80 and over , Aging , COVID-19/epidemiology , Comorbidity , Coronary Disease/physiopathology , Female , Humans , Italy/epidemiology , Male , Middle Aged , Pandemics , Risk Factors , Treatment Outcome , Vascular Diseases/epidemiology
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