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1.
Sci Rep ; 12(1): 2670, 2022 02 17.
Article in English | MEDLINE | ID: covidwho-1704157

ABSTRACT

The prognosis of heart failure (HF) patients is determined to a decisive extent by comorbidities. The present study investigates the association between a broad spectrum of diseases and the occurrence of HF in a large collective of outpatients. This retrospective case control study assessed the prevalence of 37 cardiac and extracardiac diseases in patients with an initial diagnosis of heart failure (ICD-10: I50) in 1,274 general practices in Germany between January 2005 and December 2019. The study is based on the Disease Analyzer database (IQVIA), which contains drug prescriptions, diagnoses, and basic medical and demographic data. Patients with and without heart failure were matched by sex, age, and index year. Hazard regression models were conducted to evaluate the association between different disease entities and heart failure. The present study included 162,246 patients with heart failure and 162,246 patients without heart failure. Mean age [SD] was 73.7 [12.1] years; 52.6% were women. Out of 37 predefined diagnoses, 36 were more prevalent in HF patients. The highest prevalence was primary hypertension (63.4% in HF patients vs. 53.3% in controls, p < 0.001) followed by lipid metabolism disorders (34.6% in HF patients vs. 29.1% in HF patients p < 0.001) and diabetes mellitus type II (32.2% in HF patients vs. 25.2% in controls, p < 0.001). In the regression analysis, 19 diseases were significantly associated with heart failure. Non-cardiovascular diagnoses strongly associated with HF were obesity (HR = 1.46), chronic bronchitis and COPD (HR = 1.41), gout (HR: 1.41), and chronic kidney disease (HR = 1.27). In the present study, we identified a variety of cardiac and extracardiac diseases associated with heart failure. Our data underscore the immense importance of comorbidities, even as early as at the stage of initial diagnosis of heart failure.


Subject(s)
Comorbidity , Heart Failure , Models, Cardiovascular , Registries , Aged , Aged, 80 and over , Female , Germany , Heart Failure/diagnosis , Heart Failure/epidemiology , Heart Failure/physiopathology , Humans , Male , Middle Aged , Retrospective Studies
2.
Hamostaseologie ; 41(5): 356-364, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1483185

ABSTRACT

Cardiovascular manifestations are frequent in COVID-19 infection and are predictive of adverse outcomes. Elevated cardiac biomarkers are common findings in patients with cardiovascular comorbidities and severe COVID-19 infection. Troponin, inflammatory and thrombotic markers may also improve risk prediction in COVID-19. In our comprehensive review, we provide an overview of the incidence, potential mechanisms and outcome of acute cardiac injury in COVID-19. Thereby, we discuss coagulation abnormalities in sepsis and altered immune response as contributing factors favoring myocardial injury. We further highlight the role of endothelial damage in the pathophysiological concepts. Finally, observational studies addressing the incidence of myocardial infarction during COVID-19 pandemic are discussed.


Subject(s)
COVID-19/epidemiology , Heart Injuries/epidemiology , Myocardial Infarction/epidemiology , Pandemics , SARS-CoV-2 , Biomarkers/blood , COVID-19/blood , COVID-19/mortality , Comorbidity , Heart Injuries/blood , Heart Injuries/mortality , Humans , Incidence , Models, Cardiovascular , Myocardial Infarction/blood , Myocardial Infarction/mortality , SARS-CoV-2/pathogenicity , Troponin/blood
3.
Hamostaseologie ; 41(5): 350-355, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1351995

ABSTRACT

COVID-19 bezeichnet eine der schlimmsten Krisen unserer Generation und stellt (nicht nur) für das Gesundheitssystem eine schwer bewältigbare Herausforderung dar. Mortalität und Morbidität sind im Vergleich zu anderen saisonalen Erkrankungen wie der Influenza deutlich erhöht. COVID-19 bedroht allerdings nicht die gesamte Bevölkerung in gleichem Maße. Hochrisikopatienten sind älter und leiden an kardiovaskulären Erkrankungen wie Bluthochdruck, Diabetes mellitus oder einer koronaren Herzerkrankung. Um das Risiko für einen schweren Erkrankungsverlaufs zu quantifizieren bedarf es einer multimodalen Herangehensweise. Verschiedene Risikostratifizierungssysteme stehen zu Verfügung um ungünstige Verläufe wie Intensivbehandlung oder Gesamtmortalität vorauszusagen. Biomarker wie Troponin-I, D-Dimere und NT pro-BNP kombiniert mit echokardiographischen Parametern wie links- und rechtsventrikulärer Pumpfunktion sowie pulmonalarteriellem Druck können hilfreich sein um Hochrisikopatienten zu identifizieren, die ein intensiviertes Monitoring und eine stringentere Behandlung benötigen. Da kardiovaskuläre Risikofaktoren und Komorbiditäten von großer Bedeutung zur Abschätzung des Verlaufs einer SARS-CoV-2 Infektion sind, könnten alle hospitalisierten COVID-19 Patienten von einer routinemäßigen kardiologischen Betreuung durch ein COVID-19-Heart-Team profitieren. Ein frühzeitiges Erkennen von (kardiovaskulären) Hochrisikopatienten könnte das Management erleichtern sowie die Prognose einer schweren SARS-CoV-2 Infektion verbessern.


Subject(s)
COVID-19/epidemiology , Cardiovascular Diseases/epidemiology , SARS-CoV-2 , Biomarkers/analysis , COVID-19/therapy , Cardiovascular Diseases/diagnostic imaging , Cardiovascular Diseases/physiopathology , Comorbidity , Echocardiography , Heart Disease Risk Factors , Humans , Models, Cardiovascular , Pandemics , Prognosis , Risk Assessment , SARS-CoV-2/pathogenicity , Severity of Illness Index
4.
Int J Mol Sci ; 22(13)2021 Jul 04.
Article in English | MEDLINE | ID: covidwho-1304672

ABSTRACT

Cardiovascular diseases have attracted our full attention not only because they are the main cause of mortality and morbidity in many countries but also because the therapy for and cure of these maladies are among the major challenges of the medicine in the 21st century [...].


Subject(s)
Cardiovascular Diseases/etiology , Animals , Cardiovascular Diseases/genetics , Cardiovascular Diseases/metabolism , Complement C3/genetics , Complement C3/metabolism , Extracellular Vesicles/metabolism , Genetic Markers , Humans , Membrane Proteins/genetics , Membrane Proteins/metabolism , MicroRNAs/genetics , MicroRNAs/metabolism , Models, Cardiovascular , Myosin Light Chains/genetics , Myosin Light Chains/metabolism , Risk Factors
5.
Clin Appl Thromb Hemost ; 27: 10760296211021498, 2021.
Article in English | MEDLINE | ID: covidwho-1249538

ABSTRACT

Today the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a global health problem. After more than a year with the pandemic, although our knowledge has progressed on COVID-19, there are still many unknowns in virological, pathophysiological and immunological aspects. It is obvious that the most efficient solution to end this pandemic are safe and efficient vaccines. This manuscript summarizes the pathophysiological and thrombotic features of COVID-19 and the safety and efficacy of currently approved COVID-19 vaccines with an aim to clarify the recent concerns of thromboembolic events after COVID-19 vaccination. The influx of newer information is rapid, requiring periodic updates and objective assessment of the data on the pathogenesis of COVID-19 variants and the safety and efficacy of currently available vaccines.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , SARS-CoV-2 , Thrombosis/etiology , Autoantibodies/biosynthesis , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19 Vaccines/genetics , COVID-19 Vaccines/immunology , Clinical Trials as Topic , Disseminated Intravascular Coagulation/epidemiology , Disseminated Intravascular Coagulation/etiology , Drug Approval , Female , Genetic Vectors , Glycosaminoglycans/immunology , Humans , Male , Models, Cardiovascular , Pandemics/prevention & control , Platelet Factor 4/immunology , SARS-CoV-2/genetics , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Safety , Sinus Thrombosis, Intracranial/epidemiology , Sinus Thrombosis, Intracranial/etiology , Thrombosis/epidemiology , Thrombosis/physiopathology , Vaccines, Inactivated/adverse effects , Vaccines, Inactivated/genetics , Vaccines, Inactivated/immunology , Vaccines, Synthetic/adverse effects , Vaccines, Synthetic/genetics , Vaccines, Synthetic/immunology
6.
Microcirculation ; 28(7): e12718, 2021 10.
Article in English | MEDLINE | ID: covidwho-1236400

ABSTRACT

Recently, accumulating evidence has highlighted the role of endothelial dysfunction in COVID-19 progression. Coronary microvascular dysfunction (CMD) plays a pivotal role in cardiovascular disease (CVD) and CVD-related risk factors (eg, age, gender, hypertension, diabetes mellitus, and obesity). Equally, these are also risk factors for COVID-19. The purpose of this review was to explore CMD pathophysiology in COVID-19, based on recent evidence. COVID-19 mechanisms were reviewed in terms of imbalanced renin-angiotensin-aldosterone-systems (RAAS), systemic inflammation and immune responses, endothelial dysfunction, and coagulatory disorders. Based on these mechanisms, we addressed CMD pathophysiology within the context of COVID-19, from five perspectives. The first was the disarrangement of local RAAS and Kallikrein-kinin-systems attributable to SARS-Cov-2 entry, and the concomitant decrease in coronary microvascular endothelial angiotensin I converting enzyme 2 (ACE2) levels. The second was related to coronary microvascular obstruction, induced by COVID-19-associated systemic hyper-inflammation and pro-thrombotic state. The third was focused on how pneumonia/acute respiratory distress syndrome (ARDS)-related systemic hypoxia elicited oxidative stress in coronary microvessels and cardiac sympathetic nerve activation. Fourthly, we discussed how autonomic nerve dysfunction mediated by COVID-19-associated mental, physical, or physiological factors could elicit changes in coronary blood flow, resulting in CMD in COVID-19 patients. Finally, we analyzed reciprocity between the coronary microvascular endothelium and perivascular cellular structures due to viremia, SARS-CoV-2 dissemination, and systemic inflammation. These mechanisms may function either consecutively or intermittently, finally culminating in CMD-mediated cardiovascular symptoms in COVID-19 patients. However, the underlying molecular pathogenesis remains to be clarified.


Subject(s)
COVID-19/physiopathology , Coronary Vessels/physiopathology , SARS-CoV-2 , COVID-19/complications , COVID-19/immunology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Disease Progression , Endothelium, Vascular/physiopathology , Female , Humans , Inflammation/physiopathology , Male , Microcirculation/physiology , Models, Cardiovascular , Renin-Angiotensin System/physiology , Risk Factors , Thrombosis/etiology , Thrombosis/physiopathology
7.
Int Rev Cell Mol Biol ; 363: 203-269, 2021.
Article in English | MEDLINE | ID: covidwho-1212320

ABSTRACT

An increase in intracellular Ca2+ concentration ([Ca2+]i) regulates a plethora of functions in the cardiovascular (CV) system, including contraction in cardiomyocytes and vascular smooth muscle cells (VSMCs), and angiogenesis in vascular endothelial cells and endothelial colony forming cells. The sarco/endoplasmic reticulum (SR/ER) represents the largest endogenous Ca2+ store, which releases Ca2+ through ryanodine receptors (RyRs) and/or inositol-1,4,5-trisphosphate receptors (InsP3Rs) upon extracellular stimulation. The acidic vesicles of the endolysosomal (EL) compartment represent an additional endogenous Ca2+ store, which is targeted by several second messengers, including nicotinic acid adenine dinucleotide phosphate (NAADP) and phosphatidylinositol 3,5-bisphosphate [PI(3,5)P2], and may release intraluminal Ca2+ through multiple Ca2+ permeable channels, including two-pore channels 1 and 2 (TPC1-2) and Transient Receptor Potential Mucolipin 1 (TRPML1). Herein, we discuss the emerging, pathophysiological role of EL Ca2+ signaling in the CV system. We describe the role of cardiac TPCs in ß-adrenoceptor stimulation, arrhythmia, hypertrophy, and ischemia-reperfusion injury. We then illustrate the role of EL Ca2+ signaling in VSMCs, where TPCs promote vasoconstriction and contribute to pulmonary artery hypertension and atherosclerosis, whereas TRPML1 sustains vasodilation and is also involved in atherosclerosis. Subsequently, we describe the mechanisms whereby endothelial TPCs promote vasodilation, contribute to neurovascular coupling in the brain and stimulate angiogenesis and vasculogenesis. Finally, we discuss about the possibility to target TPCs, which are likely to mediate CV cell infection by the Severe Acute Respiratory Disease-Coronavirus-2, with Food and Drug Administration-approved drugs to alleviate the detrimental effects of Coronavirus Disease-19 on the CV system.


Subject(s)
COVID-19/complications , COVID-19/drug therapy , Calcium Signaling/physiology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/metabolism , Cardiovascular System/metabolism , Lysosomes/metabolism , SARS-CoV-2 , ADP-ribosyl Cyclase 1/metabolism , Animals , Brain/blood supply , Brain/metabolism , COVID-19/metabolism , Calcium Channels/metabolism , Cardiovascular Diseases/drug therapy , Endoplasmic Reticulum/metabolism , Endothelial Cells/metabolism , Humans , Models, Cardiovascular , Myocytes, Cardiac/metabolism , NADP/analogs & derivatives , NADP/metabolism , Receptors, Adrenergic, beta/metabolism , Sarcoplasmic Reticulum/metabolism , Transient Receptor Potential Channels/metabolism
8.
Math Biosci Eng ; 18(4): 3364-3383, 2021 04 15.
Article in English | MEDLINE | ID: covidwho-1206379

ABSTRACT

Emerging studies address how COVID-19 infection can impact the human cardiovascular system. This relates particularly to the development of myocardial injury, acute coronary syndrome, myocarditis, arrhythmia, and heart failure. Prospective treatment approach is advised for these patients. To study the interplay between local changes (reduced contractility), global variables (peripheral resistances, heart rate) and the cardiac function, we considered a lumped parameters computational model of the cardiovascular system and a three-dimensional multiphysics model of cardiac electromechanics. Our mathematical model allows to simulate the systemic and pulmonary circulations, the four cardiac valves and the four heart chambers, through equations describing the underlying physical processes. By the assessment of conventionally relevant parameters of cardiac function obtained through our numerical simulations, we propose a computational model to effectively reveal the interactions between the cardiac and pulmonary functions in virtual subjects with normal and impaired cardiac function at baseline affected by mild or severe COVID-19.


Subject(s)
COVID-19 , Heart , Hemodynamics , Humans , Models, Cardiovascular , Prospective Studies , SARS-CoV-2
9.
J Appl Physiol (1985) ; 129(6): 1413-1421, 2020 12 01.
Article in English | MEDLINE | ID: covidwho-1064196

ABSTRACT

The transport of oxygen between blood and tissue is limited by blood's capillary transit time, understood as the time available for diffusion exchange before blood returns to the heart. If all capillaries contribute equally to tissue oxygenation at all times, this physical limitation would render vasodilation and increased blood flow insufficient means to meet increased metabolic demands in the heart, muscle, and other organs. In 1920, Danish physiologist August Krogh was awarded the Nobel Prize in Physiology or Medicine for his mathematical and quantitative, experimental demonstration of a solution to this conceptual problem: capillary recruitment, the active opening of previously closed capillaries to meet metabolic demands. Today, capillary recruitment is still mentioned in textbooks. When we suspect symptoms might represent hypoxia of a vascular origin, however, we search for relevant, flow-limiting conditions in our patients and rarely ascribe hypoxia or hypoxemia to short capillary transit times. This review describes how natural changes in capillary transit-time heterogeneity (CTH) and capillary hematocrit (HCT) across open capillaries during blood flow increases can account for a match of oxygen availability to metabolic demands in normal tissue. CTH and HCT depend on a number of factors: on blood properties, including plasma viscosity, the number, size, and deformability of blood cells, and blood cell interactions with capillary endothelium; on anatomical factors including glycocalyx, endothelial cells, basement membrane, and pericytes that affect the capillary diameter; and on any external compression. The review describes how risk factor- and disease-related changes in CTH and HCT interfere with flow-metabolism coupling and tissue oxygenation and discusses whether such capillary dysfunction contributes to vascular disease pathology.


Subject(s)
Capillaries/physiology , Microcirculation , Models, Cardiovascular , Oxygen Consumption , Oxygen/blood , Alzheimer Disease/blood , Alzheimer Disease/physiopathology , Anemia, Sickle Cell/blood , Anemia, Sickle Cell/physiopathology , Animals , Blood Flow Velocity , Cardiovascular Diseases/blood , Cardiovascular Diseases/physiopathology , Diffusion , Humans , Hypoxia/blood , Hypoxia/physiopathology , Regional Blood Flow , Time Factors
10.
Clin Appl Thromb Hemost ; 27: 1076029621993573, 2021.
Article in English | MEDLINE | ID: covidwho-1079192

ABSTRACT

The novel coronavirus disease 2019 (COVID-19) predisposes patients to venous thromboembolism (VTE) due to risk factors, severe infection, and severe inflammatory responses. The objective is to determine the risk of developing VTE after corticosteroid administration during COVID-19 treatment. Using PRISMA reporting guidelines, a review was conducted from inception until 20 September 2020 with MESH terms including "venous thromboembolism" and "covid-19," using MEDLINE, Scopus, CINAHL Plus, and WHO Global Database. The inclusion criteria included studies with COVID-19 patients aged 18 years and older with VTE diagnosed by duplex ultrasonography or computed tomography pulmonary angiography (CTPA). Exclusion criteria were studies with non COVID-19 patients and non-VTE patients aged less than 18 years. Quality appraisal was conducted of included studies using the Newcastle-Ottawa Scale (NOS). A random-effect model using 95% confidence intervals, and significance of findings was assessed using Review Manager V5.4.We included 12 observational studies with 2801 patients (VTE n = 434; non-VTE; n = 2367). Patients had a higher risk of presenting with VTE when being administered corticosteroids during treatment of COVID-19 (RR = 1.39, 95% CI = 1.10 to 1.77, I2 = 0%). A positive effect size was found (SMD = 1.00, 95% CI = 0.67 to 1.32, I2 = 85%) for D-dimer laboratory values (µg/mL) in the VTE group. While critically ill COVID-19 patients are more likely to require corticosteroid treatment, it may be associated with increased risk of VTE, and poor clinical prognosis. Risk assessment is warranted to further evaluate patients as case-by-case in reducing VTE and worsening clinical outcomes.


Subject(s)
Adrenal Cortex Hormones/adverse effects , COVID-19/complications , COVID-19/drug therapy , SARS-CoV-2 , Venous Thromboembolism/etiology , Adrenal Cortex Hormones/therapeutic use , COVID-19/mortality , Critical Illness , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Models, Cardiovascular , Risk Assessment , Risk Factors , SARS-CoV-2/pathogenicity , Venous Thromboembolism/blood , Venous Thromboembolism/mortality
11.
Med Hypotheses ; 146: 110454, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-969557

ABSTRACT

Takotsubo cardiomyopathy (TTS), known as stress cardiomyopathy, is a rare disorder characterized by acute and transient left ventricular systolic and diastolic dysfunction, often associated with a stressful, emotional or physical event. TTS may be closely related to SARS-CoV-2 infection and the ongoing pandemic. The enormous emotional stress caused by the pandemic and respiratory infections caused by SARS-CoV-2 could be potential triggers for TTS. The case series cited above implicates that TTS should be considered in the differential diagnosis across the entire spectrum of myocardial injury in SARS-CoV-2 infected patients. Myocardial damage associated with SARS-CoV-2 infection is usually attributed to sepsis, hypoxemia, coronary artery disease, and myocarditis. We hypothesize that TTS may also play a role among these lesions.


Subject(s)
COVID-19/complications , Pandemics , SARS-CoV-2 , Takotsubo Cardiomyopathy/etiology , Aged , Aged, 80 and over , COVID-19/physiopathology , COVID-19/psychology , Diagnosis, Differential , Female , Humans , Male , Middle Aged , Models, Cardiovascular , Risk Factors , Stress, Physiological , Stress, Psychological , Takotsubo Cardiomyopathy/physiopathology , Takotsubo Cardiomyopathy/psychology
12.
Med Hypotheses ; 146: 110410, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-939152

ABSTRACT

Coronavirus disease 2019 (COVID-19) is an ongoing pandemic that has affected millions of individuals worldwide. Prior studies suggest that COVID-19 may be associated with an increased risk for various cardiovascular disorders, such as myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism. Early reports of non-COVID-19 patients have described the concurrence of takotsubo cardiomyopathy (TTC) and spontaneous coronary artery dissection (SCAD). However, the interplay between COVID-19, TTC and SCAD has not been well established. We herein propose two sets of two-hit hypotheses for the development of SCAD and TTC in the context of COVID-19. The first two-hit hypothesis explains the development of SCAD, in which TTC-associated formation of vulnerable coronary substrate serves as the first hit (predisposing factor), and COVID-19-associated inflammation and vascular disruption serves as the second hit (precipitating factor). The second two-hit hypothesis is proposed to explain the development of TTC, in which SCAD-associated formation of vulnerable myocardial substrate serves as the first hit, and COVID-19-associated sympathetic overactivity serves as the second hit. Under this conceptual framework, COVID-19 poses a double threat for the development of SCAD (among patients with underlying TTC) as well as TTC (among patients with underlying SCAD), thereby forming a reciprocal causation. This hypothesis provides a rationale for the joint assessment of TTC and SCAD in COVID-19 patients with pertinent cardiovascular manifestations.


Subject(s)
COVID-19/complications , Coronary Vessel Anomalies/etiology , Models, Cardiovascular , SARS-CoV-2 , Takotsubo Cardiomyopathy/etiology , Vascular Diseases/congenital , Aged , Aged, 80 and over , COVID-19/epidemiology , Causality , Coronary Vessel Anomalies/epidemiology , Female , Humans , Male , Middle Aged , Pandemics , Risk Factors , SARS-CoV-2/pathogenicity , Takotsubo Cardiomyopathy/epidemiology , Vascular Diseases/epidemiology , Vascular Diseases/etiology
13.
Med Hypotheses ; 146: 110371, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-912499

ABSTRACT

The universal phenomenon of blood clotting is well known to be protective in external cellular/ tissue injury. However, the emergence of unusual thrombotic presentations in COVID-19 patients is the real concern. Interaction of the spike glycoprotein with ACE2 receptor present in the host cell surface mediates the entry of SARS-CoV-2 causing COVID-19 infection. New clinical findings of SARS-CoV-2 pathogenesis are coming out every day, and one such mystery is the formation of mysterious blood clots in the various tissues and organs of COVID-19 patients, which needs critical attention. To address this issue, we hypothesis that, high ACE2 expression in the endothelium of blood vessels facilitates the high-affinity binding of SARS-CoV-2 using spike protein, causing infection and internal injury inside the vascular wall of blood vessels. This viral associated injury may directly/indirectly initiate activation of coagulation and clotting cascades forming internal blood clots. However, the presence of these clots is undesirable as they are responsible for thrombosis and need to be treated with anti-thrombotic intervention.


Subject(s)
COVID-19/complications , Models, Cardiovascular , Pandemics , SARS-CoV-2 , Thrombosis/etiology , Angiotensin-Converting Enzyme 2/physiology , Blood Coagulation/physiology , COVID-19/physiopathology , COVID-19/virology , Endothelium, Vascular/injuries , Endothelium, Vascular/physiopathology , Endothelium, Vascular/virology , Host Microbial Interactions/physiology , Humans , Receptors, Virus/physiology , Spike Glycoprotein, Coronavirus/physiology , Thrombosis/physiopathology , Thrombosis/virology
14.
Br J Haematol ; 191(3): 390-393, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-841214

ABSTRACT

Critically ill patients with coronavirus disease 2019 (COVID-19) present with hypoxaemia and are mechanically ventilated to support gas exchange. We performed a retrospective, observational study of blood gas analyses (n = 3518) obtained from patients with COVID-19 to investigate changes in haemoglobin oxygen (Hb-O2 ) affinity. Calculated oxygen tension at half-saturation (p50 ) was on average (±SD) 3·3 (3·13) mmHg lower than the normal p50 value (23·4 vs. 26·7 mmHg; P < 0·0001). Compared to an unmatched historic control of patients with other causes of severe respiratory failure, patients with COVID-19 had a significantly higher Hb-O2 affinity (mean [SD] p50 23·4 [3·13] vs. 24·6 [5.4] mmHg; P < 0·0001). We hypothesise that, due to the long disease process, acclimatisation to hypoxaemia could play a role.


Subject(s)
Betacoronavirus , Coronavirus Infections/blood , Oxyhemoglobins/metabolism , Pneumonia, Viral/blood , Adult , Aged , COVID-19 , Carbon Dioxide/blood , Dyspnea/blood , Dyspnea/etiology , Female , Humans , Hydrogen-Ion Concentration , Hypoxia/blood , Hypoxia/etiology , Male , Middle Aged , Models, Cardiovascular , Oxygen/blood , Pandemics , Partial Pressure , Retrospective Studies , SARS-CoV-2
15.
Nat Commun ; 11(1): 4883, 2020 09 28.
Article in English | MEDLINE | ID: covidwho-801570

ABSTRACT

Early stages of the novel coronavirus disease (COVID-19) are associated with silent hypoxia and poor oxygenation despite relatively minor parenchymal involvement. Although speculated that such paradoxical findings may be explained by impaired hypoxic pulmonary vasoconstriction in infected lung regions, no studies have determined whether such extreme degrees of perfusion redistribution are physiologically plausible, and increasing attention is directed towards thrombotic microembolism as the underlying cause of hypoxemia. Herein, a mathematical model demonstrates that the large amount of pulmonary venous admixture observed in patients with early COVID-19 can be reasonably explained by a combination of pulmonary embolism, ventilation-perfusion mismatching in the noninjured lung, and normal perfusion of the relatively small fraction of injured lung. Although underlying perfusion heterogeneity exacerbates existing shunt and ventilation-perfusion mismatch in the model, the reported hypoxemia severity in early COVID-19 patients is not replicated without either extensive perfusion defects, severe ventilation-perfusion mismatch, or hyperperfusion of nonoxygenated regions.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Coronavirus Infections/physiopathology , Hypoxia/etiology , Hypoxia/physiopathology , Lung Diseases/etiology , Lung Diseases/physiopathology , Lung/blood supply , Lung/physiopathology , Models, Biological , Pneumonia, Viral/complications , Pneumonia, Viral/physiopathology , Pulmonary Circulation/physiology , COVID-19 , Computer Simulation , Coronavirus Infections/epidemiology , Humans , Hypoxia/therapy , Lung Diseases/therapy , Mathematical Concepts , Models, Cardiovascular , Oxygen Inhalation Therapy , Pandemics , Pneumonia, Viral/epidemiology , SARS-CoV-2 , Time Factors , Vasoconstriction/physiology , Vasodilation/physiology , Ventilation-Perfusion Ratio/physiology
17.
Med Hypotheses ; 143: 110125, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-665482

ABSTRACT

The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.


Subject(s)
Acute Coronary Syndrome/etiology , Betacoronavirus , Coronavirus Infections/complications , Models, Cardiovascular , Pandemics , Pneumonia, Viral/complications , Acute Coronary Syndrome/physiopathology , CD4-Positive T-Lymphocytes/immunology , COVID-19 , Chemokines/physiology , Coronary Artery Disease/etiology , Coronary Artery Disease/physiopathology , Coronary Vessels/metabolism , Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Cytokines/physiology , Humans , Immunity, Innate , Plaque, Atherosclerotic/etiology , Plaque, Atherosclerotic/physiopathology , Platelet Activation , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Vasoconstriction , Virus Diseases/complications , Virus Diseases/immunology
19.
J Thromb Haemost ; 18(8): 1849-1852, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-616203

ABSTRACT

Hypercoagulability has been recognized as a common complication of COVID-19. Exact mechanisms for this extreme coagulation activation have not yet been elucidated. However, one of the consistent laboratory finding is the increase in fibrinogen, in some cases, marked elevation. High circulating levels of fibrinogen have been linked to thrombosis for years and for this reason, hyperfibrinogenemia is considered one of the mechanisms for COVID-19 coagulopathy. In this forum article, instead of the prothrombotic role, a protective function for fibrinogen is discussed. Fibrinogen, like the other well-known acute phase reactants, is increased in COVID-19 possibly to protect the host.


Subject(s)
Betacoronavirus , Coronavirus Infections/blood , Fibrinogen/physiology , Inflammation/blood , Pneumonia, Viral/blood , Thrombophilia/blood , Thrombosis/prevention & control , Acute Disease , Acute-Phase Proteins/physiology , Biomarkers , Blood Platelets/physiology , COVID-19 , Coronavirus Infections/complications , Fibrin Fibrinogen Degradation Products/analysis , Fibrin Fibrinogen Degradation Products/physiology , Fibrinogen/analysis , Humans , Models, Cardiovascular , Pandemics , Pneumonia, Viral/complications , Risk , SARS-CoV-2 , Thrombophilia/etiology , von Willebrand Factor/analysis , von Willebrand Factor/physiology
20.
Biomed Res Int ; 2020: 7413673, 2020.
Article in English | MEDLINE | ID: covidwho-619953

ABSTRACT

Some patients with coronavirus disease 2019 (COVID-19) show abnormal changes in laboratory myocardial injury markers, suggesting that patients with myocardial injury have a higher mortality rate than those without myocardial injury. This article reviews the possible mechanism of myocardial injury in patients with COVID-19. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) affects the patients with COVID-19 in aspects of direct infection of myocardial injury, specific binding to functional receptors on cardiomyocytes, and immune-mediated myocardial injury. During hospitalization, the monitoring of laboratory myocardial injury markers in patients of COVID-19 should be strengthened.


Subject(s)
Betacoronavirus , Coronavirus Infections/blood , Coronavirus Infections/complications , Heart Injuries/blood , Heart Injuries/etiology , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Angiotensin-Converting Enzyme 2 , Biomarkers/blood , Biomarkers/metabolism , COVID-19 , Coronavirus Infections/metabolism , Cytokines/blood , Cytokines/immunology , Heart Injuries/metabolism , Humans , Inflammation Mediators/blood , Inflammation Mediators/immunology , Models, Cardiovascular , Models, Immunological , Myocytes, Cardiac/immunology , Myocytes, Cardiac/metabolism , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/metabolism , SARS-CoV-2
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