Subject(s)
COVID-19 , Cardiovascular Diseases , Heart Diseases , Cardiovascular Diseases/etiology , Humans , SARS-CoV-2ABSTRACT
Currently, myocardial injury has been reported in patients hospitalized with coronavirus disease 2019 (COVID-19). The studies also show a correlation between cardiac events and severe forms of the disease. COVID-19 begins with an early infection phase in which the virus infiltrates the lung parenchyma and proliferates. It then progresses to the pulmonary phase, where the initial inflammatory process, characterized by vasodilation, vascular permeability, and leukocyte recruitment, leads to lung damage, hypoxemia, and cardiovascular stress. The renin angiotensin aldosterone system is important in the pathophysiology of severe acute respiratory syndrome coronavirus 2 infection and in the propagation of systemic inflammation. Within this system, the pathway mediated by angiotensin-converting enzyme 2 (ACE2) produces vasodilation, cardioprotection, anti-oxidation, and anti-inflammation. Furthermore, the free form of ECA2 prevents binding of the virus to host cells and reduces its damage to the lung.
Actualmente, se ha reportado injuria miocárdica en pacientes hospitalizados por enfermedad por coronavirus 2019 (COVID-19). Los estudios, además, demuestran una correlación entre los eventos cardiacos y formas severas de la enfermedad. La COVID-19 comienza con una fase de infección temprana en la que el virus infiltra el parénquima pulmonar y prolifera. Luego progresa a la fase pulmonar, donde el proceso inflamatorio inicial, caracterizado por vasodilatación, permeabilidad vascular y reclutamiento de leucocitos, lleva a daño pulmonar, hipoxemia y estrés cardiovascular. El sistema renina angiotensina aldosterona es importante en la fisiopatología de la infección por el coronavirus 2 del síndrome respiratorio agudo grave y en la propagación de la inflamación sistémica. Dentro de este sistema, la vía mediada por la enzima convertidora de angiotensina 2 (ECA2) produce vasodilatación, cardioprotección, antioxidación y antiinflamación. Además, la forma libre de la ECA2 previene la unión del virus a las células huésped y reduce su daño al pulmón.
Subject(s)
COVID-19 , Cardiovascular System , Heart Diseases/virology , Angiotensin-Converting Enzyme 2 , COVID-19/complications , COVID-19/physiopathology , Cardiovascular System/virology , Humans , Lung/virology , Renin-Angiotensin SystemABSTRACT
The COVID-19 pandemic has had overwhelming global impacts with deleterious social, economic, and health consequences. To assess the COVID-19 death toll, researchers have estimated declines in 2020 life expectancy at birth (e0). When data are available only for COVID-19 deaths, but not for deaths from other causes, the risks of dying from COVID-19 are typically assumed to be independent of those from other causes. In this research note, we explore the soundness of this assumption using data from the United States and Brazil, the countries with the largest number of reported COVID-19 deaths. We use three methods: one estimates the difference between 2019 and 2020 life tables and therefore does not require the assumption of independence, and the other two assume independence to simulate scenarios in which COVID-19 mortality is added to 2019 death rates or is eliminated from 2020 rates. Our results reveal that COVID-19 is not independent of other causes of death. The assumption of independence can lead to either an overestimate (Brazil) or an underestimate (United States) of the decline in e0, depending on how the number of other reported causes of death changed in 2020.
Subject(s)
COVID-19 , Cause of Death , COVID-19/complications , COVID-19/mortality , United States/epidemiology , Brazil/epidemiology , Humans , Male , Female , Infant, Newborn , Infant , Child, Preschool , Child , Adolescent , Young Adult , Adult , Middle Aged , Aged , Aged, 80 and over , Neoplasms/complications , Neoplasms/mortality , Heart Diseases/complications , Heart Diseases/mortality , Diabetes Mellitus/mortality , Diabetes Complications/mortality , Cause of Death/trends , Life Tables , Life Expectancy/trendsABSTRACT
From the onset of the pandemic, evidence of cardiac involvement in acute COVID-19 abounded. Cardiac presentations ranged from arrhythmias to ischemia, myopericarditis/myocarditis, ventricular dysfunction to acute heart failure, and even cardiogenic shock. Elevated serum cardiac troponin levels were prevalent among hospitalized patients with COVID-19; the higher the magnitude of troponin elevation, the greater the COVID-19 illness severity and in-hospital death risk. Whether these consequences were due to direct SARS-CoV-2 infection of cardiac cells or secondary to inflammatory responses steered early cardiac autopsy studies. SARS-CoV-2 was reportedly detected in endothelial cells, cardiac myocytes, and within the extracellular space. However, findings were inconsistent and different methodologies had their limitations. Initial autopsy reports suggested that SARS-CoV-2 myocarditis was common, setting off studies to find and phenotype inflammatory infiltrates in the heart. Nonetheless, subsequent studies rarely detected myocarditis. Microthrombi, cardiomyocyte necrosis, and inflammatory infiltrates without cardiomyocyte damage were much more common. In vitro and ex vivo experimental platforms have assessed the cellular tropism of SARS-CoV-2 and elucidated mechanisms of viral entry into and replication within cardiac cells. Data point to pericytes as the primary target of SARS-CoV-2 in the heart. Infection of pericytes can account for the observed pericyte and endothelial cell death, innate immune response, and immunothrombosis commonly observed in COVID-19 hearts. These processes are bidirectional and synergistic, rendering a definitive order of events elusive. Single-cell/nucleus analyses of COVID-19 myocardial tissue and isolated cardiac cells have provided granular data about the cellular composition and cell type-specific transcriptomic signatures of COVID-19 and microthrombi-positive COVID-19 hearts. Still, much remains unknown and more in vivo studies are needed. This review seeks to provide an overview of the current understanding of COVID-19 cardiac pathophysiology. Cell type-specific mechanisms and the studies that provided such insights will be highlighted. Given the unprecedented pace of COVID-19 research, more mechanistic details are sure to emerge since the writing of this review. Importantly, our current knowledge offers significant clues about the cardiac pathophysiology of long COVID-19, the increased postrecovery risk of cardiac events, and thus, the future landscape of cardiovascular disease.
Subject(s)
COVID-19 , Heart Diseases , Myocarditis , Humans , COVID-19/complications , SARS-CoV-2 , Endothelial Cells , Hospital Mortality , Post-Acute COVID-19 Syndrome , Heart , Troponin , Myocytes, CardiacABSTRACT
BACKGROUND: COVID-19 patients with any pre-existing major cardio-vascular disease (CVD) are at the highest risk of viral infection and of developing severe disease. The pathophysiological mechanism is characterized by the viral link to angiotensin-converting enzyme 2 (ACE2) and the involvement of the endothelial system with the release of cytokines and the inflicting of direct damage to the myocardium, the induction of microthrombosis, and the initiation of alterations in oxygen diffusion. The aim of the study is to analyze the clinical course and outcomes in patients (gender-stratified) with pre-existing major CVD. METHODS: Out of the 1833 (973 M/860 F) patients admitted to the Internal Medicine COVID-19 Unit of "Castelli Hospital", Lazio, Italy, from 1 January 2021 to 31 December 2021, 600 patients (320 M/280 F) with a mean age of 77 (78.6 M/75.1 F) previously had CVD. Demographic characteristics, length of the stay (LOS) and oxygen therapy were evaluated. RESULTS: All of the CVD COVID-19 patients underwent non-invasive ventilation (NIV). CVD was linked with increased LOS (21 days F/22 M) compared to no CVD (19 days). In total, 32.7% of total patients had major CVD. CONCLUSIONS: Timely identification and evaluation of patients with pre-existing major CVD are fundamental for adequate treatment based on gender, severity, state of illness and for risk reduction.
Subject(s)
COVID-19 , Heart Diseases , Humans , Aged , SARS-CoV-2 , COVID-19/epidemiology , Polypharmacy , Heart Diseases/epidemiology , Hospitals , OxygenABSTRACT
BACKGROUND: Recently, antivirals, including remdesivir, have been repurposed to treat COVID-19 infections. Initial concerns have been raised about the adverse renal and cardiac events associated with remdesivir. OBJECTIVE: This study aimed to analyse the adverse renal and cardiac events associated with remdesivir in patients with COVID-19 infections using the US FDA adverse event reporting system. METHOD: A case/non-case method was used to determine adverse drug events associated with remdesivir as the primary suspect drug between January 1, 2020, and November 11, 2021, for patients with COVID-19 infections. Cases were reports for remdesivir with ≥1 ADEs as preferred terms included in the Medical Dictionary of Regulatory Activities (MedDRA) system organ classes 'Renal and urinary disorders' or 'cardiac' disorders. To measure disproportionality in reporting of ADEs, frequentist approaches, including the proportional reporting ratio (PRR) and reporting odds ratio (ROR), were used. The empirical Bayesian Geometric Mean (EBGM) score and information component (IC) value were calculated using a Bayesian approach. A signal was defined as the lower limit of 95% confidence intervals of ROR ≥ 2, PRR ≥ 2, IC > 0, and EBGM > 1 for ADEs with ≥4 reports. Sensitivity analyses were undertaken by excluding reports for non-Covid indications and medications strongly associated with AKI and cardiac arrhythmias. RESULTS: In the main analysis for remdesivir use in patients with COVID-19 infections, we identified 315 adverse cardiac events comprising 31 different MeDRA PTs and 844 adverse renal events comprising 13 different MeDRA PTs. Regarding adverse renal events, disproportionality signals were noted for "renal failure" (ROR = 2.8 (2.03-3.86); EBGM = 1.92 (1.58-2.31), "acute kidney injury" (ROR = 16.11 (12.52-20.73); EBGM = 2.81 (2.57-3.07), "renal impairment" (ROR = 3.45 (2.68-4.45); EBGM = 2.02 (1.74-2.33). Regarding adverse cardiac events, strong disproportionality signals were noted for "electrocardiogram QT prolonged" (ROR = 6.45 (2.54-16.36); EBGM = 2.04 (1.65-2.51), "pulseless electrical activity" (ROR = 43.57 (13.64-139.20); EBGM = 2.44 (1.74-3.33), "sinus bradycardia" (ROR = 35.86 (11.16-115.26); EBGM = 2.82 (2.23-3.53), "ventricular tachycardia" (ROR = 8.73 (3.55-21.45); EBGM = 2.52 (1.89-3.31). The risk of AKI and cardiac arrythmias were confirmed by sensitivity analyses. CONCLUSION: This hypothesis-generating study identified AKI and cardiac arrhythmias associated with remdesivir use in patients with COVID-19 infections. The relationship between AKI and cardiac arrhythmias should be further investigated using registries or large clinical data to assess the impact of age, genetics, comorbidity, and the severity of Covid infections as potential confounders.
Subject(s)
Acute Kidney Injury , COVID-19 , Heart Diseases , United States , Humans , Bayes Theorem , Adverse Drug Reaction Reporting Systems , COVID-19 Drug Treatment , Acute Kidney Injury/chemically induced , Acute Kidney Injury/epidemiology , Arrhythmias, Cardiac/chemically induced , Arrhythmias, Cardiac/epidemiology , United States Food and Drug Administration , PharmacovigilanceABSTRACT
Infection with SARS-CoV-2, the virus that causes COVID, is associated with numerous potential secondary complications. Global efforts have been dedicated to understanding the myriad potential cardiovascular sequelae which may occur during acute infection, convalescence, or recovery. Because patients often present with nonspecific symptoms and laboratory findings, cardiac imaging has emerged as an important tool for the discrimination of pulmonary and cardiovascular complications of this disease. The clinician investigating a potential COVID-related complication must account not only for the relative utility of various cardiac imaging modalities but also for the risk of infectious exposure to staff and other patients. Extraordinary clinical and scholarly efforts have brought the international medical community closer to a consensus on the appropriate indications for diagnostic cardiac imaging during this protracted pandemic. In this review, we summarize the existing literature and reference major societal guidelines to provide an overview of the indications and utility of echocardiography, nuclear imaging, cardiac computed tomography, and cardiac magnetic resonance imaging for the diagnosis of cardiovascular complications of COVID.
Subject(s)
COVID-19 , Heart Diseases , Humans , SARS-CoV-2 , COVID-19/diagnostic imaging , COVID-19/complications , Heart , Heart Diseases/etiology , Multimodal Imaging/methods , Magnetic Resonance ImagingABSTRACT
PURPOSE: We aimed to better understand the pathophysiology of SARS-CoV-2 pneumonia in non-critically ill hospitalized patients secondarily presenting with clinical deterioration and increase in oxygen requirement without any identified worsening factors. METHODS: We consecutively enrolled patients without clinical or biological evidence for superinfection, without left ventricular dysfunction and for whom a pulmonary embolism was discarded by computed tomography (CT) pulmonary angiography. We investigated lung ventilation and perfusion (LVP) by LVP scintigraphy, and, 24 h later, left and right ventricular function by Tc-99m-labeled albumin-gated blood-pool scintigraphy with late (60 mn) tomographic albumin images on the lungs to evaluate lung albumin retention that could indicate microvascular injuries with secondary edema. RESULTS: We included 20 patients with confirmed SARS-CoV-2 pneumonia. All had CT evidence of organizing pneumonia and normal left ventricular ejection fraction. No patient demonstrated preserved ventilation with perfusion defect (mismatch), which may discard a distal lung thrombosis. Patterns of ventilation and perfusion were heterogeneous in seven patients (35%) with healthy lung segments presenting a relative paradoxical hypoperfusion and hypoventilation compared with segments with organizing pneumonia presenting a relative enhancement in perfusion and preserved ventilation. Lung albumin retention in area of organizing pneumonia was observed in 12 patients (60%), indicating microvascular injuries, increase in vessel permeability, and secondary edema. CONCLUSION: In hospitalized non-critically ill patients without evidence of superinfection, pulmonary embolism, or cardiac dysfunction, various types of damage may contribute to clinical deterioration including microvascular injuries and secondary edema, inconsistencies in lung segments vascularization suggesting a dysregulation of the balance in perfusion between segments affected by COVID-19 and others. SUMMARY STATEMENT: Microvascular injuries and dysregulation of the balance in perfusion between segments affected by COVID-19 and others are present in non-critically ill patients without other known aggravating factors. KEY RESULTS: In non-critically ill patients without evidence of superinfection, pulmonary embolism, macroscopic distal thrombosis or cardiac dysfunction, various types of damage may contribute to clinical deterioration including 1/ microvascular injuries and secondary edema, 2/ inconsistencies in lung segments vascularization with hypervascularization of consolidated segments contrasting with hypoperfusion of not affected segments, suggesting a dysregulation of the balance in perfusion between segments affected by COVID-19 and others.
Subject(s)
COVID-19 , Clinical Deterioration , Heart Diseases , Pulmonary Embolism , Superinfection , Albumins , Critical Illness , Edema/diagnostic imaging , Edema/etiology , Humans , Lung/diagnostic imaging , Neovascularization, Pathologic , SARS-CoV-2 , Stroke Volume , Ventricular Function, LeftABSTRACT
Objective The effect of COVID-19 infection on the cardiovascular system is well established. However, knowledge gaps in the clinical implications of cardiac involvement in COVID-19 patients are yet to be addressed. This study aimed to investigate acute cardiac injury (ACI) risk factors and the outcomes associated with COVID-19 infection with cardiac involvement.Method In this study, we included hospitalized patients between March 2020 and May 2022 with confirmed COVID-19 infection and evidence of cardiac involvement.Results In total, 501 patients were included, of whom 396 (79%) had evidence of ACI. The median troponin level was 25.8 (interquartile range [IQR]: 10.8–71). The patients with evidence of ACI were significantly more likely to have diabetes mellitus (75% vs. 60%; p = 0.003), cardiovascular disease (48% Vs. 37%; p = 0.042), chronic lung disease (22.2% vs. 12.4%; p = 0.02), and chronic kidney disease (32.3% vs. 16.2%; p = < 0.001). Additionally, the patients with ACI were significantly more likely to have cardiomegaly (60.6% vs. 44.8%; p = 0.004) and bilateral lobe infiltrates (77.8% vs. 60%; p < 0.001) on X-ray. The patients with ACI were significantly more likely to suffer from complications such as cardiogenic shock (5.3% vs. 0%; p = 0.001), arrhythmias (42% vs. 30.5%; p = 0.002), pneumonia (80.1% vs. 65.7%; p = 0.003), sepsis (24.2% vs. 9.5%; p < 0.001), and acute respiratory distress syndrome (ARDS) (33.1% vs. 8.6%; p < 0.001). Patients with ACI were also significantly more likely to be admitted to the intensive care unit (ICU) (57% vs. 26.7%; p < 0.001) and significantly more likely to die (38.1% vs. 11.4%; p < 0.001). The results of the multivariate regression analysis indicated that mortality was significantly higher in patients with elevated troponin levels (adjusted odds ratio [OR]: 4.73; 95% confidence interval [CI]: 2.49–8.98).Conclusion In COVID-19 patients who exhibited evidence of ACI, age, diabetes mellitus, chronic lung disease, and chronic kidney disease were associated with increased risk of ACI. Patients with these risk factors are at risk of severe complications, such as ICU admission, sepsis, and death.
Subject(s)
Pulmonary Disease, Chronic Obstructive , Arrhythmias, Cardiac , Acute Disease , Diabetes Mellitus , Heart Diseases , Shock, Cardiogenic , Sepsis , Cardiomegaly , Pneumonia , Cardiovascular Diseases , Renal Insufficiency, Chronic , Respiratory Distress Syndrome , Death , COVID-19ABSTRACT
Introduction: Influenza is an acute viral infection with significant morbidity and mortality. It occurs annually each winter, which is called seasonal influenza, and is preventable through safe vaccine. Aim: The aim of this work is to know the epidemiological pattern of patients with seasonal influenza in Iraqi sentinel sites. Methods: A cross-sectional study was carried out on records of patients who attended four sentinel sites and registered to have influenza-like illness (ILI) or severe acute respiratory infection (SARI), and laboratory investigated. Results: The total number of cases was 1124; 36.2% of them aged 19-39 years; 53.9% were female; 74.9% lived in urban areas; 64.3% diagnosed as ILI; and 35.7% as SARI; 15.9% had diabetes, 12.7% had heart disease, 4.8% had asthma, 3% had a chronic lung disease, and 2% had hematological disease; 94.6% did not get influenza vaccine. About COVID-19 vaccine, 69.4% were not vaccinated, 3.5% got only one dose, and 27.1% completed two doses. Only the SARI cases needed admission; among them, 95.7% were cured. 6.5% were diagnosed with influenza-A virus, 26.1% had COVID-19, and 67.5% were negative. Among those with influenza, 97.3% had H3N2 subtype and 2.7% had H1N1 pdm09. Conclusions: The percentage of influenza virus in Iraq is relatively small. The age, classification of case (ILI or SARI), having diabetes, heart disease, or immunological disease, and taking COVID-19 vaccine have a significant association with influenza. Recommendations: It is needed for similar sentinel sites in other health directorates and for rising health education about seasonal influenza and its vaccine.
Subject(s)
COVID-19 , Heart Diseases , Influenza A Virus, H1N1 Subtype , Influenza Vaccines , Influenza, Human , Humans , Female , Infant , Male , Influenza, Human/epidemiology , Influenza, Human/prevention & control , Iraq/epidemiology , Influenza A Virus, H3N2 Subtype , Seasons , COVID-19 Vaccines , Cross-Sectional Studies , Sentinel SurveillanceABSTRACT
Heart disease is a significant burden on global health care systems and is a leading cause of death each year. To improve our understanding of heart disease, high quality disease models are needed. These will facilitate the discovery and development of new treatments for heart disease. Traditionally, researchers have relied on 2D monolayer systems or animal models of heart disease to elucidate pathophysiology and drug responses. Heart-on-a-chip (HOC) technology is an emerging field where cardiomyocytes among other cell types in the heart can be used to generate functional, beating cardiac microtissues that recapitulate many features of the human heart. HOC models are showing great promise as disease modeling platforms and are poised to serve as important tools in the drug development pipeline. By leveraging advances in human pluripotent stem cell-derived cardiomyocyte biology and microfabrication technology, diseased HOCs are highly tuneable and can be generated via different approaches such as: using cells with defined genetic backgrounds (patient-derived cells), adding small molecules, modifying the cells' environment, altering cell ratio/composition of microtissues, among others. HOCs have been used to faithfully model aspects of arrhythmia, fibrosis, infection, cardiomyopathies, and ischemia, to name a few. In this review, we highlight recent advances in disease modeling using HOC systems, describing instances where these models outperformed other models in terms of reproducing disease phenotypes and/or led to drug development.
Subject(s)
Cardiomyopathies , Heart Diseases , Induced Pluripotent Stem Cells , Pluripotent Stem Cells , Animals , Humans , Heart Diseases/therapy , Heart Diseases/metabolism , Myocytes, Cardiac/metabolism , Cardiomyopathies/metabolism , Pluripotent Stem Cells/metabolism , Lab-On-A-Chip DevicesABSTRACT
PURPOSE: To evaluate myocardial status through the assessment of extracellular volume (ECV) calculated at computed tomography (CT) in patients hospitalized for novel coronavirus disease (COVID-19), with regards to the presence of pulmonary embolism (PE) as a risk factor for cardiac dysfunction. METHOD: Hospitalized patients with COVID-19 who underwent contrast-enhanced CT at our institution were retrospectively included in this study and grouped with regards to the presence of PE. Unenhanced and portal venous phase scans were used to calculate ECV by placing regions of interest in the myocardial septum and left ventricular blood pool. ECV values were compared between patients with and without PE, and correlations between ECV values and clinical or technical variables were subsequently appraised. RESULTS: Ninety-four patients were included, 63/94 of whom males (67%), with a median age of 70 (IQR 56-76 years); 28/94 (30%) patients presented with PE. Patients with PE had a higher myocardial ECV than those without (33.5%, IQR 29.4-37.5% versus 29.8%, IQR 25.1-34.0%; p = 0.010). There were no correlations between ECV and patients' age (p = 0.870) or sex (p = 0.122), unenhanced scan voltage (p = 0.822), portal phase scan voltage (p = 0.631), overall radiation dose (p = 0.569), portal phase scan timing (p = 0.460), and contrast agent dose (p = 0.563). CONCLUSIONS: CT-derived ECV could help identify COVID-19 patients at higher risk of cardiac dysfunction, especially when related to PE, to potentially plan a dedicated, patient-tailored clinical approach.
Subject(s)
COVID-19 , Heart Diseases , Pulmonary Embolism , Male , Humans , Middle Aged , Aged , Retrospective Studies , Myocardium , Tomography, X-Ray Computed/methods , Pulmonary Embolism/diagnostic imagingABSTRACT
BACKGROUND: While young adults 18-24 years old bear a significant proportion of COVID-19 diagnoses, the risk factors for hospitalisation and severe COVID-19 complications in this population are poorly understood. OBJECTIVE: The objective of this study was to identify risk factors for hospitalisation and other COVID-19 complications across the health spectrum of young adults diagnosed with COVID-19 infection. STUDY DESIGN: Retrospective cohort study. PARTICIPANTS: Young adults (aged 18-24) with confirmed COVID-19 infection from the American Heart Association (AHA) COVID-19 Cardiovascular Disease Registry of hospitalised patients and the Outcomes Registry for Cardiac Conditions in Athletes (ORCCA) study of collegiate athletes. The AHA registry included 636 young adults from 152 hospitals. The ORCCA registry consisted of 3653 competitive college athletes from 42 colleges and universities. INTERVENTION: None (exposure to COVID-19). PRIMARY AND SECONDARY OUTCOME MEASURES: Main outcomes included hospitalisation, death, major adverse cardiovascular events (MACE) and other severe clinical events. RESULTS: In comparison to the ORCCA registry, patients in the AHA registry were more likely to be female (59% vs 33%); had higher average body mass index (BMI) (32.4 vs 25.6); and had increased prevalence of diabetes (10% vs 0.4%), hypertension (7% vs 0.6%), chronic kidney disease (2% vs 0%) and asthma (14% vs 8%), all with p<0.01. There were eight (2%) deaths in the AHA hospitalised registry compared with zero in the ORCCA cohort. BMI was a statistically significant predictor of death in the hospitalised cohort (OR 1.05, 95% CI 1.00, 1.10). No significant predictors of MACE or other severe clinical events were identified. CONCLUSIONS: The risk of cardiac events in young adults aged 18-24 diagnosed with COVID-19 infection is low. Patients who were hospitalised (AHA registry) were more likely to have pre-existing medical comorbidities and higher BMI than healthy collegiate athletes (ORCCA registry). Once hospitalised, elevated BMI is associated with increased mortality although other drivers of MACE and other severe clinical events remain unclear.
Subject(s)
COVID-19 , Cardiovascular Diseases , Heart Diseases , United States/epidemiology , Humans , Female , Young Adult , Adolescent , Adult , Male , COVID-19/complications , COVID-19/epidemiology , Retrospective Studies , American Heart Association , Heart Diseases/complications , Athletes , RegistriesABSTRACT
Coronavirus disease (COVID-19) has affected children differently from adults worldwide. Data on the clinical presentation of the infection in children are limited. We present a detailed account of pediatric inpatients infected with severe acute respiratory syndrome coronavirus 2 virus at our institution during widespread local transmission, aiming to understand disease presentation and outcomes. A retrospective chart review was performed of children, ages 0 to 18 years, with a positive polymerase chain reaction test for severe acute respiratory syndrome coronavirus 2 on nasopharyngeal specimens admitted to our hospital over a 4-week period. We present clinical data from 22 patients and highlight the variability of the presentation. In our study, most children presented without respiratory illness or symptoms suggestive of COVID-19; many were identified only because of universal testing. Because children may have variable signs and symptoms of COVID-19 infection, targeted testing may miss some cases.
Subject(s)
Coronavirus Infections/physiopathology , Cough/physiopathology , Dyspnea/physiopathology , Fatigue/physiopathology , Fever/physiopathology , Pneumonia, Viral/physiopathology , Seizures/physiopathology , Adolescent , Age Distribution , Alanine Transaminase/metabolism , Aspartate Aminotransferases/metabolism , Betacoronavirus , C-Reactive Protein/metabolism , COVID-19 , COVID-19 Testing , Child , Child, Preschool , Chronic Disease , Clinical Laboratory Techniques , Comorbidity , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Coronavirus Infections/metabolism , Coronavirus Infections/therapy , Female , Heart Diseases/epidemiology , Hospitalization , Hospitals, Pediatric , Humans , Infant , Infant, Newborn , Lung Diseases/epidemiology , Lymphopenia/epidemiology , Male , Mass Screening , Neoplasms/epidemiology , New York City/epidemiology , Noninvasive Ventilation , Pandemics , Pneumonia, Viral/epidemiology , Pneumonia, Viral/metabolism , Pneumonia, Viral/therapy , Procalcitonin/metabolism , Respiration, Artificial , Retrospective Studies , SARS-CoV-2 , Sex Distribution , United StatesABSTRACT
Coronavirus disease 2019 (COVID-19) is an ongoing global pandemic that has affected nearly 600 million people to date across the world. While COVID-19 is primarily a respiratory illness, cardiac injury is also known to occur. Cardiovascular magnetic resonance (CMR) imaging is uniquely capable of characterizing myocardial tissue properties in-vivo, enabling insights into the pattern and degree of cardiac injury. The reported prevalence of myocardial involvement identified by CMR in the context of COVID-19 infection among previously hospitalized patients ranges from 26 to 60%. Variations in the reported prevalence of myocardial involvement may result from differing patient populations (e.g. differences in severity of illness) and the varying intervals between acute infection and CMR evaluation. Standardized methodologies in image acquisition, analysis, interpretation, and reporting of CMR abnormalities across would likely improve concordance between studies. This consensus document by the Society for Cardiovascular Magnetic Resonance (SCMR) provides recommendations on CMR imaging and reporting metrics towards the goal of improved standardization and uniform data acquisition and analytic approaches when performing CMR in patients with COVID-19 infection.
Subject(s)
COVID-19 , Heart Diseases , Magnetic Resonance Imaging , Humans , COVID-19/complications , Heart/diagnostic imaging , Magnetic Resonance Imaging/methods , Magnetic Resonance Imaging/standards , Magnetic Resonance Spectroscopy , Myocarditis/diagnostic imaging , Predictive Value of Tests , Heart Diseases/diagnostic imaging , Heart Diseases/etiologyABSTRACT
BACKGROUND: COVID-19 is associated with cardiac dysfunction. This study tested the relative prognostic role of left (LV), right and bi- (BiV) ventricular dysfunction on mortality in a large multicenter cohort of patients during and after acute COVID-19 hospitalization. METHODS/RESULTS: All hospitalized COVID-19 patients who underwent clinically indicated transthoracic echocardiography within 30 days of admission at four NYC hospitals between March 2020 and January 2021 were studied. Images were re-analyzed by a central core lab blinded to clinical data. Nine hundred patients were studied (28% Hispanic, 16% African-American), and LV, RV and BiV dysfunction were observed in 50%, 38% and 17%, respectively. Within the overall cohort, 194 patients had TTEs prior to COVID-19 diagnosis, among whom LV, RV, BiV dysfunction prevalence increased following acute infection (p<0.001). Cardiac dysfunction was linked to biomarker-evidenced myocardial injury, with higher prevalence of troponin elevation in patients with LV (14%), RV (16%) and BiV (21%) dysfunction compared to those with normal BiV function (8%, all p<0.05). During in- and out-patient follow-up, 290 patients died (32%), among whom 230 died in the hospital and 60 post-discharge. Unadjusted mortality risk was greatest among patients with BiV (41%), followed by RV (39%) and LV dysfunction (37%), compared to patients without dysfunction (27%, all p<0.01). In multivariable analysis, any RV dysfunction, but not LV dysfunction, was independently associated with increased mortality risk (p<0.01). CONCLUSIONS: LV, RV and BiV function declines during acute COVID-19 infection with each contributing to increased in- and out-patient mortality risk. RV dysfunction independently increases mortality risk.
Subject(s)
COVID-19 , Heart Diseases , Ventricular Dysfunction, Left , Humans , COVID-19/complications , Outpatients , Aftercare , COVID-19 Testing , Cardiac Pacing, Artificial/methods , Patient Discharge , HospitalsABSTRACT
PURPOSE OF REVIEW: Cardiac consequences occur in both acute COVID-19 and post-acute sequelae of COVID-19 (PASC). Here, we highlight the current understanding about COVID-19 cardiac effects, based upon clinical, imaging, autopsy, and molecular studies. RECENT FINDINGS: COVID-19 cardiac effects are heterogeneous. Multiple, concurrent cardiac histopathologic findings have been detected on autopsies of COVID-19 non-survivors. Microthrombi and cardiomyocyte necrosis are commonly detected. Macrophages often infiltrate the heart at high density but without fulfilling histologic criteria for myocarditis. The high prevalences of microthrombi and inflammatory infiltrates in fatal COVID-19 raise the concern that recovered COVID-19 patients may have similar but subclinical cardiac pathology. Molecular studies suggest that SARS-CoV-2 infection of cardiac pericytes, dysregulated immunothrombosis, and pro-inflammatory and anti-fibrinolytic responses underlie COVID-19 cardiac pathology. The extent and nature by which mild COVID-19 affects the heart is unknown. Imaging and epidemiologic studies of recovered COVID-19 patients suggest that even mild illness confers increased risks of cardiac inflammation, cardiovascular disorders, and cardiovascular death. The mechanistic details of COVID-19 cardiac pathophysiology remain under active investigation. The ongoing evolution of SARS-CoV-2 variants and vast numbers of recovered COVID-19 patients portend a burgeoning global cardiovascular disease burden. Our ability to prevent and treat cardiovascular disease in the future will likely depend on comprehensive understanding of COVID-19 cardiac pathophysiologic phenotypes.
Subject(s)
COVID-19 , Heart Diseases , Myocarditis , Thrombosis , Humans , COVID-19/complications , COVID-19/epidemiology , SARS-CoV-2/genetics , Heart/diagnostic imaging , Myocarditis/etiology , Heart Diseases/complications , Thrombosis/complicationsABSTRACT
Since the start of the COVID-19 pandemic, studies emerged reporting the occurrence of cardiovascular complications in patients affected by SARS-CoV-2. Initial data were likely skewed by higher risk populations and those with severe disease. Recent, larger studies have corroborated this association and provide estimates for risk of cardiovascular complications. Patients affected by COVID-19 are at increased risk of myocardial infarction, myocarditis, venous thromboembolism, arrhythmias, and exacerbation of heart failure. Furthermore, a subset of patients who recover from the acute illness have persistent symptoms, a condition termed "long COVID", and management of these symptoms is challenging. Clinicians treating patients affected by COVID-19 should remain vigilant for cardiac complications during the acute illness, particularly in high-risk populations.
Subject(s)
COVID-19 , Heart Diseases , Humans , COVID-19/complications , SARS-CoV-2 , Pandemics , Acute Disease , New Zealand/epidemiology , Heart Diseases/epidemiology , Heart Diseases/etiologyABSTRACT
OBJECTIVE: To characterize myocardial injury and cardiovascular complications and their predictors in severe and critical COVID-19 patients admitted to the intensive care unit. METHODS: This was an observational cohort study of severe and critical COVID-19 patients admitted to the intensive care unit. Myocardial injury was defined as blood levels of cardiac troponin above the 99th percentile upper reference limit. Cardiovascular events considered were the composite of deep vein thrombosis, pulmonary embolism, stroke, myocardial infarction, acute limb ischemia, mesenteric ischemia, heart failure and arrhythmia. Univariate and multivariate logistic regression or Cox proportional hazard models were used to determine predictors of myocardial injury. RESULTS: Of 567 patients with severe and critical COVID-19 admitted to the intensive care unit, 273 (48.1%) had myocardial injury. Of the 374 patients with critical COVID-19, 86.1% had myocardial injury, and also showed more organ dysfunction and higher 28-day mortality (56.6% versus 27.1%, p < 0.001). Advanced age, arterial hypertension and immune modulator use were predictors of myocardial injury. Cardiovascular complications occurred in 19.9% of patients with severe and critical COVID-19 admitted to the intensive care unit, with most events occurring in patients with myocardial injury (28.2% versus 12.2%, p < 0.001). The occurrence of an early cardiovascular event during intensive care unit stay was associated with higher 28-day mortality compared with late or no events (57.1% versus 34% versus 41.8%, p = 0.01). CONCLUSION: Myocardial injury and cardiovascular complications were commonly found in patients with severe and critical forms of COVID-19 admitted to the intensive care unit, and both were associated with increased mortality in these patients.
OBJETIVO: Caracterizar a lesão miocárdica e as complicações cardiovasculares e seus preditores em pacientes graves e críticos com COVID-19 admitidos à unidade de terapia intensiva. MÉTODOS: Este foi um estudo de coorte observacional em pacientes graves e críticos com COVID-19 admitidos à unidade de terapia intensiva. A lesão miocárdica foi definida como níveis sanguíneos de troponina cardíaca acima do limite de referência superior ao percentil 99. Os eventos cardiovasculares considerados foram combinação de trombose venosa profunda, embolia pulmonar, acidente vascular cerebral, infarto do miocárdio, isquemia aguda de membros, isquemia mesentérica, insuficiência cardíaca e arritmia cardíaca. Regressão logística univariada e multivariada ou modelos de risco proporcional de Cox foram utilizados para determinar os preditores de lesão miocárdica. RESULTADOS: Foram admitidos à unidade de terapia intensiva 567 pacientes graves e críticos com COVID-19, dos quais 273 (48,1%) apresentavam lesão miocárdica. Dos 374 pacientes críticos com COVID-19, 86,1% tinham lesão miocárdica, além de apresentarem mais disfunção orgânica e maior mortalidade aos 28 dias (56,6% versus 27,1%; p < 0,001). Foram preditores de lesão miocárdica idade avançada, hipertensão arterial e uso de imunomoduladores. Complicações cardiovasculares ocorreram em 19,9% dos pacientes graves e críticos com COVID-19 admitidos à unidade de terapia intensiva, e a maioria dos eventos deu-se em pacientes com lesão miocárdica (28,2% versus 12,2%; p < 0,001). A ocorrência de evento cardiovascular precoce durante internação em unidade de terapia intensiva estava associada à maior mortalidade aos 28 dias em comparação com eventos tardios ou inexistentes (57,1% versus 34,0% versus 41,8%; p = 0,01). CONCLUSÃO: Pacientes com formas graves e críticas de COVID-19 admitidos à unidade de terapia intensiva foram comumente diagnosticados com lesão miocárdica e complicações cardiovasculares, e ambas estavam associadas à maior mortalidade nesses pacientes.