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1.
Kardiologiia ; 62(3): 21-27, 2022 Mar 31.
Article in Russian, English | MEDLINE | ID: covidwho-1789754

ABSTRACT

Aim      To evaluate the incidence and features of left atrial appendage (LAA) thrombosis in patients with persistent atrial fibrillation (AF) after novel coronavirus infection (COVID-19).Material and methods  Percutaneous echocardiography (pcEchoCG) was performed for 128 patients with persistent AF prepared for cardioversion, 36 (28.1 %) of whom had had COVID-19. In 3 (8.3 %) patients, the lung lesion area was 50-75 %; in 31 (86.1 %) patients, 25-50 %; in 1 (2.8 %) patient, less than 25 %. One patient had no lung lesion. Median time from the onset of COVID-19 to the patient enrollment in the study was 76.5 days. At the time of enrollment, the polymerase chain reaction test for SARS-CoV-2 was negative in all patients.Results Patients after COVID-19 and those who had not had COVID-19 were comparable by age (62.5±9.2 and 62.4±9.1 years, respectively; р=0.956), gender (men 52.8 and 59.8 %, respectively; р=0.471), and risk of stroke (score 2.19±1.28 and score 1.95±1.35, respectively; р=0.350). Duration of the last arrhythmia episode was longer for patients after COVID-19 than for the comparison group (76.5 and 45.0 days, respectively; р=0.011). All patients received oral anticoagulants. 55.6 % of COVID-19 patients received rivaroxaban, whereas 62.0% of patients who had not had COVID-19 were treated with apixaban. Median duration of the anticoagulant treatment was longer for COVID-19 patients than for the comparison group (61.5 and 32.0 days; р=0.051). LAA thrombus was detected in 7 (19.4 %) patients after COVID-19 and in 6 (6.5 %) patients of the comparison group (р=0.030). In COVID-19 patients, the thrombus adhered to LAA wall over the entire thrombus length whereas in patients who had not have COVID-19, the thrombus had a free part that formed a sharp angle with LAA walls. In the presence of LAA thrombus, the LAA blood flow velocity was considerably higher for COVID-19 patients than for the comparison group (31.0±8.9 and 18.8±4.9 cm/sec, respectively; p=0.010). At the follow-up examination performed at 24.0 days on the average, the thrombus was found to be dissolved in 80 and 50% of patients after and without COVID-19, respectively (р=0.343).Conclusion      In patients with persistent AF after the novel coronavirus infection, LAA thrombosis was detected more frequently than in patients who had never had COVID-19; it was characterized by mural localization and was not associated with a decrease in LAA blood flow velocity.


Subject(s)
Atrial Appendage , Atrial Fibrillation , COVID-19 , Heart Diseases , Thrombosis , Aged , Anticoagulants/therapeutic use , Atrial Appendage/diagnostic imaging , Atrial Fibrillation/complications , Atrial Fibrillation/diagnosis , Atrial Fibrillation/epidemiology , COVID-19/complications , Echocardiography, Transesophageal/adverse effects , Heart Diseases/complications , Humans , Male , Middle Aged , SARS-CoV-2 , Thrombosis/diagnosis , Thrombosis/epidemiology , Thrombosis/etiology
4.
6.
Circulation ; 143(24): 2346-2354, 2021 06 15.
Article in English | MEDLINE | ID: covidwho-1304328

ABSTRACT

BACKGROUND: Cardiovascular deaths increased during the early phase of the COVID-19 pandemic in the United States. However, it is unclear whether diverse racial/ethnic populations have experienced a disproportionate rise in heart disease and cerebrovascular disease deaths. METHODS: We used the National Center for Health Statistics to identify heart disease and cerebrovascular disease deaths for non-Hispanic White, non-Hispanic Black, non-Hispanic Asian, and Hispanic individuals from March to August 2020 (pandemic period), as well as for the corresponding months in 2019 (historical control). We determined the age- and sex-standardized deaths per million by race/ethnicity for each year. We then fit a modified Poisson model with robust SEs to compare change in deaths by race/ethnicity for each condition in 2020 versus 2019. RESULTS: There were a total of 339 076 heart disease and 76 767 cerebrovascular disease deaths from March through August 2020, compared with 321 218 and 72 190 deaths during the same months in 2019. Heart disease deaths increased during the pandemic in 2020, compared with the corresponding period in 2019, for non-Hispanic White (age-sex standardized deaths per million, 1234.2 versus 1208.7; risk ratio for death [RR], 1.02 [95% CI, 1.02-1.03]), non-Hispanic Black (1783.7 versus 1503.8; RR, 1.19 [95% CI, 1.17-1.20]), non-Hispanic Asian (685.7 versus 577.4; RR, 1.19 [95% CI, 1.15-1.22]), and Hispanic (968.5 versus 820.4; RR, 1.18 [95% CI, 1.16-1.20]) populations. Cerebrovascular disease deaths also increased for non-Hispanic White (268.7 versus 258.2; RR, 1.04 [95% CI, 1.03-1.05]), non-Hispanic Black (430.7 versus 379.7; RR, 1.13 [95% CI, 1.10-1.17]), non-Hispanic Asian (236.5 versus 207.4; RR, 1.15 [95% CI, 1.09-1.21]), and Hispanic (264.4 versus 235.9; RR, 1.12 [95% CI, 1.08-1.16]) populations. For both heart disease and cerebrovascular disease deaths, Black, Asian, and Hispanic populations experienced a larger relative increase in deaths than the non-Hispanic White population (interaction term, P<0.001). CONCLUSIONS: During the COVID-19 pandemic in the United States, Black, Hispanic, and Asian populations experienced a disproportionate rise in deaths caused by heart disease and cerebrovascular disease, suggesting that these groups have been most impacted by the indirect effects of the pandemic. Public health and policy strategies are needed to mitigate the short- and long-term adverse effects of the pandemic on the cardiovascular health of diverse populations.


Subject(s)
COVID-19/pathology , Cerebrovascular Disorders/mortality , Health Status Disparities , Heart Diseases/mortality , Adult , African Americans/statistics & numerical data , Aged , Asian Americans/statistics & numerical data , COVID-19/complications , COVID-19/epidemiology , COVID-19/virology , Cerebrovascular Disorders/complications , Cerebrovascular Disorders/ethnology , Cerebrovascular Disorders/pathology , Female , Heart Diseases/complications , Heart Diseases/ethnology , Hospital Mortality/ethnology , Humans , Male , Middle Aged , Pandemics , Risk , SARS-CoV-2/isolation & purification , United States/epidemiology , /statistics & numerical data
7.
Intern Emerg Med ; 16(8): 2051-2061, 2021 11.
Article in English | MEDLINE | ID: covidwho-1245735

ABSTRACT

Growing reports since the beginning of the pandemic and till date describe increased rates of cardiac complications (CC) in the active phase of coronavirus disease 2019 (COVID-19). CC commonly observed include myocarditis/myocardial injury, arrhythmias and heart failure, with an incidence reaching about a quarter of hospitalized patients in some reports. The increased incidence of CC raise questions about the possible heightened susceptibility of patients with cardiac disease to develop severe COVID-19, and whether the virus itself is involved in the pathogenesis of CC. The wide array of CC seems to stem from multiple mechanisms, including the ability of the virus to directly enter cardiomyocytes, and to indirectly damage the heart through systemic hyperinflammatory and hypercoagulable states, endothelial injury of the coronary arteries and hypoxemia. The induced CC seem to dramatically impact the prognosis of COVID-19, with some studies suggesting over 50% mortality rates with myocardial damage, up from ~ 5% overall mortality of COVID-19 alone. Thus, it is particularly important to investigate the relation between COVID-19 and heart disease, given the major effect on morbidity and mortality, aiming at early detection and improving patient care and outcomes. In this article, we review the growing body of published data on the topic to provide the reader with a comprehensive and robust description of the available evidence and its implication for clinical practice.


Subject(s)
COVID-19 Testing , COVID-19/complications , Heart Diseases/etiology , Arrhythmias, Cardiac/etiology , COVID-19/therapy , Disease Management , Heart Diseases/complications , Heart Diseases/therapy , Humans , Myocarditis/etiology , Prognosis , Risk Factors
9.
Circulation ; 143(24): 2346-2354, 2021 06 15.
Article in English | MEDLINE | ID: covidwho-1232383

ABSTRACT

BACKGROUND: Cardiovascular deaths increased during the early phase of the COVID-19 pandemic in the United States. However, it is unclear whether diverse racial/ethnic populations have experienced a disproportionate rise in heart disease and cerebrovascular disease deaths. METHODS: We used the National Center for Health Statistics to identify heart disease and cerebrovascular disease deaths for non-Hispanic White, non-Hispanic Black, non-Hispanic Asian, and Hispanic individuals from March to August 2020 (pandemic period), as well as for the corresponding months in 2019 (historical control). We determined the age- and sex-standardized deaths per million by race/ethnicity for each year. We then fit a modified Poisson model with robust SEs to compare change in deaths by race/ethnicity for each condition in 2020 versus 2019. RESULTS: There were a total of 339 076 heart disease and 76 767 cerebrovascular disease deaths from March through August 2020, compared with 321 218 and 72 190 deaths during the same months in 2019. Heart disease deaths increased during the pandemic in 2020, compared with the corresponding period in 2019, for non-Hispanic White (age-sex standardized deaths per million, 1234.2 versus 1208.7; risk ratio for death [RR], 1.02 [95% CI, 1.02-1.03]), non-Hispanic Black (1783.7 versus 1503.8; RR, 1.19 [95% CI, 1.17-1.20]), non-Hispanic Asian (685.7 versus 577.4; RR, 1.19 [95% CI, 1.15-1.22]), and Hispanic (968.5 versus 820.4; RR, 1.18 [95% CI, 1.16-1.20]) populations. Cerebrovascular disease deaths also increased for non-Hispanic White (268.7 versus 258.2; RR, 1.04 [95% CI, 1.03-1.05]), non-Hispanic Black (430.7 versus 379.7; RR, 1.13 [95% CI, 1.10-1.17]), non-Hispanic Asian (236.5 versus 207.4; RR, 1.15 [95% CI, 1.09-1.21]), and Hispanic (264.4 versus 235.9; RR, 1.12 [95% CI, 1.08-1.16]) populations. For both heart disease and cerebrovascular disease deaths, Black, Asian, and Hispanic populations experienced a larger relative increase in deaths than the non-Hispanic White population (interaction term, P<0.001). CONCLUSIONS: During the COVID-19 pandemic in the United States, Black, Hispanic, and Asian populations experienced a disproportionate rise in deaths caused by heart disease and cerebrovascular disease, suggesting that these groups have been most impacted by the indirect effects of the pandemic. Public health and policy strategies are needed to mitigate the short- and long-term adverse effects of the pandemic on the cardiovascular health of diverse populations.


Subject(s)
COVID-19/pathology , Cerebrovascular Disorders/mortality , Health Status Disparities , Heart Diseases/mortality , Adult , African Americans/statistics & numerical data , Aged , Asian Americans/statistics & numerical data , COVID-19/complications , COVID-19/epidemiology , COVID-19/virology , Cerebrovascular Disorders/complications , Cerebrovascular Disorders/ethnology , Cerebrovascular Disorders/pathology , Female , Heart Diseases/complications , Heart Diseases/ethnology , Hospital Mortality/ethnology , Humans , Male , Middle Aged , Pandemics , Risk , SARS-CoV-2/isolation & purification , United States/epidemiology , /statistics & numerical data
10.
J Med Virol ; 93(3): 1512-1519, 2021 03.
Article in English | MEDLINE | ID: covidwho-1196466

ABSTRACT

As coronavirus disease 2019 (COVID-19) crashed into the influenza season, clinical characteristics of both infectious diseases were compared to make a difference. We reported 211 COVID-19 patients and 115 influenza patients as two separate cohorts at different locations. Demographic data, medical history, laboratory findings, and radiological characters were summarized and compared between two cohorts, as well as between patients at the intensive care unit (ICU) andnon-ICU within the COVID-19 cohort. For all 326 patients, the median age was 57.0 (interquartile range: 45.0-69.0) and 48.2% was male, while 43.9% had comorbidities that included hypertension, diabetes, bronchitis, and heart diseases. Patients had cough (75.5%), fever (69.3%), expectoration (41.1%), dyspnea (19.3%), chest pain (18.7%), and fatigue (16.0%), etc. Both viral infections caused substantial blood abnormality, whereas the COVID-19 cohort showed a lower frequency of leukocytosis, neutrophilia, or lymphocytopenia, but a higher chance of creatine kinase elevation. A total of 7.7% of all patients possessed no abnormal sign in chest computed tomography (CT) scans. For both infections, pulmonary lesions in radiological findings did not show any difference in their location or distribution. Nevertheless, compared to the influenza cohort, the COVID-19 cohort presented more diversity in CT features, where certain specific CT patterns showed significantly more frequency, including consolidation, crazy paving pattern, rounded opacities, air bronchogram, tree-in-bud sign, interlobular septal thickening, and bronchiolar wall thickening. Differentiable clinical manifestations and CT patterns may help diagnose COVID-19 from influenza and gain a better understanding of both contagious respiratory illnesses.


Subject(s)
COVID-19/diagnosis , Influenza, Human/diagnosis , Lung/diagnostic imaging , Lung/pathology , Adult , Aged , Bronchitis/complications , Comorbidity , Diabetes Complications/complications , Diagnosis, Differential , Female , Heart Diseases/complications , Humans , Hypertension/complications , Length of Stay/statistics & numerical data , Male , Middle Aged , SARS-CoV-2 , Thorax/diagnostic imaging , Tomography, X-Ray Computed
11.
Nutr Hosp ; 37(5): 1039-1042, 2020 Oct 21.
Article in English | MEDLINE | ID: covidwho-1128242

ABSTRACT

INTRODUCTION: Background: coronavirus disease 2019 (COVID-19) can induce an exaggerated inflammatory response. Vitamin D is a key modulator of the immune system. We hypothesized that vitamin D deficiency (VDD) could increase the risk of developing severe COVID-19 infection. Methods: patients with confirmed COVID-19 seen at the emergency department of our hospital with recent measurements of 25(OH)D were recruited. We explored the association of vitamin D deficiency (VDD), defined as 25-hydroxyvitamin D < 20 ng/mL, with a composite of adverse clinical outcomes. Results: we included 80 patients, of which 31 (39 %) presented the endpoint. VDD tended to predict an increased risk of developing severe COVID-19 after adjusting for age, gender, obesity, cardiac disease, and kidney disease [OR 3.2 (95 % CI: 0.9-11.4), p = 0.07]. Age had a negative interaction with the effect of VDD on the composite outcome (p = 0.03), indicating that the effect was more noticeable at younger ages. Furthermore, male gender was associated with VDD and with severe COVID-19 at younger ages. Conclusions: in this retrospective study, vitamin D deficiency showed a signal of association with severe COVID-19 infection. A significant interaction with age was noted, suggesting VDD may have a greater impact in younger patients. These findings should be confirmed in larger, prospective, adequately powered studies.


INTRODUCCIÓN: Antecedentes: la enfermedad por coronavirus 2019 (COVID-19) puede inducir una respuesta inflamatoria exagerada. La vitamina D es un modulador clave del sistema inmune. Planteamos que la deficiencia de vitamina D (VDD) podría aumentar el riesgo de desarrollar infección grave por COVID-19. Métodos: se reclutaron pacientes consecutivos que acudieron al servicio de urgencias de nuestro centro con diagnóstico de COVID-19 confirmado (PCR-COVID-19 positiva) y mediciones recientes de 25(OH)D. Exploramos la asociación de la deficiencia de vitamina D (VDD), definida como una 25-hidroxivitamina D < 20 ng/ml, con un compuesto de resultados clínicos adversos. Resultados: se incluyeron 80 pacientes, de los cuales 31 (39 %) presentaron el criterio de valoración primario. El VDD tendió a predecir un mayor riesgo de desarrollar COVID-19 grave después de ajustar edad, sexo, obesidad, enfermedad cardíaca y enfermedad renal [OR: 3,2 (IC 95 %: 0,9-11,4), p = 0,07]. La edad tuvo una interacción negativa con el efecto de la VDD en el resultado compuesto (p = 0,03), lo que indica que el efecto fue más notable a edades más tempranas. Además, el género masculino se asoció con la VDD y con la COVID-19 grave en las edades más jóvenes. Conclusiones: en este estudio retrospectivo, la deficiencia de vitamina D mostró una tendencia de asociación con la infección grave por COVID-19. Se observó una interacción significativa con la edad, lo que sugiere que la VDD puede tener un mayor impacto en los pacientes más jóvenes. Estos hallazgos deben confirmarse en estudios más grandes, prospectivos y con potencia adecuada.


Subject(s)
Age Factors , Betacoronavirus , Coronavirus Infections/etiology , Pneumonia, Viral/etiology , Vitamin D Deficiency/complications , Vitamin D/analogs & derivatives , Adult , Aged , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/epidemiology , Female , Heart Diseases/complications , Humans , Kidney Diseases/complications , Male , Middle Aged , Obesity/complications , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/epidemiology , Retrospective Studies , SARS-CoV-2 , Sex Factors , Spain/epidemiology , Vitamin D/blood
12.
Eur Rev Med Pharmacol Sci ; 25(4): 2114-2122, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1116635

ABSTRACT

OBJECTIVE: To determine the incidence and risk factors for acute cardiac injury (ACI) and acute kidney injury (AKI), and then investigate their effect on severity and mortality in patients with COVID-19. PATIENTS AND METHODS: A total of 1249 patients with COVID-19 were included in this retrospective study. Predictors of ACI and AKI were investigated. Multivariable-logistic regression models were used to determine the association of ACI (or AKI) with severity and mortality. RESULTS: Median age of patients was 36 years and 61.9% were male. ACI and AKI were observed in 53 (4.2%) and 91 (7.3%) of patients, respectively. Patients with age > 60 years, chronic heart disease, decreased lymphocyte and increased CRP, PCT, and ESR on hospital admission, and Lopinavir/Ritonavir use showed higher odds of ACI. Patients with age > 60 years, male, obesity, hypertension, chronic kidney disease, decreased lymphocyte and increased CRP, PCT, and ESR on hospital admission showed higher odds of AKI. Increased Hs-cTnI (> 300 ng/L), Pro-BNP (> 2500 pg/ml) and decreased e-GFR (< 60 ml/min) revealed higher adjusted mortality. CONCLUSIONS: ACI and AKI were not common in COVID-19 patients in Shanghai, China. However, patients with ACI/AKI had higher severity-rate and mortality-rate when compared to those without ACI/AKI.


Subject(s)
Acute Kidney Injury/mortality , COVID-19/mortality , Heart Diseases/mortality , SARS-CoV-2 , Acute Kidney Injury/complications , Aged , COVID-19/complications , China/epidemiology , Female , Heart Diseases/complications , Hospitalization/statistics & numerical data , Humans , Kaplan-Meier Estimate , Male , Middle Aged , Retrospective Studies , Severity of Illness Index
13.
PLoS One ; 16(2): e0247800, 2021.
Article in English | MEDLINE | ID: covidwho-1105824

ABSTRACT

Myocardial injury in hospitalized patients is associated with poor prognosis. This study aimed to evaluate risk factors for myocardial injury in hospitalized patients with coronavirus disease 2019 (COVID-19) and its prognostic value. We retrieved all consecutive patients who were hospitalized in internal medicine departments in a tertiary medical center from February 9th, 2020 to August 28th with a diagnosis of COVID-19. A total of 559 adult patients were hospitalized in the Sheba Medical Center with a diagnosis of COVID-19, 320 (57.24%) of whom were tested for troponin levels within 24-hours of admission, and 91 (28.44%) had elevated levels. Predictors for elevated troponin levels were age (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.01-1.06), female sex (OR, 3.03; 95% CI 1.54-6.25), low systolic blood pressure (OR, 5.91; 95% CI 2.42-14.44) and increased creatinine level (OR, 2.88; 95% CI 1.44-5.73). The risk for death (hazard ratio [HR] 4.32, 95% CI 2.08-8.99) and a composite outcome of invasive ventilation support and death (HR 1.96, 95% CI 1.15-3.37) was significantly higher among patients who had elevated troponin levels. In conclusion, in hospitalized patients with COVID-19, elevated troponin levels are associated with poor prognosis. Hence, troponin levels may be used as an additional tool for risk stratification and a decision guide in patients hospitalized with COVID-19.


Subject(s)
COVID-19/complications , Heart Diseases/complications , Aged , Aged, 80 and over , Blood Pressure , COVID-19/blood , COVID-19/diagnosis , Female , Heart Diseases/blood , Heart Diseases/diagnosis , Hospitalization , Humans , Male , Middle Aged , Myocardium/pathology , Prognosis , Retrospective Studies , SARS-CoV-2/isolation & purification , Troponin/analysis
14.
Acta Diabetol ; 58(7): 831-843, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1083870

ABSTRACT

The outbreak of coronavirus disease 2019 (COVID-19) caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a pandemic. The cellular receptor for SARS-CoV-2 entry is the angiotensin-converting enzyme 2, a membrane-bound homolog of angiotensin-converting enzyme. Henceforth, this has brought the attention of the scientific community to study the interaction between COVID-19 and the renin-angiotensin system (RAS), as well as RAS inhibitors. However, these inhibitors are commonly used to treat hypertension, chronic kidney disorder, and diabetes. Obesity is a known risk factor for heart disease, diabetes, and hypertension, whereas diabetes and hypertension may be indirectly related to each other through the effects of obesity. Furthermore, people with hypertension, obesity, diabetes, and other related complications like cardiovascular and kidney diseases have a higher risk of severe COVID-19 infection than the general population and usually exhibit poor prognosis. This severity could be due to systemic inflammation and compromised immune response and RAS associated with these comorbid conditions. Therefore, there is an urgent need to develop evidence-based treatment methods that do not affect the severity of COVID-19 infection and effectively manage these chronic diseases in people with COVID-19.


Subject(s)
COVID-19/mortality , Diabetes Mellitus/epidemiology , Hypertension/epidemiology , Obesity/epidemiology , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antihypertensive Agents/pharmacology , Antihypertensive Agents/therapeutic use , COVID-19/complications , COVID-19/epidemiology , Comorbidity , Diabetes Complications/drug therapy , Diabetes Complications/epidemiology , Diabetes Complications/mortality , Diabetes Mellitus/drug therapy , Disease Progression , Heart Diseases/complications , Heart Diseases/drug therapy , Heart Diseases/epidemiology , Humans , Hypertension/complications , Hypertension/drug therapy , Obesity/complications , Pandemics , Peptidyl-Dipeptidase A/physiology , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiology , Risk Factors , SARS-CoV-2/drug effects , SARS-CoV-2/physiology
15.
Int J Cardiovasc Imaging ; 37(5): 1721-1733, 2021 May.
Article in English | MEDLINE | ID: covidwho-1070880

ABSTRACT

The pandemic of coronavirus disease 2019 (COVID-19) secondary to the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has bestowed an unprecedented challenge upon us, resulting in an international public health emergency. COVID-19 has already resulted in > 1,600,000 deaths worldwide and the fear of a global economic collapse. SARS-CoV-2 is notorious for causing acute respiratory distress syndrome, however emerging literature suggests various dreaded cardiac manifestations associated with high mortality. The mechanism of myocardial damage in COVID-19 is unclear but thought to be multifactorial and mainly driven by the host's immune response (cytokine storm), hypoxemia and direct myocardial injury by the virus. Cardiac manifestations from COVID-19 include but are not limited to, acute myocardial injury, cardiac arrhythmias, congestive heart failure and acute coronary syndrome. Cardiac imaging is paramount to appropriately diagnose and manage the cardiac manifestations of COVID-19. Herein, we present cardiac imaging findings of COVID-19 patients with biomarker and imaging confirmed myocarditis to provide insight regarding the variable manifestations of COVID-19 myocarditis via Cardiac MRI (CMR) coupled with CMR-edema education along with recommendations on how to incorporate advanced CMR into the clinicians' COVID-19 armamentarium.


Subject(s)
COVID-19/complications , Heart Diseases/complications , Heart Diseases/diagnostic imaging , Magnetic Resonance Imaging/methods , Heart/diagnostic imaging , Humans , SARS-CoV-2
16.
Stem Cell Res ; 51: 102168, 2021 03.
Article in English | MEDLINE | ID: covidwho-1019479

ABSTRACT

COVID-19 caused by a novel coronavirus named SARS-CoV-2, can elites severe acute respiratory syndrome, severe lung injury, cardiac injury, and even death and became a worldwide pandemic. SARS-CoV-2 infection may result in cardiac injury via several mechanisms, including the expression of angiotensin-converting enzyme 2 (ACE2) receptor and leading to a cytokine storm, can elicit an exaggerated host immune response. This response contributes to multi-organ dysfunction. As an emerging infectious disease, there are limited data on the effects of this infection on patients with underlying cardiovascular comorbidities. In this review, we summarize the early-stage clinical experiences with COVID-19, with particular focus on patients with cardiovascular diseases and cardiopulmonary injuries, and explores potential available evidence regarding the association between COVID-19, and cardiovascular complications.


Subject(s)
COVID-19/pathology , Cardiovascular Diseases/complications , Heart Diseases/complications , Animals , COVID-19/complications , COVID-19/transmission , COVID-19/virology , Cytokine Release Syndrome/etiology , Heart Diseases/prevention & control , Heart Failure/complications , Heart Failure/prevention & control , Humans , Myocarditis/complications , Myocarditis/prevention & control , SARS-CoV-2/isolation & purification
19.
J Thorac Imaging ; 36(2): 73-83, 2021 Mar 01.
Article in English | MEDLINE | ID: covidwho-972686

ABSTRACT

OBJECTIVE: Cardiac magnetic resonance imaging (CMR) with its new quantitative mapping techniques has proved to be an essential diagnostic tool for detecting myocardial injury associated with coronavirus disease 2019 (COVID-19) infection. This systematic review sought to assess the important imaging features on CMR in patients diagnosed with COVID-19. MATERIALS AND METHODS: We performed a systematic literature review within the PubMed, Embase, Google Scholar, and WHO databases for articles describing the CMR findings in COVID-19 patients. RESULTS: A total of 34 studies comprising 199 patients were included in the final qualitative synthesis. Of the CMRs 21% were normal. Myocarditis (40.2%) was the most prevalent diagnosis. T1 (109/150; 73%) and T2 (91/144; 63%) mapping abnormalities, edema on T2/STIR (46/90; 51%), and late gadolinium enhancement (LGE) (85/199; 43%) were the most common imaging findings. Perfusion deficits (18/21; 85%) and extracellular volume mapping abnormalities (21/40; 52%), pericardial effusion (43/175; 24%), and pericardial LGE (22/100; 22%) were also seen. LGE was most commonly seen in the subepicardial location (81%) and in the basal-mid part of the left ventricle in inferior segments. In most of the patients, ventricular functions were normal. Kawasaki-like involvement with myocardial edema without necrosis/LGE (4/6; 67%) was seen in children. CONCLUSION: CMR is useful in assessing the prevalence, mechanism, and extent of myocardial injury in COVID-19 patients. Myocarditis is the most common imaging diagnosis, with the common imaging findings being mapping abnormalities and myocardial edema on T2, followed by LGE. As cardiovascular involvement is associated with poor prognosis, its detection warrants prompt attention and appropriate treatment.


Subject(s)
COVID-19/complications , COVID-19/diagnostic imaging , Heart Diseases/complications , Heart Diseases/diagnostic imaging , Magnetic Resonance Imaging/methods , Heart/diagnostic imaging , Humans , SARS-CoV-2
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