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1.
Medicina (Kaunas) ; 58(10)2022 Oct 11.
Article in English | MEDLINE | ID: covidwho-2071631

ABSTRACT

Background and Objectives: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection represents a pathology with primary pulmonary involvement and multisystemic impact, including cardiovascular injuries. The present study aimed to assess the value of clinical, biochemical, and imaging factors in COVID-19 patients in determining the severity of myocardial involvement, and to create a model that can be used toevaluate myocardial injury risk based on clinical, biochemical and imaging factors. Materials and Methods: We performed an observational cohort study on 150 consecutive patients, evaluating their age, sex, hospitalization period, peripheral oxygen saturation (SpO2) in ambient air, systolic and diastolic blood pressure, heart rate, respiratory rate, biochemical markers of cardiac dysfunction (TnI, and NT-proBNP), inflammatory markers (C reactive protein (CRP), fibrinogen, serum ferritin, interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα)), D-dimers, lactate dehydrogenase (LDH), myoglobin and radio-imaging parameters. All patients underwent computerized tomography chest scan in the first two days following admission. Results: We observed elevated heart and respiratory rates, higher systolic blood pressure, and a lower diastolic blood pressure in the patients with cardiac injury; significant differences between groups were registered in TnI, NT-proBNP, LDH, CRP, and D-dimers. For the radiological parameters, we found proportional correlations with the myocardial injury for the severity of lung disease, number of pulmonary segments with alveolar consolidation, number of pulmonary lobes with pneumonia, crazy paving pattern, type of lung involvement, the extent of fibroatelectatic lesions and the mediastinal adenopathies. Conclusions: Myocardial injury occurred in 12% of patients in the study group. Ground glass opacities, interstitial interlobular septal thickening (crazy paving pattern), fibroatelectasic lesions and alveolar consolidations on CT scan were correlated with myocardial injury. Routine lung sectional imaging along with non-specific biomarkers (LDH, D-dimers, and CRP) can be further valuable in the characterization of the disease burden, thus impacting patient care.


Subject(s)
COVID-19 , Humans , COVID-19/complications , SARS-CoV-2 , Interleukin-6 , Tumor Necrosis Factor-alpha , C-Reactive Protein , Myoglobin , Lung/pathology , Biomarkers , Lactate Dehydrogenases , Ferritins , Retrospective Studies
2.
Front Cardiovasc Med ; 9: 876718, 2022.
Article in English | MEDLINE | ID: covidwho-2054996

ABSTRACT

Introduction: The impact of colchicine on hospitalized patients with Coronavirus disease-19 (COVID-19) related cardiac injury is unknown. Materials and Methods: In this multicenter randomized controlled open-label clinical trial, we randomized hospitalized adult patients with documented COVID-19 and evidence of cardiac injury in a 1:1 ratio to either colchicine 0.6 mg po twice daily for 30 days plus standard of care or standard of care alone. Cardiac injury was defined as elevated cardiac biomarkers, new arrhythmia, new/worsened left ventricular dysfunction, or new pericardial effusion. The primary endpoint was the composite of all-cause mortality, need for mechanical ventilation, or need for mechanical circulatory support (MCS) at 90 days. Key secondary endpoints included the individual components of the primary endpoint and change in and at least 2-grade reduction in the World Health Organization (WHO) Ordinal Scale at 30 days. The trial is registered with clinicaltrials.gov (NCT04355143). Results: We enrolled 93 patients, 48 patients in the colchicine arm and 45 in the control arm. There was no significant difference in the primary outcome between the colchicine and control arms (19 vs. 15%, p = 0.78), nor in the individual components of all-cause mortality (17 vs. 15%, p = 1.0) and need for mechanical ventilation (8 vs. 5%, p = 0.68); no patients in either group required MCS. The change in (-1.8 ± 2.4 vs. -1.2 ± 2.0, p = 0.12) and at least 2-grade reduction (75 vs. 75%, p = 1.0) in the WHO ordinal scale was also similar between groups. Conclusion: Patients hospitalized with COVID-19 and evidence of cardiac injury did not benefit from colchicine therapy.

3.
Cardiovasc Diabetol ; 21(1): 188, 2022 09 19.
Article in English | MEDLINE | ID: covidwho-2038758

ABSTRACT

BACKGROUND: To determine the risk-assessment role of the immune-inflammatory biomarkers on myocardial damage in COVID-19 patients with diabetes mellitus (DM). METHODS: This retrospective study was conducted on 822 COVID-19 inpatients from 1 January to 10 March 2020 at Renmin Hospital of Wuhan University. The demographic data, clinical data, and immune-inflammatory parameters of participants were collected. The predictors of cardiac injury were assessed by Logistics regression analysis. RESULTS: A total of 246 COVID-19 inpatients were diagnosed with DM (29.9%). The incidence of cardiac injury was higher in patients with DM than in non-DM cases (28.9% vs 9.0%, p < 0.001), even grouped by age, gender, and the level of fasting plasma glucose (FPG). The mortality in diabetic COVID-19 patients with cardiac injury and without cardiac injury was 42.9% and 3.4%, respectively (p < 0.001). COVID-19 patients with DM and cardiac injury presented a decreased number of immunocyte subsets, lower C3 concentration, and a higher level of interleukin-6 (IL-6) and immunoglobulin A (IgA). The independent risk factors for cardiac injury in COVID-19 patients with DM were CD3+CD4+ T cells counts ≤ 288 cells/µl (adjusted Odds ratio (OR), 2.501; 95% confidence interval (CI) 1.282-4.877; p = 0.007) and IL-6 > 25.68mpg/ml (adjusted OR, 4.345; 95% CI 2.192-10.374; p < 0.001) (all Pinteraction < 0.05). CONCLUSIONS: For diabetic patients with COVID-19, cardiac injury not only induce severer immune-inflammatory responses, but also increase in-hospital mortality. The decreased number of CD3+CD4+ T cells and increased IL-6 are recommended to distinguish the people who refer to high risk of cardiac injury and mortality from those persons. However, it remains a testable theory whether decision-making strategies based on the risk status of cardiac injury in COVID-19 patients, especially with DM, would be expected to get better outcomes.


Subject(s)
COVID-19 , Diabetes Mellitus , Biomarkers , Blood Glucose , COVID-19/diagnosis , Diabetes Mellitus/diagnosis , Diabetes Mellitus/epidemiology , Humans , Immunoglobulin A , Interleukin-6 , Retrospective Studies
4.
Viruses ; 14(8)2022 08 14.
Article in English | MEDLINE | ID: covidwho-1987993

ABSTRACT

BACKGROUND: Even though coronary artery disease (CAD) is considered an independent risk factor of an unfavorable outcome of SARS-CoV-2-infection, the clinical course of COVID-19 in subjects with CAD is heterogeneous, ranging from clinically asymptomatic to fatal cases. Since the individual C2HEST components are similar to the COVID-19 risk factors, we evaluated its predictive value in CAD subjects. MATERIALS AND METHODS: In total, 2183 patients hospitalized due to confirmed COVID-19 were enrolled onto this study consecutively. Based on past medical history, subjects were assigned to one of two of the study arms (CAD vs. non-CAD) and allocated to different risk strata, based on the C2HEST score. RESULTS: The CAD cohort included 228 subjects, while the non-CAD cohort consisted of 1956 patients. In-hospital, 3-month and 6-month mortality was highest in the high-risk C2HEST stratum in the CAD cohort, reaching 43.06%, 56.25% and 65.89%, respectively, whereas in the non-CAD cohort in the high-risk stratum, it reached: 26.92%, 50.77% and 64.55%. Significant differences in mortality between the C2HEST stratum in the CAD arm were observed in post hoc analysis only for medium- vs. high-risk strata. The C2HEST score in the CAD cohort could predict hypovolemic shock, pneumonia and acute heart failure during hospitalization, whereas in the non-CAD cohort, it could predict cardiovascular events (myocardial injury, acute heart failure, myocardial infract, carcinogenic shock), pneumonia, acute liver dysfunction and renal injury as well as bleedings. CONCLUSIONS: The C2HEST score is a simple, easy-to-apply tool which might be useful in risk stratification, preferably in non-CAD subjects admitted to hospital due to COVID-19.


Subject(s)
COVID-19 , Coronary Artery Disease , Heart Failure , COVID-19/diagnosis , Coronary Artery Disease/diagnosis , Hospitalization , Humans , Risk Assessment , Risk Factors , SARS-CoV-2
5.
Microorganisms ; 10(7)2022 Jun 21.
Article in English | MEDLINE | ID: covidwho-1964028

ABSTRACT

Myocardial injury in patients with SARS-CoV-2 infection may be attributed to the presence of the virus at the cellular level, however, it may also be secondary to other diseases, playing an essential role in the evolution of the disease. We evaluated 16 patients who died because of SARS-CoV-2 infection and analyzed the group from both clinical and pathological points of view. All autopsies were conducted in the Sibiu County morgue, taking into consideration all the national protocols for COVID-19 patients. Of the 16 autopsies we performed, two were complete, including an extensive examination of the cranial cavity. In our study, the cardiac injury was primarily cumulative. Chronic cardiac injuries included fatty infiltration of the myocardium in five cases, fibrosis in 11 cases, and coronary atherosclerosis in two cases. Among the cases with evidence of acute cardiovascular injuries, inflammatory lymphocytic infiltrate was observed in nine cases, subepicardial or visceral pericardial neutrophil-rich vascular congestion in five cases, and venous thrombosis in three cases. Acute ischemia or myocytic distress was identified by vacuolar degeneration in four cases; areas of undulated and/or fragmented myocardial fibers, with eosinophilia and nuclear pyknosis with or without enucleation of the myocytes in nine cases; and in one case, we observed a large area of myocardial necrosis. Immunohistochemical criteria confirmed the presence of the SARS-CoV-2 antigen at the level of the myocardium in only two cases. Comorbidities existing prior to SARS-CoV-2 infection associated with systemic and local inflammatory, thrombotic, hypoxic, or immunological phenomena influence the development of cardiac lesions, leading to death.

6.
J Cardiovasc Thorac Res ; 14(1): 23-33, 2022.
Article in English | MEDLINE | ID: covidwho-1955532

ABSTRACT

Introduction: Owing to the imposed burden of the coronavirus disease 2019 (COVID-19),the need for stratifying the prognosis of patients has never been timelier. Hence, we aimed to ascertain the value of CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-M (one point for male instead of female) scores to predict unfavorable outcomes in COVID-19 patients. Methods: We enrolled consecutive patients above 18 years of age with confirmed COVID-19,who were admitted between February 16 and November 1, 2020. The primary endpoint of this study was three-month all-cause mortality. The secondary endpoints were considered four major in-hospital clinical features, including acute respiratory distress syndrome, cardiac injury,acute kidney injury, and mechanical ventilation. Results: A total of 1,406 hospitalized COVID-19 patients were studied, among which 301(21.40%) patients died during the follow-up period. Regarding the risk scores, CHADS 2≥1,CHA2DS2-VASc≥2, and CHA2DS2-VASc-M≥2 were significantly associated with mortality. The performance of all risk scores for predicting mortality was satisfactory (area under the curve:0.668, 0.668, and 0.681, respectively). Appraising secondary endpoints, we found that all three risk scores were associated with increased risk of acute respiratory distress syndrome, cardiac injury, acute kidney injury, and mechanical ventilation. Lastly, we revealed that all risk scores were significantly correlated with serum levels of laboratory biomarkers. Conclusion: Our analysis illustrated that the CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-Mscores could aid prognostication of unfavorable outcomes in COVID-19 patients. Therefore,these easily calculable methods could be integrated into the overall therapeutic strategy to guide the COVID-19 management more accurately.

7.
Arch Cardiovasc Dis ; 115(6-7): 388-396, 2022.
Article in English | MEDLINE | ID: covidwho-1943941

ABSTRACT

BACKGROUND: Since 2019, coronavirus disease 2019 (COVID-19) has been the leading cause of mortality worldwide. AIMS: To determine independent predictors of mortality in COVID-19, and identify any associations between pulmonary disease severity and cardiac involvement. METHODS: Clinical, laboratory, electrocardiography and computed tomography (CT) imaging data were collected from 389 consecutive patients with COVID-19. Patients were divided into alive and deceased groups. Independent predictors of mortality were identified. Kaplan-Meier analysis was performed, based on patients having a troponin concentration>99th percentile (cardiac injury) and a CT severity score ≥18. RESULTS: The mortality rate was 29.3%. Cardiac injury (odds ratio [OR] 2.19, 95% confidence interval [CI] 1.14-4.18; P=0.018), CT score ≥18 (OR 2.24, 95% CI 1.15-4.34; P=0.017), localized ST depression (OR 3.77, 95% CI 1.33-10.67; P=0.012), hemiblocks (OR 3.09, 95% CI 1.47-6.48; P=0.003) and history of leukaemia/lymphoma (OR 3.76, 95% CI 1.37-10.29; P=0.010) were identified as independent predictors of mortality. Additionally, patients with cardiac injury and CT score ≥ 18 were identified to have a significantly shorter survival time (mean 14.21 days, 95% CI 10.45-17.98 days) than all other subgroups. There were no associations between CT severity score and electrocardiogram or cardiac injury in our results. CONCLUSIONS: Our findings suggest that using CT imaging and electrocardiogram characteristics together can provide a better means of predicting mortality in patients with COVID-19. We identified cardiac injury, CT score ≥18, presence of left or right hemiblocks on initial electrocardiogram, localized ST depression and history of haematological malignancies as independent predictors of mortality in patients with COVID-19.


Subject(s)
COVID-19 , Heart Injuries , Hospital Mortality , Humans , Lung , Retrospective Studies , SARS-CoV-2 , Tomography, X-Ray Computed/methods
8.
Pakistan Journal of Medical Sciences Quarterly ; 37(3):908, 2021.
Article in English | ProQuest Central | ID: covidwho-1898182

ABSTRACT

At the end of 2019 a novel coronavirus was identified in Wuhan, China. The disease caused by the severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) was designated COVID-19 (corona virus disease 2019) by the World Health Organization in early 2020. Up to 80% of patients with COVID-19 experience mild symptoms with severe or critical disease occurring in the remaining 20%. Severe disease is manifested by the development of pneumonia, hypoxia and radiographic lung involvement while critical disease indicates multiorgan involvement with significant respiratory or cardiac compromise. The current estimated case fatality rate from COVID-19 is approximately 1%. Epidemiological studies have shown that advanced age, male gender, previous chronic lung disease, cardiovascular and kidney disease, obesity and diabetes are risk factors for the severity of disease course. In the current focused review, we present an overview of the acute cardiovascular complications of COVID-19, their detection and impact upon prognosis.

9.
Jordan Journal of Biological Sciences ; 15(2):159-164, 2022.
Article in English | Academic Search Complete | ID: covidwho-1893782

ABSTRACT

Occurrence of cardiac arrhythmias in COVID-19 patients with myocardial injuries is common, and it is potentially a lifethreatening complication. The current study presents the published literature on cardiac arrhythmia occurrence in COVID-19 patients during 2020. We aimed to evaluate the association among cardiac arrhythmias, acute cardiac injury, and disease severity. Databases, including PubMed, Science Direct, and Scopus, were searched to find studies describing subjects with cardiac arrhythmias and COVID-19. In this study, we recruited 4,355 patients with COVID-19, collected from 13 studies. Relevant data were manually extracted and compared among two groups: arrhythmia as a complication of COVID-19 and cardiac injury as a complication of COVID-19. The pooled prevalence of cardiac arrhythmia was 19% (95%CI: 12% to 29%), compared to 9% (95%CI: 5% to 18%) in acute cardiac injury. Compared to patients without arrhythmias, the probability of developing severe symptoms was increased by ten folds in patients with arrhythmias. In addition, acute cardiac injury significantly increased the severity of COVID-19 by nearly 15-folds. No significant publication bias was indicated by either the visual symmetry or the Egger’s test. In conclusion, the incidence of cardiac arrhythmias and acute cardiac injury is highly associated with the severity and the mortality rate of COVID-19. [ FROM AUTHOR] Copyright of Jordan Journal of Biological Sciences is the property of Hashemite University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

10.
Pan Afr Med J ; 41: 45, 2022.
Article in English | MEDLINE | ID: covidwho-1856322

ABSTRACT

Many cases of severe cardiac complications due to Coronavirus disease 2019 (COVID-19) were reported. Cancer and chemotherapy appear to be risk and prognostic factors for COVID-19. A 49-year-old Female, with a history of breast cancer treated by tumorectomy and anthracycline-based chemotherapy was admitted with acute respiratory distress syndrome (ARDS) confirmed as COVID-19. She also had elevated troponin I level (up to 43 g/L), and diffuse myocardial hypokinesia along with severe left ventricle dysfunction on echocardiography. Initial treatment included hydroxychloroquine, azithromycin, corticosteroids and mechanical ventilation. The evolution was marked by QT interval prolongation (QTc=523 ms) and occurrence of cardiogenic shock. The patient died of hemodynamic instability reluctant to resuscitation measures at the 2ndday of hospitalization. COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure. Receiving chemotherapy especially anthracyclines may be a precipitating and prognostic factor of cardiac manifestations in COVID-19 cancer patients.


Subject(s)
Breast Neoplasms , COVID-19 , Heart Diseases , Heart Failure , Breast Neoplasms/complications , Breast Neoplasms/drug therapy , Female , Heart Diseases/chemically induced , Heart Diseases/diagnosis , Heart Failure/etiology , Humans , Middle Aged , Shock, Cardiogenic/etiology
11.
Front Med (Lausanne) ; 9: 808221, 2022.
Article in English | MEDLINE | ID: covidwho-1817974

ABSTRACT

BACKGROUND: Severe COVID-19 pneumonia requiring intensive care treatment remains a clinical challenge to date. Dexamethasone was reported as a promising treatment option, leading to a reduction of mortality rates in severe COVID-19 disease. However, the effect of dexamethasone treatment on cardiac injury and pulmonary embolism remains largely elusive. METHODS: In total 178 critically ill COVID-19 patients requiring intensive care treatment and mechanical ventilation were recruited in three European medical centres and included in the present retrospective study. One hundred thirteen patients (63.5%) were treated with dexamethasone for a median duration of 10 days (IQR 9-10). Sixty five patients (36.5%) constituted the non-dexamethasone control group. RESULTS: While peak inflammatory markers were reduced by dexamethasone treatment, the therapy also led to a significant reduction in peak troponin levels (231 vs. 700% indicated as relative to cut off value, p = 0.001). Similar, dexamethasone resulted in significantly decreased peak D-Dimer levels (2.16 mg/l vs. 6.14 mg/l, p = 0.002) reflected by a significant reduction in pulmonary embolism rate (4.4 vs. 20.0%, p = 0.001). The antithrombotic effect of dexamethasone treatment was also evident in the presence of therapeutic anticoagulation (pulmonary embolism rate: 6 vs. 34.4%, p < 0.001). Of note, no significant changes in baseline characteristics were observed between the dexamethasone and non-dexamethasone group. CONCLUSION: In severe COVID-19, anti-inflammatory effects of dexamethasone treatment seem to be associated with a significant reduction in myocardial injury. Similar, a significant decrease in pulmonary embolism, independent of anticoagulation, was evident, emphasizing the beneficial effect of dexamethasone treatment in severe COVID-19.

12.
Int J Biol Sci ; 18(7): 2703-2713, 2022.
Article in English | MEDLINE | ID: covidwho-1811190

ABSTRACT

Coronavirus disease 2019 (COVID-19), a global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) had resulted in considerable morbidity and mortality. COVID-19 primarily posed a threat to the respiratory system and violated many different organs, including the heart, kidney, liver, and blood vessels with the development of the disease. Severe patients were often accompanied by cardiac injury, and once the heart gets damaged, the mortality of patients will significantly increase. The main clinical manifestations of cardiac injury range from myocarditis, heart failure (HF), arrhythmia, and Takotsubo cardiomyopathy (TCM). A high abundance of angiotensin-converting enzyme II (ACE2) on the membrane of cardiomyocytes makes it possible that the virus can directly attack cardiomyocytes as subsequently evidenced by the detection of spike protein and virus RNA in autopsy cardiac tissues. The secondary myocardial injury through systemic inflammatory and immune response also caused obvious cardiac damage. The pathological manifestations of heart tissue were diverse, varied from mild cardiomyocyte edema, myocardial hypertrophy, cardiomyocyte degeneration, and necrosis to severe myocarditis caused by lymphocyte and macrophage infiltration. However, the mechanism of heart injury was still unclear. Here, we summarized the clinical manifestations and mechanism of SARS-CoV2 mediated cardiac injury, providing a reference for cardiac treatment in critically ill patients.


Subject(s)
COVID-19 , Heart Injuries , Myocarditis , Humans , RNA, Viral , SARS-CoV-2
13.
Pakistan Armed Forces Medical Journal ; 71:S298-S300, 2021.
Article in English | Scopus | ID: covidwho-1801626

ABSTRACT

Objective: To determine frequency of cardiac involvement in patients of COVID-19. Secondary objective was to determine association of cardiac involvement with prognosis. Study Design: Descriptive cross-sectional study. Place and Duration of Study: Pak-Emirates Military Hospital, Rawalpindi Pakistan, from Apr to Jul 2020. Methodology: We prospectively assessed the laboratory data, Electrocardiogram and transthoracic echocardiography of all the COVID-19 patients admitted to our institute. Outcomes of interest included length of hospital stay, admission to Intensive Care Unit and mortality. Acute myocardial injury was defined by a value of high-sensitivity troponin I (hs-TnI) above the 99th percentile upper reference limit. Statistical Package for the Social Sciences (SPSS) version 23 was used for all the analysis. Results: Our study included 1015 patients, mean age 50.34 (SD 13.71) years, 887 (87.3%) males and 128 (12.6%) females. Three hundred and thirty (n=330, 32.5%) patients had evidence of acute cardiac injury as shown by raised cardiac troponins, but 50, 4.92% had left ventricle dysfunction. Raised cardiac enzymes were associated with marginally prolonged hospital stay (10.03 versus 9.32 days, p-value 0.07) and higher mortality (OR 2.634, confidence interval 1.252-5.543, p-value 0.01). Conclusion: Cardiac involvement is quite common among patients suffering from COVID-19 and predicts worse prognosis. © 2021, Army Medical College. All rights reserved.

14.
Rhythmos ; 17(2):25-31, 2022.
Article in English | Academic Search Complete | ID: covidwho-1787295

ABSTRACT

A comprehensive review of current data on COVID-19 related myocarditis is herein presented. [ FROM AUTHOR] Copyright of Rhythmos is the property of Evagelismos General Hospital of Athens and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

15.
Am Heart J Plus ; 14: 100125, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1767825

ABSTRACT

Purpose: This study assessed a functional protocol to identify myocarditis or myocardial involvement in competitive athletes following SARS-CoV2 infection. Methods: We prospectively evaluated competitive athletes (n = 174) for myocarditis or myocardial involvement using the Multidisciplinary Inquiry of Athletes in Miami (MIAMI) protocol, a median of 18.5 (IQR 16-25) days following diagnosis of COVID-19 infection. The protocol included biomarker analysis, ECG, cardiopulmonary stress echocardiography testing with global longitudinal strain (GLS), and targeted cardiac MRI for athletes with abnormal findings. Patients were followed for median of 148 days. Results: We evaluated 52 females and 122 males, with median age 21 (IQR: 19, 22) years. Five (2.9%) had evidence of myocardial involvement, including definite or probable myocarditis (n = 2). Three of the 5 athletes with myocarditis or myocardial involvement had clinically significant abnormalities during stress testing including ventricular ectopy, wall motion abnormalities and/or elevated VE/VCO2, while the other two athletes had resting ECG abnormalities. VO2max, left ventricular ejection fraction and GLS were similar between those with or without myocardial involvement. No adverse events were reported in the 169 athletes cleared to exercise at a median follow-up of 148 (IQR108,211) days. Patients who were initially restricted from exercise had no adverse sequelae and were cleared to resume training between 3 and 12 months post diagnosis. Conclusions: Screening protocols that include exercise testing may enhance the sensitivity of detecting COVID-19 related myocardial involvement following recovery from SARS-CoV2 infection.

16.
Curr Pharm Des ; 28(19): 1581-1588, 2022.
Article in English | MEDLINE | ID: covidwho-1765615

ABSTRACT

Besides acute respiratory distress syndrome, acute cardiac injury is a major complication in severe coronavirus disease 2019 (COVID-19) and is associated with a poor clinical outcome. Acute cardiac injury with COVID-19 can be of various etiologies, including myocardial ischemia or infarction and myocarditis, and may compromise cardiac function, resulting in acute heart failure or cardiogenic shock. Systemic inflammatory response increases heart rate (HR), which disrupts the myocardial oxygen supply/demand balance and worsens cardiac energy efficiency, thus further deteriorating the cardiac performance of the injured myocardium. In fact, the combination of elevated resting HR and markers of inflammation synergistically predicts adverse cardiovascular prognosis. Thus, targeted HR reduction may potentially be of benefit in cardiovascular pathologies associated with COVID-19. Ivabradine is a drug that selectively reduces HR via If current inhibition in the sinoatrial node without a negative effect on inotropy. Besides selective HR reduction, ivabradine was found to exert various beneficial pleiotropic effects, either HR-dependent or HR-independent, including anti-inflammatory, anti-atherosclerotic, anti-oxidant and antiproliferative actions and the attenuation of endothelial dysfunction and neurohumoral activation. Cardioprotection by ivabradine has already been indicated in cardiovascular pathologies that are prevalent with COVID-19, including myocarditis, acute coronary syndrome, cardiogenic shock or cardiac dysautonomia. Here, we suggest that ivabradine may be beneficial in the management of COVID-19- related cardiovascular complications.


Subject(s)
COVID-19 , Myocarditis , Benzazepines/pharmacology , COVID-19/complications , COVID-19/drug therapy , Heart Rate , Humans , Ivabradine/pharmacology , Ivabradine/therapeutic use , Shock, Cardiogenic
17.
J Electrocardiol ; 72: 44-48, 2022.
Article in English | MEDLINE | ID: covidwho-1734724

ABSTRACT

OBJECTIVE: The aim of this study is to examine the probability of de-novo fQRS in patients with mild COVID-19 disease, as an indicator of cardiac injury. METHODS: Data of 256 patients with normal admission electrocardiography and no comorbidities between 1.12.2020-31.12.2021, were examined retrospectively 6-month after mild COVID-19 disease. Patients were divided into two groups: fQRS+ group (n = 102) and non-fQRS group (n = 154). Relation between fQRS and other electrocardiography, echocardiographic and laboratory findings were investigated. RESULTS: No significant difference was found between the groups among age and gender. Troponin-I and creatine kinase myocardial band values (retrospectively 9.10 ± 1.76 vs 0.74 ± 1.43, 34.05 ± 82.20 vs. 14.68 ± 4.42), COVID-19 IgG levels (45.78 ± 14.82 vs. 36.49 ± 17.68), diastolic dysfunction (39.21% vs. 15.07%), EF value (58.02 ± 1.95 vs. 64.27 ± 3.07), dyspnea (41.17% vs. 6.84%), post-COVID-19 tachycardia syndrome (19.6% vs. 2.74) were more frequent in fQRS+ group compared to non-fQRS group. The EF value was lower in the presence of fQRS in the high lateral leads (57.12 ± 1.99, 58.47 ± 1.79, p:0.018). There was a positive correlation between IgG value and endsystolic diameter, septum thickness and left atrium diameter. In multivariate analysis de-novo fQRS, dyspnea, high troponin and IgG values, diastolic dysfunction, low EF value and left atrial diameter were determined as independent risk factors for post-COVID-19 tachycardia syndrome in follow-up. CONCLUSION: In COVID-19 disease de-novo fQRS, dyspnea, high IgG and troponin value, left atrial diameter, lower EF value, diastolic dysfunction were associated with post-COVID-19 tachycardia syndrome. The de-novo fQRS in SARS-COV-2 may be a predictor of future more important adverse cardiovascular outcomes and this should alert clinicians.


Subject(s)
COVID-19 , Electrocardiography , Heart Diseases , COVID-19/complications , COVID-19/physiopathology , Dyspnea/physiopathology , Dyspnea/virology , Follow-Up Studies , Heart Diseases/physiopathology , Heart Diseases/virology , Humans , Immunoglobulin G , Retrospective Studies , SARS-CoV-2 , Troponin
18.
Front Endocrinol (Lausanne) ; 13: 801260, 2022.
Article in English | MEDLINE | ID: covidwho-1731767

ABSTRACT

Type 2 diabetes (T2D) patients with SARS-CoV-2 infection hospitalized develop an acute cardiovascular syndrome. It is urgent to elucidate underlying mechanisms associated with the acute cardiac injury in T2D hearts. We performed bioinformatic analysis on the expression profiles of public datasets to identify the pathogenic and prognostic genes in T2D hearts. Cardiac RNA-sequencing datasets from db/db or BKS mice (GSE161931) were updated to NCBI-Gene Expression Omnibus (NCBI-GEO), and used for the transcriptomics analyses with public datasets from NCBI-GEO of autopsy heart specimens with COVID-19 (5/6 with T2D, GSE150316), or dead healthy persons (GSE133054). Differentially expressed genes (DEGs) and overlapping homologous DEGs among the three datasets were identified using DESeq2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses were conducted for event enrichment through clusterProfile. The protein-protein interaction (PPI) network of DEGs was established and visualized by Cytoscape. The transcriptions and functions of crucial genes were further validated in db/db hearts. In total, 542 up-regulated and 485 down-regulated DEGs in mice, and 811 up-regulated and 1399 down-regulated DEGs in human were identified, respectively. There were 74 overlapping homologous DEGs among all datasets. Mitochondria inner membrane and serine-type endopeptidase activity were further identified as the top-10 GO events for overlapping DEGs. Cardiac CAPNS1 (calpain small subunit 1) was the unique crucial gene shared by both enriched events. Its transcriptional level significantly increased in T2D mice, but surprisingly decreased in T2D patients with SARS-CoV-2 infection. PPI network was constructed with 30 interactions in overlapping DEGs, including CAPNS1. The substrates Junctophilin2 (Jp2), Tnni3, and Mybpc3 in cardiac calpain/CAPNS1 pathway showed less transcriptional change, although Capns1 increased in transcription in db/db mice. Instead, cytoplasmic JP2 significantly reduced and its hydrolyzed product JP2NT exhibited nuclear translocation in myocardium. This study suggests CAPNS1 is a crucial gene in T2D hearts. Its transcriptional upregulation leads to calpain/CAPNS1-associated JP2 hydrolysis and JP2NT nuclear translocation. Therefore, attenuated cardiac CAPNS1 transcription in T2D patients with SARS-CoV-2 infection highlights a novel target in adverse prognostics and comprehensive therapy. CAPNS1 can also be explored for the molecular signaling involving the onset, progression and prognostic in T2D patients with SARS-CoV-2 infection.


Subject(s)
COVID-19/epidemiology , Computational Biology , Diabetes Mellitus, Type 2/epidemiology , Diabetes Mellitus, Type 2/genetics , Diabetic Cardiomyopathies/epidemiology , SARS-CoV-2 , Adult , Aged , Aged, 80 and over , Animals , Calpain/genetics , Calpain/physiology , Comorbidity , Diabetes Mellitus, Type 2/physiopathology , Diabetic Cardiomyopathies/genetics , Diabetic Cardiomyopathies/physiopathology , Humans , Male , Membrane Proteins/metabolism , Mice , Mice, Inbred C57BL , Middle Aged , Mitochondria, Heart/ultrastructure , Muscle Proteins/metabolism , Myocardium/chemistry , Myocardium/metabolism , Myocardium/ultrastructure , Prognosis , Sequence Analysis, RNA , Transcriptome
19.
Front Cardiovasc Med ; 8: 798897, 2021.
Article in English | MEDLINE | ID: covidwho-1731763

ABSTRACT

PURPOSE: This study investigated the incidence, disease course, risk factors, and mortality in COVID-19 patients who developed both acute kidney injury (AKI) and acute cardiac injury (ACI), and compared to those with AKI only, ACI only, and no injury (NI). METHODS: This retrospective study consisted of hospitalized COVID-19 patients at Montefiore Health System in Bronx, New York between March 11, 2020 and January 29, 2021. Demographics, comorbidities, vitals, and laboratory tests were collected during hospitalization. Predictive models were used to predict AKI, ACI, and AKI-ACI onset. Longitudinal laboratory tests were analyzed with time-lock to discharge alive or death. RESULTS: Of the 5,896 hospitalized COVID-19 patients, 44, 19, 9, and 28% had NI, AKI, ACI, and AKI-ACI, respectively. Most ACI presented very early (within a day or two) during hospitalization in contrast to AKI (p < 0.05). Patients with combined AKI-ACI were significantly older, more often men and had more comorbidities, and higher levels of cardiac, kidney, liver, inflammatory, and immunological markers compared to those of the AKI, ACI, and NI groups. The adjusted hospital-mortality odds ratios were 17.1 [95% CI = 13.6-21.7, p < 0.001], 7.2 [95% CI = 5.4-9.6, p < 0.001], and 4.7 [95% CI = 3.7-6.1, p < 0.001] for AKI-ACI, ACI, and AKI, respectively, relative to NI. A predictive model of AKI-ACI onset using top predictors yielded 97% accuracy. Longitudinal laboratory data predicted mortality of AKI-ACI patients up to 5 days prior to outcome, with an area-under-the-curve, ranging from 0.68 to 0.89. CONCLUSIONS: COVID-19 patients with AKI-ACI had markedly worse outcomes compared to those only AKI, ACI and NI. Common laboratory variables accurately predicted AKI-ACI. The ability to identify patients at risk for AKI-ACI could lead to earlier intervention and improvement in clinical outcomes.

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R I Med J (2013) ; 105(2):25-32, 2022.
Article in English | PubMed | ID: covidwho-1710789

ABSTRACT

BACKGROUND: The causes of death in COVID-19 patients with cardiac injury are uncertain. METHODS: We conducted a case-control study and reviewed the electronic medical record of 109 deceased COVID-19 patients with cardiac injury on admission and 32 deceased COVID-19 patients without cardiac injury at two hospitals in Rhode Island. RESULTS: Among the 109 deceased COVID-19 patients who had cardiac injury on admission, 79 patients (72.5%) died of hypoxic respiratory failure, 21 patients (19.2%) of multi-organ failure and septic shock, 6 patients (5.5%) of cardiac arrhythmia, 3 patients (2.8%) of severe kidney failure as the immediate causes of death. We observed a similar pattern of distribution when compared to deceased patients without cardiac injury on admission (n=32). CONCLUSION: The main causes of death of COVID-19 patients with cardiac injury were non-cardiac, mostly hypoxic respiratory failure. Cardiac-related arrhythmia only accounted for a small proportion of cases.

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