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1.
Open Access Macedonian Journal of Medical Sciences ; 10:332-339, 2022.
Article in English | EMBASE | ID: covidwho-1939097

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a health problem that is still engulfing the world that contributes to the high mortality rate globally. Death arises from the severity of the disease due to complications in important organs such as the heart. AIM: The purpose of this study was to systematically review the manifestations of cardiovascular disease in COVID-19 patients and their management in terms of published articles. METHODS: This research is a systematic review research. The research was conducted using the PRISMA method. Article searches are carried out by online publications through PubMed, Science Direct, and Google Scholar that meet the inclusion and exclusion criteria. The population is articles about the manifestations of cardiovascular disease in COVID-19 patients and their management between 2011 and 2021. Inclusion criteria are studies that examine the manifestations of cardiovascular disease in COVID-19 patients and their management using primary data in the form of cohort research designs in English and full text available. The exclusion criteria were a case study, review study, and used secondary data. The data were analyzed by univariate analysis by calculating the frequency and percentage. RESULTS: The results show that several manifestations of cardiovascular disease in COVID-19 patients include cardiac injury, heart failure, myocardial infarction, myocarditis, cardiomegaly, and others. Complications of these diseases occur with or without comorbidities, and the risk increases with comorbid cardiovascular disease. The management of COVID-19 patients is basically done with antiviral agents, reducing symptoms and protecting important organs such as the heart. CONCLUSION: In the treatment of COVID-19 patients with cardiovascular complications, the use of antiviral agents such as lopinavir or ritonavir should be used with caution because: may interact with cardiovascular drugs. Mechanical circulation support is suggested, and the use of extracorporeal membrane oxygenation can also be performed to treat cardiovascular complications in COVID-19 patients.

2.
Heart International ; 16(1):1, 2022.
Article in English | EMBASE | ID: covidwho-1938574
3.
Journal of Hypertension ; 40:e180, 2022.
Article in English | EMBASE | ID: covidwho-1937744

ABSTRACT

Objective: Red blood cell (RBC) role is both passive action, oxygen delivery to the tissues as well as carbon dioxide to the lungs and active action involvement in the regulation of vascular tone. The aim was to investigate pathophysiological and ultrastructural changes of RBC in heart failure (HF) patients with hypertension (HT) and long Covid. Design and method: In total 12 patients with HF of Coronary Artery Disease origin, HT, and long Covid were examined. Mean age of patients was 62 ± 5.8 years. The control group consisted of 10 apparently healthy people. The functional state and ultrastructure of RBC were studied using electron microscopy. Results: During ultrastructure examination, structural pathologies of RBC in HF patients with HT and long Covid were revealed. RBC anisocytosis and poikilocytosis as structural damage variations in size and shape were found respectively. Reticulocytes were found much more often in HF patients with HT and long Covid than in the control group. In healthy control group, RBC had a typical discoid shape. In the presence of long Covid, both calcification as a marker of RBC apoptosis and destruction was also detected (Fig.1). Neutrophil extracellular traps (NETs) were found in RBC surrounding (Fig.1). Conclusions: Altered RBC function has important implications for HF patients with HT and long Covid. RBC has been shown to induce endothelial cell dysfunction and to increase cardiac injury as well as increased inflammatory processes in long Covid. The presence of HF, HT and long Covid leads to RBC calcification and activation of blood cell apoptosis. Prognostic role of RBC calcium distribution in combination with other important prognostic measures, such as biomarkers like Thrombospondin - 1, NT-proBNP and ST2 is subject of interest and requires further research.

4.
World Journal of Clinical Cases ; 10(20):6784-6793, 2022.
Article in English | EMBASE | ID: covidwho-1928899

ABSTRACT

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In some patients, COVID-19 is complicated with myocarditis. Early detection of myocardial injury and timely intervention can significantly improve the clinical outcomes of COVID-19 patients. Although endomyocardial biopsy (EMB) is currently recognized as the ‘gold standard’ for the diagnosis of myocarditis, there are large sampling errors, many complications and a lack of unified diagnostic criteria. In addition, the clinical methods of treating acute and chronic COVID-19-related myocarditis are different. Cardiac magnetic resonance (CMR) can evaluate the morphology of the heart, left and right ventricular functions, myocardial perfusion, capillary leakage and myocardial interstitial fibrosis to provide a noninvasive and radiation-free diagnostic basis for the clinical detection, efficacy and risk assessment, and followup observation of COVID-19-related myocarditis. However, for the diagnosis of COVID-19-related myocarditis, the Lake Louise Consensus Criteria may not be fully applicable. COVID-19-related myocarditis is different from myocarditis related to other viral infections in terms of signal intensity and lesion location as assessed by CMR, which is used to visualize myocardial damage, locate lesions and quantify pathological changes based on various sequences. Therefore, the standardized application of CMR to timely and accurately evaluate heart injury in COVID-19-related myocarditis and develop rational treatment strategies could be quite effective in improving the prognosis of patients and preventing potential late-onset effects in convalescent patients with COVID-19.

5.
European Heart Journal, Supplement ; 24(SUPPL C):C96-C97, 2022.
Article in English | EMBASE | ID: covidwho-1915557

ABSTRACT

Already from the first data in China it emerged that patients with cardiovascular comorbidities had an increased risk of contracting SARS-CoV-2 infection and a more unfavourable clinical course. From March to May 2020, 85 patients affected by COVID-19 were enrolled, hospitalized at the Hospital of Reggio Calabria. All patients underwent anamnesis, clinical evaluation, chest CT, ECG and measurement of markers of cardiovascular damage (Troponin I, CK-MB, LDH, D-dimer, BNP) and of inflammation (PCR, IL-6, and PCT). Thirty-one patients underwent echocardiography. In particular, we evaluated parietal dimensions and thicknesses, biventricular function and transvalvular tricuspid and pulmonary flows and correlated the data obtained with ECG, radiological, clinical, and biohumoral parameters. The aim of our study was to evaluate the prognostic impact of cardiovascular involvement in COVID- 19, investigating the effect of cardiovascular risk factors, levels of cardiovascular damage markers and newly emerging ECG and echocardiographic changes on a composite primary endpoint, consisting of the combination of death and the need for intensive care (ICU). The enrolled patients were divided into two subpopulations: those with better prognosis and those with poorer prognosis (ICU/exitus). We analysed the reciprocal correlation of each of the parameters and searched for the presence of echocardiographic signs of repercussion on the right sections of the pulmonary pathology. All markers of cardiovascular damage had significantly higher values in the most critically ill patients and similar behaviour had indices of inflammation. Patients with poorer prognosis had significantly lower lung AcT values, which correlated with higher D-dimer levels and more complicated hospital stays. There were no statistically significant differences between PAPs, right ventricular size, TAPSE and pulmonary trunk diameter in the two subpopulations. Larger right ventricular diameters were associated with more dilated lung trunks and higher IL-6 levels. The most interesting data of our study is the behaviour of pulmonary AcT: lower values of AcT were associated with higher levels of D-dimer, expression of a greater pulmonary microthrombotic burden, and a poorer prognosis, in the presence of PAPs normal. The dynamic analysis of this parameter, which is easy to calculate in the patient's bed, can play a crucial role in the instrumental follow-up of patients hospitalized for SARS-CoV-2 infection.

6.
International Journal of Pharmaceutical and Clinical Research ; 14(6):176-181, 2022.
Article in English | EMBASE | ID: covidwho-1912995

ABSTRACT

Objective: Covid-19 has impacted the health of the people and 20% of the patients were critical and hospitalized with the need for ventilation and intensive care unit (ICU) support. This study aimed to study the association of inflammatory biomarkers with severity of COVID-19 infection. Material & Method: For this study, 545 Covid-19 infected patients admitted in New Civil hospital, Bharuch were selected. The infection related to Covid-19 was confirmed using the Real-Time Reverse Transcription Polymerase Chain Reaction (RT-PCR) test. Pearson correlation was used to assess the correlation between inflammatory markers and laboratory indicators. A p-value of <0.05 was used as a cut-off value for significance. Results: The inflammatory markers and WBC count was significantly elevated in the critical COVID-19 patients. Moreover, patients with lower absolute lymphocyte count (ALC) were significantly associated with severe to critical COVID-19 infection compared to the mild to moderate form that showed higher lymphocyte count (P<0.0001). Moreover, patients with evidence of acute cardiac injury showed a significantly lower ALC (1.08±0.628× 103 cells/μL) compared to (1.38±0.72× 103 cells/μL) (P<0.0001). Conclusion: From the study, it can be concluded that there is a significant association between different inflammatory markers, clinical as well as the laboratory profile of the Covid-19 patients affecting the recovery.

7.
Italian Journal of Medicine ; 16(SUPPL 1):13, 2022.
Article in English | EMBASE | ID: covidwho-1912959

ABSTRACT

Background: COVID-19 disease is characterized by respiratory symptoms, but acute cardiovascular complications are reported in severe infections that adversely affect prognosis. Clinical Case: A patient is hospitalized for fever, chest pain, and dyspnoea. Clinical examination: pulmonary and peripheral congestion, low blood pressure values, oxygen saturation in ambient air 91%. Increased myocardiocytolysis and inflammatory indices. Nasopharyngeal swab: positive for COVID-19. Chest CT scan: interstitial pneumonia. ECG: sinus tachycardia, changes in ventricular repolarization. Echocardiogram: left ventricle dilated, hypertrophic and with severe global systolic dysfunction. Therapy: furosemide, high flow oxygen alternating CPAP, antiretrovirals, antibiotics, low molecular weight heparin, beta blocker. Cardiac MRI: focal edema of the anterior wall. Coronary angiography: moderate coronary artery disease. Control chest CT scan: resolution of pulmonary interstitial disease. Cardiac MRI after 2 months: improvement of the overall systolic function of the left ventricle. Conclusions: An entity defined as “acute myocardial damage” characterized by an increase in troponin with ECG and/or echocardiographic changes, is reported in COVID patients. These forms are not related to coronary artery disease but are the consequence of the septic state and the excessive activation of the infectious- inflammatory systems and can manifest themselves with myocarditis/stress myocardiopathy causing heart failure and left ventricular systolic dysfunction.

8.
Critical Care and Shock ; 25(3):129-134, 2022.
Article in English | EMBASE | ID: covidwho-1912935

ABSTRACT

Due to its expression by macrophages, galectin-3 is among the most recently studied biomarkers. It is likely involved in the inflammatory process that leads to remodeling and eventually fibrosis of organs such as the heart, brain, and kidneys. Coronavirus disease 19 (COVID-19) infection causes excessive inflammatory reactions in the whole body, playing a role in the development of fibrosis due to the activation of the galectin-3-macrophage-fibroblast axis. Heart failure or cardiac dysfunction occurred not only due to pro-inflammatory activation but also due to the overactivation of sympathetic nerves and failure of the respiratory system. The latter increases. the possibility of direct infection or necrosis of the heart due to the heart-lung interaction observed in our pilot study. Forty-five intensive care unit (ICU) patients were recruited consecu-tively in this study to be observed their galectin-3 and troponin I levels. This pilot study demonstrates the correlation between galectin-3 as a proinflammatory biomark-er and troponin I as a definitive biomarker for direct heart injury and highlights its potential use in COVID-19 patients. With the assessment of appropriate biomarkers such as cardiac fibro-sis markers, possible worsening of cardiac conditions in COVID-19 patients treated in the ICU can be detected in its early stages.

9.
Egyptian Journal of Chest Diseases and Tuberculosis ; 71(2):162-169, 2022.
Article in English | EMBASE | ID: covidwho-1884548

ABSTRACT

Background Medical information regarding critically ill coronavirus disease 2019 (COVID-19) patient course of disease and outcomes are fundamental to providing the best medical care and avoiding possible complications. Objective To evaluate the clinical characters, outcomes, and mortality risk factors in COVID-19 critically ill patients Patients and methods In our study, 31 adult ICU patients admitted to Sohag General Hospital and Health Insurance Hospital in Sohag Governorate were included from September 2020 to October 2020. Coronavirus was affirmed by an reverse transcriptase-PCR of a nasopharyngeal swab. Clinical information was separated from clinical sheets. Results The mean age of the patients was 60 years, 61.3% were males, 64.5% had comorbidities, which were more in improved than dead cases (P<0.04). The dead cases had a significantly longer symptom duration till ICU admission than the improved (P<0.0001). The improved cases had considerably higher oxygen saturation on admission than dead cases (P<0.02). Mechanical ventilation was indicated in eight out of 31 patients with a mean duration of 4±2.56 days and all of them died. Mortality rate was 41.9%. The dead cases needed a vasopressor therapy more than the improved (P<0.001). Acute respiratory distress syndrome was higher in the dead cases (P<0.003). Acute cardiac injury was higher in the dead cases (P<0.02). Conclusion Several predictors influence survival in COVID-19 critically ill patients including comorbidities, duration of symptoms till ICU admission, O 2 saturation on admission, development of complication, and laboratory findings including ferritin, C-reactive protein, D-dimer, and thrombocytopenia on ICU admission.

10.
Journal of Oncology Pharmacy Practice ; 28(2 SUPPL):40, 2022.
Article in English | EMBASE | ID: covidwho-1868954

ABSTRACT

Introduction: Around 1 in 10 childhood cancer survivors who receive an anthracycline develop a symptomatic cardiac event over time.1 Dexrazoxane, a free radical scavenger, has been shown to reduce surrogate markers of cardiac damage in children and young people receiving anthracycline chemotherapy.2 In February 2020, NHS England (NHSE) published a new clinical commissioning policy entitled: “Dexrazoxane for preventing cardiotoxicity in children and young people (under 25 years) receiving high-dose anthracyclines or related drugs for the treatment of cancer”.1 Given uncertainties regarding the robustness of the supporting data,1,2 a general unfamiliarity with the product and the timing of the publication of the policy (at the start of the COVID-19 pandemic) we hypothesised that these factors may all have impacted on the speed and degree of its adoption. Consequently we decided to undertake a survey of practice, with the aim of exploring awareness of the policy and use of the drug amongst UK TYA centres. Methods: A short questionnaire was designed using the www.onlinesurveys.ac.uk platform. The questionnaire was sent electronically to senior oncology/ haematology pharmacists from all 17 TYA Cancer Centres in the UK in March 2021 and was kept open for six weeks to allow centres sufficient time to respond. Responses were transferred to Microsoft Excel for data analysis. Results: Responses were received from all 17 UK TYA centres. All centres in England (n=13) were either very aware (69%) or somewhat aware (31%) of the dexrazoxane commissioning policy. The majority (three out of four) of the centres from the devolved nations were unaware of the policy. Five centres (29%) had used dexrazoxane as a cardioprotectant since February 2020 and a further five centres (29%) were considering its use. Reasons for not using the drug included: unconvinced by efficacy data (n=4), concerned re short and long-term side effects (n=3). Of those centres that had used the drug, three had only given it to 1-3 patients, one centre had given it to 7-9 patients and one centre had given it to >9 patients. None of the centres had a TYA Unit policy or guideline for the use dexrazoxane as a cardioprotectant, although two were in the process of writing one. Furthermore, although stipulated in the commissioning policy, only three out of five centres using the drug required MDT discussion prior to use. From a clinical perspective, there was a lack of consensus as to when in the treatment pathway to start the drug (i.e. with cycle one of chemotherapy or when a threshold dose had been reached). And from a practical perspective, concerns were raised about the short shelf-life of dexrazoxane and the workload implications for aseptic units. Conclusions: Despite generally good awareness of the dexrazoxane commissioning policy, use of the drug by TYA centres has been limited to date and clinical practice has not uniformly matched the recommendations contained within the policy. Further work is required to explore reasons for the slow and variable uptake and to also investigate potential differences in practice between TYA and paediatric centres.

11.
U.S. Pharm. ; 47:8-12, 2022.
Article in English | EMBASE | ID: covidwho-1865974

ABSTRACT

Patients with heart failure (HF) who contract coronavirus disease 2019 (COVID-19) are at increased risk for morbidity and mortality. Numerous pathophysiologic mechanisms exist by which COVID-19 infection inflicts cardiovascular damage. For HF patients with reduced ejection fraction (HFrEF), guideline-directed medical therapy should be maintained and optimized in the absence of contraindications. Clinicians should assess currently authorized COVID-19 treatment options prior to initiation. Pharmacists play an essential role in managing patients who have HFrEF and recommending preventive therapy, such as lifestyle modifications and vaccinations, with the goal of optimizing health outcomes during the COVID-19 pandemic.

12.
European Heart Journal Cardiovascular Imaging ; 23(SUPPL 1):i130, 2022.
Article in English | EMBASE | ID: covidwho-1795325

ABSTRACT

Background: SARS-CoV-2 infection is associated with multiple cardiac manifestations (1,2). Global longitudinal strain (GLS) by speckle tracking echocardiography (STE) is a novel transthoracic echocardiography (TTE) measure of myocardial deformation, which could early recognize subclinical cardiac injury in COVID-19 patients (3,4). Purpose: We aimed to explore GLS profiles in post-hospitalized COVID-19 patients to identify features of eventual subclinical cardiac injury and to investigate the possible correlation with the severity of infection. Methods: We enrolled 33 patients (mean age 59.2 ± 13, 64% men) with positive SARS-CoV-2 RT-PCR, hospitalized for moderate COVID-19 disease, with no admission to intensive care unit. Patients were submitted to TTE 1-2 months after discharge. Images were anonymised and analysed offline by two accredited cardiologists. Clinical parameters and laboratory findings from hospitalization were also collected. Acute myocardial infarction and pulmonary embolism were exclusion criteria. Results: Mean duration of hospitalization was 12.9 ± 8.0 days. Study population had normal systolic function with a mean LV ejection fraction 58.6% (±3.6) while the majority of patients had relative low values of LV global longitudinal strain, mean 15.2% (±2.3). Arterial hypertension was present in 51.5% of patients and a history of previous myocardial infarction was referred in 6.1% of the population. Only 24.2% of patients had elevated troponin levels during the previous in-hospital period (mean maximal value of hs-troponin was 18.1 ±16.6 pg/mL) whereas 81.8% had abnormal D-Dimers values (mean 2424 μg /L, range ±2825) and 93.1% had high hs-CRP values (138.2 ±92.0 mg/L) . Duration of hospitalization had strong significant correlation with D-Dimers (rho: 0.708, p: <0.001) and hs CRP (rho:0383, p:0.028) and marginal association with troponin ( rho: 0.335, p:0.056). Moreover, global longitudinal strain showed significant association with duration of hospitalization (rho:-0.545, p: 0.007). Traditional systolic indices as LVEF and the various diastolic parameters showed no significant association with severity of disease reflected by the duration of hospitalization and the other clinical and laboratory biomarkers. Conclusion: Cardiac manifestations of SARS-CoV-2 infections could be present in mild to moderate disease and seems to associate with the severity of infection. The novel echocardiographic parameters such as GLS could add valuable information and identify possible subclinical cardiac injury often unrecognized by traditional TTE examination.

13.
European Heart Journal, Supplement ; 23(SUPPL F):F19, 2021.
Article in English | EMBASE | ID: covidwho-1769260

ABSTRACT

Aims: Cardiac injury is common in novel coronavirus disease-2019 (COVID-19) patients and is associated with an increased risk of mortality. However, the prognostic accuracy of cardiac biomarkers in predicting mortality in COVID-19 patients remains unclear. A meta-analysis of diagnostic test accuracy was conducted to find cost-effective biomarkers, particularly those frequently evaluated to enable risk stratification and sensible resource allocation. Methods: We systematically searched PubMed, Europe PMC, and SCOPUS for studies published up to June 2021. Studies were enrolled, if they included assessment of the accuracy of predetermined cardiac biomarkers (troponin, lactate dehydrogenase (LDH), creatine kinase, and N-terminal pro-brain natriuretic peptide (NT-proBNP)) in predicting mortality of COVID-19 patients and provided sufficient data to construct a 2 x 2 contingency table. Results: This meta-analysis showed cardiac troponin was the most reliable biomarker in prognosticating mortality in COVID-19 patients (area under curve (AUC) = 0.79 (0.76-0.83), sensitivity = 0.63 (0.52-0.73), specificity = 0.80 (0.74-0.84)), followed by LDH (AUC = 0.75 (0.71-0.78), sensitivity = 0.72 (0.63-0.80), specificity = 0.65 (0.54-0.75)), NT-proBNP (AUC = 0.73 (0.69-0.77), sensitivity = 0.55 (0.41-0.68), specificity = 0.79 (0.68-0.87)), and creatine kinase (AUC = 0.35 (0.31-0.39), sensitivity = 0.27 (0.19-0.36), specificity = 0.76 (0.49-0.92)). Conclusion: Increased cardiac injury biomarkers may aid in the identification of individuals who are most at risk, especially cardiac troponin with AUC 0.79, 63% sensitivity and 80% specificity.

14.
Indian Journal of Clinical Biochemistry ; 36(SUPPL 1):S3-S4, 2021.
Article in English | EMBASE | ID: covidwho-1767673

ABSTRACT

However, it is this very set of tests that have come Hin question. First, what is the normal and acceptable range (upper & lower limits) of different Clinical Chemistry and Immunoassay biomarkers in a particular population has been debated in different scientific fora. This is because the level of markers can change in relation to other biochemicals, biomolecules and hormones, which themselves vary considerably with race, gender, age, different physiological conditions (like pregnancy, new-born) and other illnesses & interfering substances. The variation can be to an extent that each individual can seem to have their own set-point of these parameters. A second problem which the diagnosticians have to grapple with is the variability of test-results in itself;even a broadly similar set of instruments and methods can provide variable results. It is then a real challenge to physicians, to decide whether the patient is suffering from a disease or not, since other factors can also cause changes in test levels. Standardization and harmonization of clinical chemistry and immunoassay testingis therefore still a formidable challenge, due to the lack of proper reference intervals and sometimes due to standardized measurement procedures. Laboratory medicine community the world over has realized that, variability in test results in different platforms can create a lot of confusion to clinicians and the general population;harmonization of procedures is therefore the need of the hour. In this talk, I will provide few examples and technical solutions to address laboratory challenges and to take it forward from both Clinical Chemistry as well as Immunoassay platforms. To begin with, harmonization and standardization of TSH and other thyroid function tests are still a formidable challenge, due to the lack of proper reference intervals and standardized measurement procedures. It has been documented that even a broadly similar set of instruments and methods can give up to 40% more or less values in TSH levels. Based on a particular population's demographic variations, reference interval can be different for immunoassay like TSH. Therefore, we have verified the reference interval for the Indian population for TSH in our laboratory. We have screened 800 subjects, of which 630 healthy subjects were chosen in the study group for reference interval verification. The reference interval (90% Confidence interval) for TSH by non-parametric procedure (bootstrap) was 0.48- 4.52, and by parametric one (after transformation of the data) was 0.45-4.27 for the adult population, which is little different from the manufacturer's guidelines. Similarly, we have conducted a study of 2797 female patients and 2805 male patients in a six month period and have observed that, women have a greater risk of being 14% under-diagnosed of acute coronary syndrome, if we donot use gender specific cut off (Male: 32.3 pg/ml and Female: 14.6pg/ml for the Indian population), with high th sensitive troponin I assay near the 99 percentile of a reference control population. Therefore, implementation of sex-specific hs-cTnI assay was able to identify 14% of under-diagnosed women with ACS in 6 months period. This in turn also decreased the number of men being diagnosed by 3%. On a similar note, there has been a continuous challenge in the health care system in U.S, Europe and other countries to standardize and harmonize the HbA1c reporting: the decision on what to report in NGSP (%) and/or IFCC (mmol/mol) units along with eAG (in either mmol/L or mg/dL). This globalization places a responsibility on laboratory medicine specialists to work together to reduce the current variability in patient results, which arises from differences between units, methods and laboratory practices in different countries. Due to the standardization efforts of IFCC, NGSP, and also due to ongoing efforts of manufacturers and laboratories, the quality of HbA1c reporting has increased dramatically. Consequently, there has been a paradigm shift: HbA1c is now considered the gold standard, not only for monitoring, but also for diagnosis of diabetes. We have performed verification studies of HbA1c by different methods: HPLC, Capillary Electrophoresis, Enzymatic, Immunoassays in 200 samples and compared 60 samples with hemoglobinopathies. Finally, we have also explored harmonizing the clinical protocol based on the use of inflammatory and routine laboratory biomarkers in 2,654 COVID-19 patients. To explain the role of harmonizing routine laboratory parameters in disease monitoring, two adult males, two adult females and one adolescent girl were selected. These are representative examples of different manifestations of COVID 19, with Adult Respiratory Distress Syndrome (ARDS), Cardiac Injury, Neurological manifestations and Pediatric Multi system inflammatory syndrome (PIMS), admitted in the Intensive care unit (ICU) of the hospital, which will be discussed. Therefore, the road map for laboratory medicine will involve strategies for harmonizing, communicating and integrating with all stakeholders, like, clinicians, diagnosticians and IVD industry, in order to formulate guidelines for assisting in correct measurement, diagnosis and management of diseases.

15.
Open Forum Infectious Diseases ; 8(SUPPL 1):S331, 2021.
Article in English | EMBASE | ID: covidwho-1746539

ABSTRACT

Background. Up until this day, over 3.5 million fatalities related to coronavirus disease 2019 (COVID-19) have been registered worldwide by the World Health Organization. Healthcare professionals require prognostic tools for COVID-19 patients in order to guide treatment strategies. Elevated troponin levels, a biomarker of cardiac injury, have been detected among patients with COVID-19, hence associating it with cardiac injury. Although several studies have mentioned it, the role of troponin as a prognosis biomarker is unclear. Elevation in troponin levels has been observed in patients with community-acquired pneumonia (CAP). However, its association with mortality is scarcely mentioned in literature. Thus, we sought to determine the utility of serum troponin I levels as a mortality predictor for patients with COVID-19 and CAP. Methods. A prospective observational study was carried out at Clinica Universidad de La Sabana, Colombia, with patients hospitalized due to CAP and COVID-19. Troponin biomarker was quantified in serum samples using the PATHFAST system within the first 24 hours of hospital admission. Serum concentrations of troponin were compared among study groups. To assess the biomarkeŕs capacity to predict mortality, ROC curves were used, quantifying their differences through the DeLonǵs test. Results. A total of 88 patients with CAP and 152 with COVID-19 were included in the study. In all cohort the median [IQR] serum concentration of troponin (ng/ml) was higher in those who died (34.2, [9.74-384] vs 5.89, [2.44-27.9] p< 0.001). Furthermore, troponin was higher in deceased patients with COVID-19 vs those who survived (77.35 [11.9-346.5] vs. 4.88 [2.10-13.02], p< 0.001). However, there was no significant difference between CAP deceased and not deceased patients (18.1 [8.52-398] vs 15.7 [3.75-62.8], p=0.16). Although sample size might be a limitation when analyzing these results, the AUC ROC of troponin I to predict mortality was 0.799 for COVID-19 and 0.615 for CAP, the DeLongs test for compared ROC curves was a p= 0.0351. A. Serum troponin I and mortality due to lower respiratory tract infections B. Serum troponin I to predict mortality in patients with lower tract infections C. ROC curve for serum troponin I to predict risk of mortality Conclusion. Overall, troponin levels were higher among deceased patients. Our findings suggest that high troponin levels are a mortality predictor for patients with COVID-19.

16.
Journal of the Hong Kong College of Cardiology ; 28(2):72, 2020.
Article in English | EMBASE | ID: covidwho-1743557

ABSTRACT

Regarding the most critical health threat in 21st century, caused by the coronavirus, identifying its controlling methods and treatments is the first priority of the medical society. Up-to-date methods are required for identifying and controlling coronavirus, due to its raising pervalence and mutations. In this presentation, we discuss cardiac, pulmonary, and musculoskeletal side effects of coronavirus. While COVID-19 may affect multiple organ systems, symptoms are most often located in the respiratory tract. Approximately 80% of symptomatic patients present with mild disease: symptoms of fever, runny nose, sore throat or dry cough. Moderate to severe disease is characterized by pneumonia. Underlying CVD and/or development of acute cardiac injury are associated with significantly worse outcome in these patient, Information about other cardiovascular manifestations is very limited at patients with coronavirus disease 2019 (COVID-19) have underlying cardiovascular (CV) disease or develop acute cardiac injury during the course of the illness. Adequate understanding of the interplay between COVID-19 and CV disease is required for optimum management of these patients. COVID-19 is primarily a respiratory illness but cardiovascular involvement can occur through several mechanism Acute cardiac injury is the most reported cardiovascular abnormality in COVID-19, with average incidence 8-12%. Recently research about musculoskeletal disorders in COVID-19 represent, COVID-19 that has an affinity for neural tissue. There are reports of encephalitis, encephalopathy, cranial neuropathy, Guillain-Barrè syndrome, and myositis/rhabdomyolysis in patients with COVID-19. Moreover, Rehabilitation methods, especially exercise therapy, are discussed as supporting treatments for COVID-19. Considering cardiac side effects, like Myocarditis, and other pulmonary side effects, especially pneumonia, as well as identifying musculoskeletal side effects of COVID-19, including Neuropathy, have great importance. Furthermore, secondary side effects, caused by this disease due to deconditioning;results in a decrease in cardiac, respirational, and mobility performance of the patients after an acute period;however, by using an exact, scientific rehabilitation program, the recovery process can become shorter, and the patients can return to their normal lives cycles in a quicker way.

17.
Journal of Investigative Medicine ; 70(2):473, 2022.
Article in English | EMBASE | ID: covidwho-1699844

ABSTRACT

Case Report Multisystem inflammatory syndrome (MIS-C) involves severe multi-organ inflammatory injury 2-6 weeks after COVID-19 infection. Seventy to 85% of patients have cardiovascular involvement, including diminished left ventricular ejection fraction (EF), coronary aneurysm, arrhythmias, valvular dysfunction, and pericardial effusion. Here we present a patient who arrived to the pediatric emergency department (ED) with MIS-C and suspected cardiogenic shock, though without the echocardiogram abnormalities commonly associated with MIS-C. A 7 year old African American male presented for a third time to our ED over the course of 4 days of febrile illness and was found to have MIS-C. During this time, he had no chest pain, palpitations, shortness of breath, or abnormal cardiopulmonary exam. At the first 2 ED visits, he was generally well appearing and after treating fever, had vital signs normal for his age. At his third visit, his vital signs were notable for borderline hypotension 86/48 (threshold 83/39 for his height of 1.25 meters). Troponins, chest X-ray, and EKG were normal. Bedside ultrasound was normal, with EF 55-60% so the hypotension was presumed to be secondary to hypovolemia and sepsis. However, despite 40 mL/kg of fluid boluses and maintenance fluid x1.5, his blood pressure continued to downtrend to a nadir of 79/39. He soon developed an S3 gallop and facial edema indicating fluid overload. His proBNP 4986 pg/mL also resulted at this time, suggesting cardiac injury was present. A formal cardiology echocardiogram confirmed the bedside ultrasound findings, noting normal ventricular size and motion, trivial pericardial effusion, and normal coronary artery size. However, it also detected diastolic dysfunction evident in mildly elevated E/e' of 10.86 of lateral mitral annulus, and 12.7 at medial mitral annulus. Three hours after starting solumedrol for treatment of MIS-C, his blood pressure improved to 110/52. The patient had no further episodes of hypotension, though it is unclear if steroids had resolved this by alleviating the underlying inflammation or as a secondary effect. We present a case of MIS-C that led to diastolic heart failure detected by mild hypotension, elevated proBNP, and subtle findings on formal echocardiogram. Although less common than systolic dysfunction in MIS-C, early recognition of diastolic heart failure is important for effective fluid management and initiation of vasoactive agents in criticallly 'ill patients. Diastolic heart failure with preserved systolic function has been seen on echo of MIS-C patients, and is hypothesized to be the subacute period after recovery of systolic function. However, we did not find clinical symptoms of systolic heart failure prior to the patient's development of diastolic heart failure. It is therefore essential to recognize that a patient with MIS-C may present with diastolic heart failure without preceding symptoms or echo findings of other cardiac anomalies.

18.
Circulation ; 144(SUPPL 1), 2021.
Article in English | EMBASE | ID: covidwho-1636999

ABSTRACT

Introduction: As defined by MB-CPK, hsTn-I, MB, or EKG and/or cardiac echo abnormalities, cardiac injury (CI) determines a median survival time (MST) of 10 days for hospitalized COVID patients (HCPs). HCPs without defined CI have an MST beyond 39 days (Huang, et al., see Figure). Hypertension (HTN) presents in 17-41% of HCPs in various studies, with COVID mortality independent of HTN. Therefore, a randomized clinical trial (RCT) is proposed for HCPs with CI and incidental BP elevation to compare IV isosorbide dinitrate (ISDN) with usual anti-HTN care (UC). Vasodilatory ISDN lowers BP, and has been proposed an an anti-SARS-CoV-2 drug. Others report improved survival of ISDN treated Coxsackie B3 virus-infected mice as evidence for anti-viral activity. The endpoint for this CI RCT pilot of 100 ISDN-treat HCPs and 100 UC controls is mortality. Secondary endpoints are interval biomarkers to dissect ISDN anti-viral action. Methods: Log-rank analysis was performed with 1:1 allocation. Accrual time was 180 days with a 60-day follow-up. Power was 0.8 with a type I error of 0.05. Results: For 200 total subjects, an MST greater than 14.9 days in the ISDN arm was significant if UC stays at 10 days (see Figure). Conclusions: Testing repurposed ISDN as a COVID drug is feasible. A successful pilot with improved MST suggests ISDN has anti-SARS-CoV-2 action, since COVID mortality is independent of HTN. Biomarkers could include viral clearance, oxygenation, D-dimer, IL-6, LDH, as well as platelet and lymphocyte counts. The need to treat HCPs with elevated BP per guidelines permits study entry. Cross-over treatment occurs if a regimen fails. Immunomodulators and remdesivir are administered per COVID treatment guidelines for all HCPs. IV ISDN, bolused and/or infused, avoids 1 pass hepatic effects. IV IDSN is approved in most countries, but not in the USA or Canada. A successful pilot would permit larger IV ISDN RCTs as IND RCTs, and can serve as a template for other treatments for HCPs with defined CI.

19.
Circulation ; 144(SUPPL 1), 2021.
Article in English | EMBASE | ID: covidwho-1635643

ABSTRACT

Introduction: Cardiac injury occurs in about 20-30% of patients hospitalized for COVID-19 and influence the prognosis but many aspects like the role of age and magnitude of cardiac damage in determining the prognosis, remains vague. Hypothesis: Age and magnitude of cardiac damage may influence the mortality of patients hospitalized for COVID-19. Methods: We considered all patients consecutively admitted at a third-level European Hospital for COVID-19 between February and June 2020. Cardiac injury was defined as a high-sensitivity cardiac Troponin I (hs-cTnI) value greater than the upper reference limit (URL) of 47 ng/dL. Firstly, we analyzed the data by hs-cTnI across age tertiles (<62 years, 62-73 years and >73 years). Then, we compared patients with no-damage, mid-damage (hs-cTnI up to 10-fold URL) and high-damage (more than 10-fold URL). The primary endpoint was in-hospital mortality. Results: We enrolled 543 patients (median age 69, 67% males);hs-cTnI was available in 509. The survival was lower in elderly patients and high levels of hs-cTnI worsened the prognosis across all age tertiles (Fig. 1A). Surprisingly, the magnitude of cardiac damage did not influence the overall in-hospital mortality (Fig. 1B), but patients with high-damage died earlier (survival at 15 days: 86% nodamage vs 61% mid-damage vs 49% high-damage;p<0.001). Of note, among patients with highdamage, only 7 received coronary angiography, cardiac magnetic resonance or heart biopsy. Conclusions: Cardiac injury dramatically increased the mortality across all ages in patients hospitalized for COVID-19. The magnitude of cardiac damage did not influence overall in-hospital mortality but almost all patients with high-damage died within 15 days from admission. A secondlevel diagnostic test was performed seldomly in high-damage patients, suggesting that the unexpected high burden of the first COVID-19 wave negatively influenced the health system and our clinical daily practice.

20.
Circulation ; 144(SUPPL 1), 2021.
Article in English | EMBASE | ID: covidwho-1634063

ABSTRACT

Introduction: The global pandemic of the coronavirus 2019 disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to respiratory failures, COVID-19 patients exhibited cardiac complications. Studies observed the direct infection and replication of SARS-CoV2 in human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) accompanied by cytopathic effects. However, the underlying mechanisms of SARS-CoV-2-mediated CM death remain poorly understood. In addition, the therapeutic potential of remdesivir (RDV) on CMs has yet to be answered. Methods and Results: We confirmed that SARS-CoV-2 is infectious to and effectively replicates in hPSC-CMs and is cytopathic to hPSC-CMs. We also found that RDV effectively inhibited viral replication at a concentration of 50 nM. RNA-seq analyses demonstrated that expression of immune responsive genes was elevated in SARS-CoV-2 infected hPSC-CMs. Immunostaining and an ELISA assay further revealed formation of inflammasomes and secretion of inflammasome-mediated cytokines, such as IL-1β, IL-18, and IL-6 in SARS-CoV-2 infected hPSC-CMs. RNA-seq analyses showed gene profile changes in SARS-CoV-2 infected hPSC-CMs corroborating with activation of inflammatory signals and cell death pathways. While gene profiles of 0.1 μM RDV-treated SARS-CoV-2-infected hPSC-CMs showed reversal of such changes, a high dose (10 μM) RDV-treated CoV-2-infected hPSC-CMs showed changes in 44% of genes expressed compared to non-RDVtreated CoV2-infected hPSC-CMs. Among those, expression of protein stability related genes, such as genes associated with autophagy and protein ubiquitination increased while expression of antiviral responsive genes decreased. In addition, a high dose of RDV inhibited expression of mitochondrial genes, particularly MitoComplex I and V compositions, which are related to energy production. Conclusions: This study demonstrates that SARS-CoV2 induced inflammasome in hPSC-CMs, which can underlie cardiac damage in addition to direct cytopathic effects. In addition, RDV can reduce inflammasome when introduced early after SARS-CoV2 infection while a high-dose can aggravate cytopathic effects by potential toxicity to mitochondria.

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