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Background: The 2019 novel coronavirus disease (COVID-19) has been reported as pandemy and the number of patients continues to rise. Based on recent data, cardiac injury is a prominent feature of the disease, leading to increased morbidity and mortality. In the present study we aimed to evaluate myocardial dysfunction using transthoracic echocardiography (TTE) and tissue Doppler imaging (TDI) in hospitalized COVID-19 patients. Methods and Results: We recruited 30 patients (56.7% male, 55.80 +/- 14.949 years) who were hospitalized with the diagnosis COVID-19 infection. We analyzed left ventricular (LV) and right ventricular (RV) conventional and TDI parameters at the time of hospitalization and during the course of the disease. Patients without any cardiac disease and with preserved LV ejection fraction (EF) were included. TTE examination was performed and all the variables were recorded and analyzed retrospectively. We observed that both LV and RV conventional echocardiographic parameters were similar when the day of admission to the hospital was compared to the 5th day of the disease. Regarding TDI analysis, we demonstrated significant impairment in LV septal and lateral deformation (P < 0.001). In the correlation analysis no marked correlation was observed between impairment in LV deformation and inflammation biomarkers. Conclusion(s): Cardiac involvement is an important feature of the COVID-19 infection but the exact mechanism is still undefined. Echocardiography is an essential technique to describe myocardial injury and provide new concepts for the possible definitions of cardiac dysfunction.Copyright © 2023 The Author(s).
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Introduction: Lactate is a common biomarker used in multiple surgical subspecialties. No one has previously measured coronary sinus lactate reduction as a result of drug administration. We therefore tested the hypothesis that IV geranylgeranylacetone (GGA), a novel agent used to treat human peptic ulcer disease, would result in reduced coronary sinus lactate production. Method(s): New Zealand adult rabbits (N=5 each) received IV 50 mg/kg GGA 24 hours before intervention, which consisted of Langendorff perfusion, 30 min of global normothermic cardioplegic arrest, followed by reperfusion. Myocardial release of lactate was measured. HSP70 was quantified by western blot. Differences between GGA+ and GGA- groups pre- and post-ischemia were analyzed by unpaired t-tests. Result(s): In the GGA- group, lactate increased immediately at one minute and throughout the duration of reperfusion. However, in GGA+ hearts, lactate also increased at one min of reperfusion but then continued to decrease throughout the remainder of reperfusion. Lactate was significantly less at every time point of reperfusion in GGA+. Integrated lactate area was significantly less throughout reperfusion in GGA+. Conclusion(s): GGA induced caused a marked decrease in coronary sinus lactate release during reperfusion. Simultaneously intravenously GGA induced myocardial HSP70i and reduced myocardial damage. Further study of the effects and mechanisms involved is indicated. Application to other organs is useful as well. Heat shock proteins (HSPS) are also antithrombotic. Given the thrombotic nature of Covid, induction of HSPS may be beneficial in decreasing the cardiac thoracic and vascular complications of Covid and allowing faster resolution of this disease during to vascular complications.
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High-sensitivity cardiac troponins expedite the evaluation of patients with chest pain in the emergency department. The utility of troponins extends beyond the acute coronary syndromes to accurate the diagnosis of myocardial injury. Troponins are best friends for physicians;however, they are a double-edged sword if not interpreted appropriately. Misdiagnosis is harmful with regard to patient outcomes. The present review focuses on the recent updates in the understanding and interpretation of high-sensitivity troponins in various acute clinical settings. Common mistakes and gray zones in the interpretation of troponins, the concept of myocardial injury versus infarction, newer entities like myocardial infarction (MI) with Nonobstructive Coronary Arteries, recent controversies over the definition of periprocedural MI, complementary role of imaging in the diagnosis of myocardial injury and the role of troponins in the current COVID-19 pandemic are discussed.Copyright © 2022 Saudi Center for Organ Transplantation.
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The most common clinical manifestation of new coronavirus infection is bilateral pneumonia. At the same time, COVID-19 has a wide range of cardiovascular complications, with the development of acute heart failure, arrhythmias, acute coronary syndrome, and myocarditis. Myocardial injury is relatively common in COVID-19, accounting 7-23 % of cases. The presented clinical case describes a 56-year-old patient with a confirmed coronavirus infection. The peculiarity of this clinical case is that it is the first report on COVID-19 with systemic manifestations: lungs, heart, kidneys and skin lesions. It should be noted that despite viral pneumonia typical for COVID-19, clinical picture and severity of the patient's condition were determined by the developed myocardial injury. The presented clinical case is specific due to skin lesions.Copyright © 2021, Krasnoyarsk State Medical University. All rights reserved.
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The proceedings contain 385 papers. The topics discussed include: racial and ethnic differences in the population burden of dementia attributable to modifiable risk factors in the United States;higher visit-to-visit variability in fasting glucose and HbA1c is associated with decline in global cognitive performance: the Multi-Ethnic Study of Atherosclerosis (MESA);prevalence of stroke symptoms among Hispanic/Latino adults in the Hispanic community health study/study of Latinos (HCHS/SOL);educational attainment and dementia risk: mediation by vascular risk factors at mid-life in the atherosclerosis risk in communities (ARIC) study;a healthy plant-based diet was associated with slower cognitive decline in African Americans: a biracial community-based cohort of older adults;outcome preferences related to cardiovascular preventive therapies in older adults: an online survey;subclinical myocardial injury, coagulopathy, and inflammation in Covid-19: a meta-analysis;COVID-19 and type II NSTEMI: a comprehensive overview;association of antecedent statin use with outcomes of people with Covid-19 admitted at northwestern medicine health system;and social determinants of health and ambulatory outcomes among Covid-19 positive patients: differences by race/ethnicity.
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Background: Multisystem inflammatory syndrome in children (MIS-C), associated with coronavirus disease 2019 (COVID-19) is a rare but serious condition, affecting children mostly after acute SARS CoV2 infection. MISC presents with fever, laboratory evidence of inflammation, and multiorgan dysfunction, including heart. Purpose(s): We analized the degree of cardiac involvement and clinical outcomes of MIS-C patients hospitalized in Pediatric department of Cantonal hospital Zenica, to compare with previously reported findings. Method(s): Cardiac testing results in pediatric patients hospitalized with MIS-C from November 2020. until March 2022. were retrospectively analized. For this study, MIS-C patients with positive cardiac testing were defined as having an abnormality of one or more of the following on admission: Cardiac biomarkers, electrocardiogram, and/or echocardiogram. Result(s): Cardiac abnormal findings were present in almost all of our ten patients with MIS-C, but the extent of cardial injury was lower than we expected it to be. Abnormal EKG was found in 80% patients with the most common electrocardiography findings: Low voltage (50%) and T wave abnormality (70%). Echocardiography abnormalities were present in 80% patients mostly including valvular regurgitation (mitral, pulmonal), and rarely pericardial effusion or left ventricular diastolic disfunction (20%). Elevated cardiac biomarkers were seen in 70% patients. By the time of hospital discharge or short time follow-up all cardiological findings were diminished. Six months follow-up found no cardiac sequellae and 24h electrocardiogram with heart rate variability parametres found no disturbancies outside physiological or underlying chronic disease. Conclusion(s): While most patients in our study had evidence of abnormal cardiac testing on hospital admission, all cardiac findings were normal by hospital discharge. Cardiologic findings were representative for subacute myocardial injury with good clinical outcome and no sequellae. The degree of cardiac involvement was mild compared with previous reports.
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Background: Coronavirus disease 2019 (COVID-19) has been associated with significant morbidity and mortality, with cardiovascular involvement being usual. Elevations in cardiac Troponin-I level has proposed as an independent biomarker for mortality among patients with COVID-19. Aim(s): To evaluate the role of high sensivity Troponin-I (hs-TnI) level at hospital admission in predicting 30 day in-hospital mortality and 6-month mortality in patients hospitalized with a COVID-19 diagnosis. Method(s): We performed a retrospective single-center cohort study including consecutive patients aged 18 years and older who were admitted for COVID-19, during a 1-year period (n=818). We excluded patients with acute coronary syndrome (n=23), patients with acute heart failure (n=42), and patients in which hs-TnI level was not dosed at admission (n=163). Patients were divided into two groups according to hs-TnI levels: Hs-TnI <19.8 vs hs-TnI >=19.8 pg/mL. Primary outcomes were 30-day in-hospital mortality and 6-months mortality. According to the data distribution, appropriate statistical tests were conducted to compare independent samples. Multivariable logistic regression was used to analyze mortality risk. Receiver operator characteristics (ROC) curve and area under the curve (AUC) were obtained to determine the discriminative power of hs-TnI as a predictor of mortality. (Figure 1). Result(s): This cohort included 590 patients. Mean age was 71 >=+/-15 years and 52.4% were men. Overall, 209 patients (35.4%) had elevated hs- TnI levels and 381 patients had normal hs-TnI levels. Individuals in the hs-TnI >=19.8 pg/mL group were older (80+/-11 vs 66+/-14 years, p<0.001) and presented higher prevalence of chronic heart failure (24.9% vs 7.1%, p<0.001), hypertension (77.0% vs 57.5%, p<0.001), atrial fibrillation/flutter (19.1% vs 5.5%, p<0.001), prior stroke (12.4% vs 5.2%, p=0.001) and ischemic heart disease (12.4% vs 3.7%, p<0.001). There was no difference in length of hospital stay between the groups (8.0 [IQR 9.6] in hs-TnI 19.8 pg/mL group vs 9.0 [IQR 8.0] normal hs-TnI group, p=0.669). Troponin-I was the only independent predictor of in-hospital mortality (OR 3.80, CI 95%: 2.44-5.93, p<0.001), see Table 1. The troponin levels had the highest area under the receiver operating characteristic curv (AUC) with an AUC of 0.705 (95% CI: 0.667-0.742, p<0.001) for association with the inhospital mortality (figure 1). There was no difference in 6-months mortality between the two groups. Conclusion(s): Acute myocardial injury is common in patients hospitalized with COVID-19. In the present study a TnI level >=19.8 pg/mL was predictor of 30 days in-hospital mortality, suggesting that raised levels of this biomarker is associated with adverse prognosis. This tool might be useful for COVID-19 patient risk stratification. Further studies are needed to provide robust data and reliable recommendations on this theme.
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Background: Myocarditis after SARS-CoV2 infection or vaccination is rare, but seems to be relatively more frequent in young population. Cardiac magnetic resonance (CMR) T2 weighted sequences have the potential to detect subclinical myocarditis. However, there is paucity of data on the potential myocardial involvement after SARS-CoV2 infection or vaccination in asymptomatic adolescents. Purpose(s): To evaluate the presence of subclinical myocardial damage in adolescents who were infected with SARS-CoV2 or vaccinated against SARS-CoV2 using non-contrast CMR imaging. Method(s): Asymptomatic adolescents enrolled in the Early ImaginG Markers of unhealthy lifestyles in Adolescents (EnIGMA) project were scanned using a 3-Tesla CMR scanner between March 2021 and October 2021. CMR scans included CINE imaging and myocardial T2-mapping sequences. SARS-CoV2 IgG antibody testing was performed in capillary blood samples, and date of confirmed SARS-CoV2 infection and/or vaccination if any was collected. Participants were assigned to three different groups according to SARS-CoV2 status: Group 1 (non-infected and nonvaccinated), Group 2 (infected and non-vaccinated), and Group 3 (vaccinated, independently of past infection status). CMR images were analyzed by experienced observers blinded to adolescent's SARS-CoV2 status. ANOVA and multiple regression analysis, together with correlation coefficients, were used to study between-group differences and associations among variables of interest. Result(s): A total of 115 adolescents with a mean age of 16.0 years (standard deviation (SD)=0.4), 54% girls, completed the CMR study and SARSCoV2 data successfully, and were assigned to Group 1 (n=72), Group 2 (n=22), and Group 3 (n=21). Left and right ventricular ejection fraction (LVEF/RVEF) did not significantly differ among groups: Mean LVEF was 62.8% (SD=4.1), 63.0% (SD=3.7) and 60.9% (SD=3.9) [p=0.12] and mean RVEF was 56.5% (SD=4.2), 56.5% (SD=5.5) and 54.5% (SD=5.1) [p=0.23] in Groups 1, 2 and 3, respectively. Similarly, there were no between-group significant differences in myocardial T2 relaxation values: Mean T2 values were 44.1 ms (SD=2.2), 44.1 ms (SD=1.8) and 44.4 ms (SD=1.9) in Groups 1, 2, and 3, respectively (p=0.63) (Figure 1). No differences were found either after adjusting for age and gender. Median time (interquartile range) from date of infection or vaccination to CMR acquisition was 133 (121) days and 28 (38) days in Group 2 and Group 3, respectively. No correlation between time from infection/vaccination to CMR acquisition and T2 values was detected (Figure 2). Conclusion(s): This observational study did not find evidence of subclinical myocardial involvement after SARS-CoV2 infection or vaccination in asymptomatic adolescents, as assessed with T2-mapping magnetic resonance imaging.
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Background: Advances in computational methodologies have enabled processing of large datasets originating from imaging studies. However, most imaging biomarkers suffer from a lack of direct links with underlying biology, as they are only observationally correlated with pathophysiology. Purpose(s): To develop and validate a novel AI-assisted image analysis platform, by applying quantitative radiotranscriptomics that quantifies cytokinedriven vascular inflammation from routine CT angiograms (CTA) performed as part of clinical care in COVID-19. Method(s): We used this platform to train the radiotranscriptomic signature C19-RS, derived from the perivascular space around the aorta and the internal mammary artery in routine chest CTAs, to best describe cytokinedriven vascular inflammation, defined using transcriptomic profiles from RNA sequencing data from human arterial biopsies (A). This signature was validated externally in 358 clinically indicated CT pulmonary angiograms from patients with or without COVID-19 from 3 different geographical regions. Result(s): First, 22 patients who had a CTA before the pandemic underwent repeat CTA <6 months post COVID-19 infection (B). Compared with 22 controls (matched for age, gender, and BMI) C19-RS was increased only in the COVID-19 group (C). Next, C19-RS was calculated in a cohort of 331 patients hospitalised during the pandemic, and was higher in COVID-19 positives (adjusted OR=2.97 [95% CI: 1.43-6.27], p=0.004, D). C19-RS had prognostic value for in-hospital mortality in COVID-19, with HR=3.31 ([95% CI: 1.49-7.33], p=0.003) and 2.58 ([95% CI: 1.10-6.05], p=0.028) in two testing cohorts respectively (E, F), adjusted for clinical factors and biochemical biomarkers of inflammation and myocardial injury. The corrected HR for in-hospital mortality was 8.24 [95% CI: 2.16-31.36], p=0.002 for those who received no treatment with dexamethasone, but only 2.27 [95% CI: 0.69-7.55], p=0.18 in those who received dexamethasone subsequently to the C19-RS based image analysis, suggesting that vascular inflammation may have been a therapeutic target of dexamethasone in COVID-19. Finally, C19-RS was strongly associated (r=0.61, p=0.0003) with a whole blood transcriptional module representing dysregulation of coagulation and platelet aggregation pathways. Conclusion(s): We present the first proof of concept study that combines transcriptomics with radiomics to provide a platform for the development of machine learning derived radiotranscriptomics analysis of routine clinical CT scans for the development of non-invasive imaging biomarkers. Application in COVID-19 produced C19-RS, a marker of cytokine-driven inflammation driving systemic activation of coagulation, that predicts inhospital mortality and identifies people who will have better response to anti-inflammatory treatments, allowing targeted therapy. This AI-assisted image analysis platform may have applications across a wide range of vascular diseases, from infections to autoimmune diseases.
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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. Method(s): 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. 113 patients (63.5%) were treated with dexamethasone for a median duration of 10 days (IQR 9-10). 65 patients (36.5%) constituted the nondexamethasone control group. Result(s): 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. 6.14mg/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(s): In severe COVID-19, antiinflammatory 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. (Figure Presented).
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Introduction: COVID-19 infection has been associated with acute myocardial dysfunction. However, long-term effects of myocardial injury during COVID-19 infection are not well characterized. Novel speckle tracking echocardiography (STE) may lend further insights into COVID-19 myocardial dysfunction. Method(s): Patients hospitalized with acute COVID-19 infection from March 2020 to September 2021 who underwent STE and had evidence of myocardial dysfunction (defined as left ventricular ejection fraction (LVEF) less than 55% and/or global longitudinal strain (GLS) less negative than -18%) were enrolled in follow-up 3-12 months after hospitalization. Clinical and laboratory data were collected, and follow-up STE was performed, including LVEF, GLS, myocardial work index (MWI) and myocardial work efficiency (MWE) measurements. Statistical analysis was performed to determine risk factors for worsening myocardial dysfunction at follow-up. Result(s): Twenty-four patients were enrolled at an average 239+/-102 days after the initial hospitalization echocardiogram: 13 (54%) male, 14 (58%) Black, and average age 56+/-14 years. Average duration of initial admission was 24+/-25 days;14 patients (58%) were admitted to the intensive care unit. Ten (42%) patients had acute respiratory distress syndrome, 1 (4%) had ST-elevation myocardial infarction and 1 (4%) had cardiac arrest. Eleven (46%) patients required mechanical ventilation and 2 (8%) required extracorporeal membrane oxygenation. Five (21%) patients had elevated troponin on admission and average peak troponin was 1.35+/-3.83 ng/ml. Follow-up STE showed significant improvement in average GLS (-13.7+/-3.2% vs -16.0+/-3.7%, P=0.03). There were no significant changes in average LVEF (55.9+/-12.6% vs 55.5+/-8.8%, P=0.90), MWI (1519+/-425 vs 1681+/-412, P=0.24) and MWE (93+/-4 vs 92+/-4, P=0.65) at follow-up compared to during COVID-19 infection. Patients with lower LVEF at follow-up as compared to acute infection (n=11, 46%) were more likely to have had longer duration of symptoms prior to initial presentation (11+/-5 days vs 6+/-5 days, P=0.02) and higher peak erythrocyte sedimentation rate (94+/-30 mm/h vs 44+/-36 mm/h, P=0.007) compared to those with stable or improved LVEF. Conclusion(s): Approximately 8 months after COVID-19 infection, average GLS was significantly improved in patients with myocardial dysfunction during acute COVID-19 infection. Close follow-up is recommended for patients with evidence of myocardial injury during COVID-19 infection, especially those who present with prolonged symptoms and those with high inflammatory markers.Copyright © 2022
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Introduction: Cardiac sarcoidosis (CS) classically manifests as a restrictive cardiomyopathy or conduction abnormalities, though the full scope of phenotypes may be underrecognized. We present an atypical case of mitral regurgitation (MR) and aortic regurgitation (AR) attributed to CS. Case Presentation: A 33-year-old woman with a history of hypertension, tobacco use, and COVID-19 infection two months prior presented with worsening dyspnea on exertion, orthopnea and lower extremity edema. Initial work up revealed elevated pro-BNP and troponin, and a CXR with pulmonary edema. A prior CTA showed mediastinal and hilar lymphadenopathy. Echocardiogram was notable for mildly dilated LV, severe hypokinesis of the basal inferior myocardium, LVEF 50-55%, moderate MR and moderate AR. cMR revealed multiple foci of predominantly mid-wall late gadolinium enhancement (LGE) in the LV, including a focus adjacent to the posteromedial papillary muscle (Fig. 1). Cardiac PET showed extensive patchy, focal hypermetabolic activity in the LV inferobasal, anterobasal and anterolateral walls. With high suspicion for CS, the patient opted for treatment with steroids and follow-up PET over extracardiac lymph node biopsy due to procedural risk. Discussion(s): Isolated CS is underdiagnosed and can present with a wide range of symptoms. Detection is limited by current diagnostic criteria, namely difficulty ascertaining affected tissue, which may limit recognition of the full range of presentations. Diagnosis and treatment vary widely among institutions but there is consensus on starting immunosuppression and pursuing follow-up cardiac PET for suppression of inflammatory activity in cases of high clinical suspicion. Our patient plans to undergo repeat PET and have ongoing discussion about lymph node biopsy. COVID-19 myocarditis remains on our differential, however given the patchy nature of LGE on cMR which correlated with the FDG uptake on PET, CS is considered the most probable diagnosis. Conclusion(s): CS should be considered in the differential diagnosis for young patients with structural valve abnormalities, even in the absence of arrhythmias or cardiomyopathy. High clinical suspicion may justify early immunosuppressive treatment to prevent irreversible myocardial injury and/or fatal arrhythmias. Whether this treatment will result in resolution of the structural defects remains to be seen and further investigated.Copyright © 2022
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Objective: Covid-19 infection has been declared as a pandemic disease by the World Health Organization (WHO) and has been associated with increased morbidity and mortality. More than 400 million people diagnosed with the disease has been reported until February 2022 [1]. Covid-19 infection mostly progresses with lung involvement and pneumonia, however, its effects on the cardiovascular system are also well-known. Studies have reported that Covid 19 infection can trigger cardiac events such as acute myocardial damage, acute myocarditis, acute coronary syndrome (ACS), ventricular arrhythmias, cardiogenic shock, and cardiac arrest [2]. Electrocardiogram (ECG) is an important tool to diagnose cardiac involvement. QTc interval, QT dispersion, Tp-e interval, Tp-e/QTc ratio are defined as ventricular repolarization parameters and these parameters are associated with increased risk of ventricular arrhythmia [3,4]. In our study, we aimed to evaluate to predict ventricular arrhythmia by ECG in Covid-19 patients. Method(s): Our study is a single-center, cross-sectional study. Patients diagnosed with Covid-19 in our center between July and October 2020 were included. 408 patients with positive SARS-CoV2 PCR test were detected and the ECGs of the patients were recorded at admission and 15 days after symptomatic recovery. After the exclusion criteria, remained 91 patients were analyzed. Conduction parameters (PR and QRS durations) and repolarization parameters (QTc interval, QT dispersion, Tp-e interval and Tp-e/QTc ratio) were evaluated in 12-lead ECG recordings. Result(s): Ninety-one patients with Covid-19 infection were included. The group were consisted of 47 male (52%) and 44 female (48%). The mean age was 50.4 years. As a result of the statistical analysis, no significant difference was observed between the groups in terms of PR interval (142.2+/-21.4 ms vs. 140.1+/-19.0 ms;p=0.312). QRS duration was found significantly higher during active infection (91.4+/-12.2 ms vs. 88.8+/-10.9 ms;p=0.022). The mean QTc duration was detected longer in the first ECG, but no statistically significant difference was observed between the two groups (426.1+/-23.6 ms vs. 422.5+/-26.2 ms;p=0.237). QT dispersion (35.2+/-7.3 ms vs. 27.7+/-7.8 ms;p<0.001), Tp-e interval (86.7+/-10.1 ms vs. 76.1+/-9.9 ms;p<0.001) and Tp-e/QTc ratio (0.204+/-0.026 vs 0.180+/-0.025;p<0.001) were found significantly higher during active infection Conclusion(s): In our study, QRS complex, QT dispersion, Tp-e interval, Tpe/ QTc ratio were significantly higher during active infection. We considered these parameters as a contributor of the increased mortality by inducing ventricular arrhythmia and sudden death in Covid-19 patients during active infection.
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Background Biochemical markers of cardiac injury and strain are proven indicators of severe COVID-19. Whether enzyme elevation is a product of cardiopulmonary strain versus myocardial viral injury is not well defined. CARDIO-COVID is a registry designed to study COVID-19 patients admitted to ICUs with evidence of cardiac injury. Methods Inclusion criteria for the CARDIO-COVID registry are PCR positive test for SARS-CoV2, ICU admission and either elevated troponin, elevated NT-proBNP/BNP, or new onset heart failure. Registry contains 1328 cases from 16 centers in the US, Canada, and Europe. 838 cases were included for analysis. Cases were collected between March 2020 - May 2021. Multivariate regression analyses were performed. Results Patients were 51.3% male, average age of 67.4 years and 32% Caucasian. 63% had pre-existing cardiovascular disease. Morbidity and mortality were common: 40% died, 50% underwent intubation, 20% required renal replacement therapy, and 5% had cardiac arrest requiring CPR. New onset arrhythmias were common (26%), but VT/VF was rare (4.8%). Cardiovascular complications were minor drivers of morbidity: 4.8% had ACS requiring catheterization, 8.0% had new onset heart failure (median EF 43% (IQR 31 - 47.75%), 4.4% had a CVA, and 6.7% had PE. Of patients who died, 65% died from hypoxemic respiratory failure, 10.5% from septic shock, 9.3% from PEA, and 3.1% from cardiogenic shock. Modeling showed insignificant increased odds of death in patients with MACE (p-value 0.22, OR 1.94 CI 0.67 - 5.82). Age (p-value 0.005) and intubation (p-value 0.001, OR 5.8 CI 2.1 - 18) were strongest predictors of death. Every increase in age by one year was associated with 5% increase in odds of death. Degree of cardiac enzyme elevation was not associated with MACE, death, or intubation. Conclusion While elevated cardiac enzymes are common in severe COVID-19, cardiac complications are not common drivers of mortality. Respiratory failure and septic shock are leading causes of death. These findings suggest that in severe COVID-19 cardiac enzyme elevation usually reflects cardiopulmonary strain from respiratory distress rather than myocardial injury portending cardiac failure or death.Copyright © 2023 American College of Cardiology Foundation
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Objective In 2021, accumulated coronavirus disease 2019 (COVID-19) confirmed cases exceeded 100 million worldwide. We sought the long term sequale on COVID-19. Design and Method Although there is a hope for vaccination, continuous infection is observed with case fatality rate over 2%. Patients with cardiovascular disease are more susceptible to COVID-19 and show more severe clinical course after the infection. COVID-19 related myocardial injury evidenced by increased troponin plasma levels occur in at least 10% of hospitalized patients and 25% to 35% or more, of critically ill patients. Patients with SARS-CoV-2 infection related cardiac complications are heart failure, arrhythmia, acute thrombosis, and stress induced cardiomyopathy. Results Myocardial injury is an important entity that cause long term sequale. The extent of the local tissue damage and cytokine storm triggered by the host immune response both contribute to the severity of the myocarditis. An exaggerated inflammatory response can be extremely fatal, and immunomodulators such as corticosteroids are considered in selected cases even though the efficacy and safety is questionable. Combined with these mechanisms related to a host immune response, multiple factors are responsible for the cardiac consequence of COVID-19, such as an oxygen supply and demand imbalance (with or without coronary artery disease), increased right ventricular afterload due to respiratory acidosis, hypoxemia and positive pressure ventilation. Even though it is difficult to discriminate all the possible mechanisms related to myocarditis, accordingly the effort to identify the dominant cause is necessary for the selection of the proper target treatment. Conclusions Substantial evidence has suggested a non-negligible incidence of cardiac injury related to COVID-19. Although the clinical significance and exact mechanisms are under investigation, we should be aware of the potentially fatal cardiac manifestations when dealing with patients with COVID-19. Long-term complications are also noticed from the recent publications and need further attention.
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Background SARS-CoV-2 infection, the cause of COVID-19, has been associated with myocarditis. Fulminant myocarditis (FM) is rare. Case A 30-year-old male with a past medical history of SARS-CoV-2 infection 7 months prior, presented with a 2-week history of malaise, cough, dyspnea, and signs of cardiogenic shock. He was fully vaccinated 9 months prior. Respiratory viral PCR testing, including SARSCoV-2, was negative. HS-troponin was >20,000 ng/L (NR: 0-53 ng/L). An echocardiogram revealed a dilated cardiomyopathy with an EF of 15-20%. Cardiac catheterization revealed no CAD. Workup for an autoimmune etiology was unrevealing. His condition worsened and he required inotropic support, eventual placement of an LVAD, and initiation of ECMO. He was not able to tolerate cardiac MRI or endomyocardial biopsy. Ultimately, he underwent orthotopic heart transplantation. Pathologic examination of the explanted heart confirmed lymphocytic myocarditis. Decision-making Myocardial injury due to the cardiotropic nature of SARS CoV-2 has been increasingly reported. There has been a 42% increase in viral myocarditis, and the risk is 16 times greater with a history of COVID-19. Symptomatic myocarditis typically manifests within weeks of infection. Such a delayed presentation has not been described. Data from autopsies of deceased COVID-19 patients revealed a 25% to 50% detection rate of SARS-CoV-2 mRNA in the myocardium. One case report described a deceased FM patient with multiple negative SARS-CoV-2 PCR tests, including bronchial lavage samples, having confirmed SARS-CoV-2 within the myocardium postmortem. Hence SARS-Cov-2 can persist in the heart after the resolution of respiratory infection, possibly leading to ongoing inflammation and myocardial damage. This may explain why our patient presented 7 months after a resolved infection. Conclusion SARS-CoV-2 is cardiotropic and can cause fulminant myocarditis even in the absence of a detectable respiratory infection. Hence closer monitoring of post-COVID-19 patients, including screening for subclinical myocarditis, may be prudent. Further research on monitoring and an evaluation of the clinical utility of medical therapy, is also warranted.Copyright © 2023 American College of Cardiology Foundation
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Introduction: In December 2019, a novel Coronavirus disease 2019 (COVID-19) was discovered and spread rapidly worldwide. The virus spared no country in its contagiousness. The most common clinical manifestations are respiratory symptoms;but COVID-19 may induce arrhythmias, myocardial infarction, heart failure, and other cardiovascular diseases due to the systemic inflammatory response coupled with localized vascular inflammation. The study aims to provide knowledge about the clinical profile, cardiovascular complications, and clinical outcomes among adult COVID-19 patients admitted to a tertiary hospital. Method(s): This study is a single-centered cross-sectional retrospective study of hospitalized adult COVID-19 patients between March 2020 to May 2022. COVID-19 confirmed patients who met the inclusion criteria with clinical data upon hospitalization are followed up for occurrence of critical illness. The study's primary outcome is determining the demographic profile and clinical course of COVID-19 infection regarding cardiovascular signs and symptoms. Data were retrieved from electronic health records. All outcomes were obtained with standardized data collection forms, and clinical severity was defined based on the National Institute of Health guidelines. Result(s): A total of 1341 hospitalized adult COVID-19 patients were admitted with a mean age of 50.41+/-15.92 years. More males than females account for 60.2% of the total number of patients. Hypertension is the most common comorbidity among COVID-19 patients, comprising 44% of cases, followed by diabetes at 31.9% and dyslipidemia at 11.4%. About 5.4% had coronary artery disease, followed by heart disease 6 (3.6%) and arrhythmia (0.6%). Most COVID-19 patients were smokers 12% and alcoholic beverage drinkers (11.4%). A univariate analysis associated with mortality showed diabetes mellitus (odds ratio 2.7, p = 0.029) and hypertension (odds ratio 3.4, p = 0.11). In the multiple logistic regression analysis, factors' age (OR 1.095, estimate coefficient 0.091, standard error 0.028, p-value <0.05) and admission duration (OR 0.906, estimate coefficient -0.099, standard error 0.028, p-value <0.05) were significantly associated with mortality. Based on the fitted model, older people are more likely to be deceased than younger people. The log odds for mortality increase by 0.091 units for each year. During hospital admission, 24.43% of patients developed acute COVID-19 infection, with an in-hospital casefatality rate of 13.89%. During hospital stay, COVID-19 patients had a significant QTc (.43 +/- 0.04, p'0.001). Patients admitted to Non-ICU had lower QTc (.44 +/- 0.045) compared to ICU patients (.45 +/- .05). Conclusion(s): Myocardial injury and significant cardiovascular risk factors increased mortality among critically-ill COVID-19 patients. Hence, aside from risk factor modification, emphasis on cardiovascular protection should also be considered during treatment for COVID-19.
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Cardiovascular complications are frequently reported in COVID-19 patients and are associated with increased mortality during hospitalization. However, no data exists on cardiac involvement in patients recovered from COVID-19 infection. Our study suggests a need for closer follow-up among COVID-19 recovered subjects including echocardiographic assessment of left ventricular function to elucidate long-term cardiovascular outcomes by early detection of left ventricular dysfunction.Copyright © 2022 Wolters Kluwer Medknow Publications. All rights reserved.
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The role of cardiac biomarkers in diagnosing acute myocardial infarction is undoubted. In the 2020 guidelines of the European Society of Cardiology, the measurement of cardiac peptides to gain prognostic information has a class IIa indication in all patients with ACS. In emergency care, ruling out a non-ST elevation myocardial infarction requires documentation of normal levels of cardiac biomarkers, which remain stable or have very small variations within several hours. This review aims to summarize the current knowledge and recent progresses in the field of cardiac biomarker discovery, from their routine use in emergency rooms to their prognostic roles in modern risk assessment tools. Integrated approaches combining cardiac troponin with other biomarkers of ventricular dysfunction or inflammation, or with modern cardiac imaging in emergency care are also presented, as well as the role of modern algorithms for serial troponin measurement in the modern management of emergency departments.
ABSTRACT
Background/Purpose: Multisystem inflammatory syndrome in children (MIS-C), associated with COVID-19 infection is a life-threatening condition, required intensive care. The aim of this study was to determine risk factors for severe/life-threatening course of MIS-C. Method(s): The retrospective study included 166 children (99 male, 67 female), aged from 4 months to 17 years (median 8.2 years), who met the WHO criteria for MIS-C. The criterion of severity was the fact of the ICU admission. The analysis of the obtained data was performed using the STATISTICA software package, version 10.0 (StatSoft Inc., USA). Result(s): To assess the factors associated with the severe course of MIS-C, patients were divided into two groups: those who were hospitalized in the ICU (n = 84;50.6%), and those who did not (n = 82;49.4%). Patients with a more severe course of MIS-C were significantly older. They had a high frequency of signs such as rash, edema, hepatomegaly, splenomegaly, neurological and respiratory symptoms. Hypotension/shock and myocardial damage were much more common in patients hospitalized in the ICU. Among the laboratory changes there were significant differences in the levels of hemoglobin, leukocytes and platelets, CRP, creatinine, troponin and D-dimer. The presence of macrophage activation syndrome was higher in patients, admitted in the ICU. Children, required intensive care required high dose corticosteroids and IVIG more often (table 1). FIGURE: 1) The first symptoms of progeria in infancy: scleroderma-like changes in the skin of the lower extremities and stiffness of knee joints at the age of 2 months. 2) Girl at the age of 3 years 5 months. Almost total alopecia with the absence of eyebrows and eyelashes. Pronounced venous pattern in the forehead, nasal bridge and nasolabial triangle. Conclusion(s): MIS-C is potentially a severe life-threatening condition, in which more than half (50.6%) of patients needed the ICU admission. The main factors determining the severity of MIS-C were: cardiovascular, resiratory and central nervous system disorders. It has been found that factors such as hepatomegaly, splenomegaly, D-dimer >2568 ng/ml, troponin >10 pg/ml, make it possible to identify a group of patients with high risk of severe MIS-C who may potentially need hospitalization in the ICU.