Cardiac Injury In Patients Research Articles

Blunt Cardiac Injury in Patients With Sternal Fractures.

BackgroundBlunt cardiac injury (BCI) is a possible consequence of sternal fractures (SF). There is a scarcity of studies addressing BCI in patients with different types of SF and with pre-existing cardiac conditions. The goal of this study was to delineate diagnostic patterns of BCI in different cohorts of SF patients.MethodsThis retrospective cohort study included 380 blunt trauma patients admitted to two level 1 trauma centers between January 2015 and March 2020 with radiologically confirmed SF. Electrocardiography, cardiac enzymes and echocardiography were evaluated for BCI diagnosis. Analyzed variables included: age, comorbidities, injury severity score, Glasgow coma score, type of SF (isolated, combined, displaced), incidence of traumatic brain injury, co-injuries, retrosternal hematoma, intensive care unit admissions, hospital lengths of stay, and mortality.ResultsIn 380 SF patients there were 250 (66%) females and 130 (34%) males and the mean age was 63 years old. Electrocardiography was done in all patients, cardiac enzymes in 234 (62%) and echocardiography in 181 (48%). BCI was diagnosed in 19 (5%) of patients, all having combined SF. BCI patients had higher injury severity score (mean 18.4) and 14 (74%) had pulmonary co-injuries. Multivariable analysis confirmed pulmonary co-injuries as a statistically significant predictor of BCI (p<0.001). BCI patients compared to no BCI patients had all three tests (electrocardiography, cardiac enzymes and echocardiography) performed statistically more often (90% vs 36%, p<0.001). SF patients with pre-injury cardiac comorbidities had similar incidence of BCI as without cardiac comorbidities (5% vs 6%, p=0.6). In SF patients with traumatic brain injury, cardiac enzymes (troponin, creatine kinase) were elevated significantly more often compared to patients without traumatic brain injury (58% vs 38%, p=0.02). SF displacement or retrosternal hematoma presence were not associated with BCI. Mortality in SF patients with BCI versus without was not statistically different (16 vs 9%, p=0.4).ConclusionsBlunt cardiac injury is rare in patients with SF. Higher degree of BCI suspicion must be applied in combined SF patients, especially those with pulmonary co-injuries. Cardiac comorbidities did not affect the rate of BCI. Echocardiography for BCI diagnosis is essential in SF patients with traumatic brain injury, as cardiac enzymes may be less informative, however is less important in isolated SF patients. Performing all three diagnostic tests in combined SF patients improves the accuracy of BCI diagnosis.

Persistent cardiac injury - An important component of long COVID-19 syndrome.

Persistent cardiac injury - An important component of long COVID-19 syndrome.

Morphologically, immunohistochemically and PCR proven lymphocytic viral peri-, endo-, myocarditis in patients with fatal COVID-19

BackgroundDespite a reported cardiac injury in patients with new coronavirus infection, the possibility and specifics of genuine viral myocarditis in COVID-19 remains not fully clear.PurposeTo study the presence of SARS-CoV-2 in the myocardium and the morphological properties of myocarditis in patients with severe coronavirus infection (COVID-19).MethodsAutopsy data of eight elderly patients (75.6 ± 7.4 years), four male and four female, with severe new coronavirus infection were studied. The lifetime diagnosis of COVID-19 is based on a positive result of the PCR study. The inclusion criterion was the presence of morphological signs of myocarditis according to the Dallas criteria. A standard histological examination included staining by hematoxylin and eosin, toluidin blue and Van Gieson. An immunohistochemical study was performed using antibodies to CD3, CD 68, CD20, perforin, toll-like receptor (TLR) types 4 and 9. PCR in real-time was performed to determine the viral RNA in the myocardium.ResultsAll patients had severe bilateral viral pneumonia. In all cases, myocarditis was not clinically diagnosed. Morphological examination of the heart found signs of active lymphocytic myocarditis. PCR identified the SARS-Cov2 RNA in all cases. There were also signs of destructive coronaritis in all cases, thrombovasculitis, lymphocytic pericarditis (in 3 cases) and endocarditis (in 2 cases). The absence of neutrophils confirms the aseptic nature of inflammation. An immunohistochemical study showed the CD3-positive T lymphocytes in the infiltrates. Increased expression of TLR type 4 and less 9 was also detected.ConclusionMorphological and immunohistochemical evidence of myocarditis in COVID-19 was presented. Lymphocytic infiltrations and positive PCR confirm the viral nature of inflammation. Myocarditis in COVID-19 is also characterized by coronaritis with microvascular thrombosis and associated with lymphocytic endo- and pericarditis.

Abstract TP223: Association Between Stroke Severity And Cardiac Troponins In Acute Stroke

Introduction: Cardiac troponins are often elevated in patients with acute stroke and have been associated poor outcomes. Whether the elevation in cardiac troponins, a marker of acute myocardial injury, is due to neurogenic mechanisms or the underlying cardiac risk factors is unknown. We evaluated the association between stroke severity and serum cardiac troponin levels in people with acute stroke. Methods: We conducted a retrospective study of adults (≥ 40 years) with a discharge diagnosis of imaging confirmed stroke admitted to a quaternary stroke centre in Toronto, Canada between January 1, 2018 and December 31, 2018. We collected demographic and clinical information, including stroke severity using the National Institutes of Health Stroke Scale [NIHSS], modelled as a continuous variable. We recorded serum cardiac troponin levels on admission. We modelled serum troponin level both as a continuous and a categorical variable (normal vs. high, ≥ 15 ng/L). We evaluated the association between admission NIHSS and serum troponin level using multivariable negative binomial models and logistic regression models, adjusting for demographics (age and sex) and comorbidities [history of congestive heart failure or stroke, stroke type (ischemic vs. hemorrhagic), ST elevation on ECG, and creatinine levels]. Results: We included 218 patients with acute stroke (median age 76 years, 48.6% women), of whom 190 (87.2%) had an ischemic stroke. Median NIHSS was 6 (Q1-Q3, 2-14), and median cardiac troponin level was 17 ng/L (Q1-Q3, 9-30), with 108 (53.2%) patients having higher than normal levels. A one-point increase in NIHSS (stroke severity) was associated with a higher serum troponin level in age- and sex- (RR 1.03; 1.00-1.05) and multivariable- (RR 1.03; 1.01-1.05) adjusted models. However, stroke severity was not associated with the odds of having high troponin levels in adjusted models (OR 1.03; 0.98-1.08). Conclusions: The modest, yet independent, association between greater stroke severity and higher cardiac troponins in patients with acute stroke could suggest a neurogenic basis for mild cardiac injury in patients with acute stroke. Future work on the association between elevated troponin and poor stroke outcomes should account for stroke severity on admission.

COVID-19 Hastalarında Hastane İçi Mortalitenin Kardiyak Hasar ile İlişkisi: Retrospektif Kohort Çalışması

Objective: Coronavirus disease-2019 (COVID-19) emerged in late 2019 and has caused a pandemic, resulting in significant morbidity and mortality. However, the clinical significance of cardiac injury in patients affected by COVID-19 is still unknown. Therefore, our objective was to explore the association between cardiac injury and mortality in hospitalized patients with COVID-19. Material and Methods: The study included four hundred forty-three patients with laboratory values for troponin and follow-up. The mean age was 57.3±16.0 years. The male to female ratio was 1.53. Fever (45.6%) and cough (42.7%) were the most frequent sign and symptom at admission. Hypertension was the most common comorbidity, identified in 140 patients (31.6%). Results: In 143 (32.2%) patients, we determined cardiac injury. The median length of hospital stay was ten days. The mortality rate was 14.4%. The median length of hospital stay was longer in patients with cardiac injury (14 days vs. 9 days, respectively) (p<0.001). The mortality rate was 3.7% in the patients without cardiac injury, whereas the mortality rate was significantly higher among the patients with cardiac injury (37.7%, p<0.001). The multivariable model showed that cardiac injury was the only independent risk factor for death. There was a higher risk of death in patients with cardiac injury than in those without cardiac injury [hazard ratio, 4.01 (95% confidence interval, 1.85-8.72, p<0.001)]. Conclusion: In conclusion, cardiac injury is a common condition among hospitalized patients with COVID-19 and is associated with an elevated risk of in-hospital mortality. In addition, it is significantly more common in patients with known heart disease, complicating the treatment process.

Electrocardiographic abnormalities in patients with COVID-19 pneumonia and raised interleukin-6.

Cardiac injury is associated with high mortality in patients with COVID-19 infection. Electrocardiographic changes can give clues to the underlying cardiovascular abnormalities. Raised inflammatory markers like raised interleukin-6 (IL-6) are associated with arrhythmia, heart failure, and coronary artery disease. However, past studies have not highlighted the electrocardiographic abnormalities in patients with COVID-19 infection with raised IL- 6 levels. This study compared the electrocardiogram (ECG) changes in COVID-19 patients with high and normal IL-6 levels. A retrospective analysis of ECG of 306 patients with COVID-19 infection was done, out of which 250 patients had normal IL- 6 levels, whereas 56 patients had raised IL-6 levels. IL-6 levels were measured in all the patients. Detailed clinicodemographic profile of all the serial COVID-19 patients admitted with moderate to severe COVID-19 pneumonia was noted from the hospital record section. Electrocardiographic findings and biochemical parameters of all the patients were noted. Out of 56 patients with raised IL-6 levels, 41 (73.2%) patients had ECG abnormalities compared to 177 (70.8%) patients with normal IL-6 levels. This difference was not statistically significant. However, ECG abnormality such as sinus tachycardia was significantly more common in patients with raised IL-6 levels than those with normal levels. Among patients with raised IL-6 levels who were discharged, 5 (16.6%) had sinus tachycardia, 2 (6.6%) had ST/T wave changes as compared to 15 (57.6%), and 10 (38.4%) who had tachycardia and ST/T wave change respectably succumbed to death. This difference was statistically significant. Sinus tachycardia followed by atrial fibrillation and right bundle branch block are common ECG changes in patients with COVID-19 infection with raised IL-6. The possible association of cardiac injury in patients with COVID-19 infection with coexisting raised IL-6 levels should be explored further.

Male carriers of HLA-C*04:01 have increased risk of cardiac injury in COVID-19

Identification of factors that lead to the severe clinical course of COVID-19 is crucial for timely allocation of resources. The purpose of this study was to evaluate possible sex differences in cardiac injury associated with HLA-C*04:01. High sensitivity troponin T on admission (hs-TnTa) and maximum high sensitivity troponin T (hs-TnTmax) were used to assess for cardiac injury in patients with COVID-19 (n = 435). We tested for the association of elevated hs-TnT with HLA-C* 04:01 and evaluated for potential sex-specific differences. An association between hs-TnTa and the severity of clinical course was identified. In addition, our study revealed that hs-TnTmax was higher in men who were carriers of HLA-C*04:01 compared to men without the risk allele. Male carriers of HLA-C*04:01 with COVID-19 developed higher hs-TnTmax, suggesting a larger extent of cardiac injury. This association suggests the presence of different pathomechanisms in COVID-19 based on sex.

Detailed Analyses of the Expression Patterns of Potential Severe Acute Respiratory Syndrome Coronavirus 2 Receptors in the Human Heart Using Single-Nucleus RNA Sequencing.

Cardiac injury is a common complication of coronavirus disease 2019 (COVID-19), but the exact mechanisms have not been completely elucidated. The virus receptors on subsets of cells are key determinants of susceptibility to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Due to its high sequence similarity to SARS-CoV, SARS-CoV-2 also utilizes ACE2 as the cell entry receptor. A growing number of studies have indicated that other receptors apart from ACE2 are involved in SARS-CoV-2 infection. This study aimed to elucidate the expression characteristics of SARS-CoV-2 cellular receptors in the heart. We first investigated ACE2 expression in a comprehensive transcriptional landscape of the human heart comprising single-nucleus RNA-seq (snRNA-seq) data for >280,000 cells. Then, the expression distributions of novel SARS-CoV-2 receptors were analyzed at the single-cell level to clarify the cardiovascular complications in COVID-19. We observed a higher percentage of ACE2-positive cells in pericytes (8.3%), fibroblasts (5.1%), and adipocytes (4.4%) in the human heart, compared to other cell types. The frequency of ACE2-positive cells in each cell type from the ventricles was significantly higher than that in the atria, suggesting that the ventricular cells are more susceptible to SARS-CoV-2 infection. The distribution patterns of other receptors (BSG, HSPA5, KREMEN1, NRP1, ANPEP, AXL) were significantly different from those of ACE2, demonstrating higher expression levels in ventricular cardiomyocytes. Moreover, our results suggest that fibroblasts and adipocytes, aside from pericytes, may be vulnerable targets for SARS-CoV-2 infection in the human heart. Our study presents potential targets for future clinical studies and interventions for cardiac injury in patients with COVID-19.

Retinol-Binding Protein 4 Promotes Cardiac Injury After Myocardial Infarction Via Inducing Cardiomyocyte Pyroptosis Through an Interaction With NLRP3.

BackgroundAcute myocardial infarction (AMI) is one of the leading causes of cardiovascular morbidity and mortality worldwide. Pyroptosis is a form of inflammatory cell death that plays a major role in the development and progression of cardiac injury in AMI. However, the underlying mechanisms for the activation of pyroptosis during AMI are not fully elucidated.Methods and ResultsHere we show that RBP4 (retinol‐binding protein 4), a previous identified proinflammatory adipokine, was increased both in the myocardium of left anterior descending artery ligation‐induced AMI mouse model and in ischemia‐hypoxia‒induced cardiomyocyte injury model. The upregulated RBP4 may contribute to the activation of cardiomyocyte pyroptosis in AMI because overexpression of RBP4 activated NLRP3 (nucleotide‐binding oligomerization domain‐like receptor family pyrin domain‐containing 3) inflammasome, promoted the precursor cleavage of Caspase‐1, and subsequently induced GSDMD (gasdermin‐D)‐dependent pyroptosis. In contrast, knockdown of RBP4 alleviated ischemia‐hypoxia‒induced activation of NLRP3 inflammasome signaling and pyroptosis in cardiomyocytes. Mechanistically, coimmunoprecipitation assay showed that RBP4 interacted directly with NLRP3 in cardiomyocyte, while genetic knockdown or pharmacological inhibition of NLRP3 attenuated RBP4‐induced pyroptosis in cardiomyocytes. Finally, knockdown of RBP4 in heart decreased infarct size and protected against AMI‐induced pyroptosis and cardiac dysfunction in mice.ConclusionsTaken together, these findings reveal RBP4 as a novel modulator promoting cardiomyocyte pyroptosis via interaction with NLRP3 in AMI. Therefore, targeting cardiac RBP4 might represent a viable strategy for the prevention of cardiac injury in patients with AMI.

Laboratory biochemical markers of cardiac injury by COVID-19: an integrative review.

The damaging effects of Sars-CoV-2 on cardiac tissue may be intensified with the presence of cardiocirculatory pathologies. The use of clinical biomarkers has grown, in order to monitor this cardiotoxicity early. In this sense, this study aimed to investigate, through an integrative review, the main biomarkers of cardiac injury associated with comorbidities in patients with COVID-19. A systematic bibliographic search was conducted on July 26, 2020, in the Scopus database. Of the total of 669 publications purchased, only 40 articles were eligible for this review. From the content of these publications, 16 systemic cardiac and inflammatory biomarkers that are part of the clinical findings of critically ill patients with COVID-19 were identified. Most of these patients were male, had a mean age of 63 years, and pre-existing comorbidities, such as were hypertension, diabetes mellitus, coronary artery disease, cerebrovascular disease, and chronic obstructive pulmonary disease. Cardiac injuries in patients infected with COVID-19 are related to the increase in cardiac and systemic biomarkers observed in most of these individuals. Finally, it is expected to increase physicians' awareness of biochemical markers of non-invasive cardiac injury, for diagnosis and prognosis, of unusual extrapulmonary pathophysiological presentations during infection by COVID-19.

Cardiovascular and Cerebrovascular Complications With COVID-19.

The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 has affected the health of people across the globe. Cardiovascular diseases (CVDs) have a significant relationship with COVID-19, both as a risk factor and prognostic indicator, and as a complication of the disease itself. In addition to predisposing to CVD complications, the ongoing pandemic has severely affected the delivery of timely and appropriate care for cardiovascular conditions resulting in increased mortality. The etiology behind the cardiac injury associated with severe acute respiratory syndrome coronavirus-2 is likely varied, including coronary artery disease, microvascular thrombosis, myocarditis, and stress cardiomyopathy. Further large-scale investigations are needed to better determine the underlying mechanism of myocardial infarction and other cardiac injury in COVID-19 patients and to determine the incidence of each type of cardiac injury in this patient population. Telemedicine and remote monitoring technologies can play an important role in optimizing outcomes in patients with established CVD. In this article, we summarize the various impacts that COVID-19 has on the cardiovascular system, including myocardial infarction, myocarditis, stress cardiomyopathy, thrombosis, and stroke.

Relation between Cardiac Injury and Elevated Levels of Inflammatory Biomarkers in Patients with Severe COVID-19

Background: Since early December 2019, coronavirus disease 2019 (COVID-19) has emerged as a global pandemic and public health crisis. This study aims to explore the relationship between cardiac injury and inflammatory biomarkers in patients with severe COVID-19. Methods: We collected data on 91 patients with a confirmed diagnosis of severe COVID-19 from February 8 to March 31, 2020. Demographic characteristics, clinical data, and in-hospital outcomes were compared. The relationship between cardiac injury and inflammatory biomarkers was analyzed. Logistic regression was used to explore the independent risk factors for cardiac injury. Results: The mean age of all patients was 61 years±14 years. About half of the patients were male. Hypertension and coronary heart disease were more common in the cardiac injury group. The levels of inflammatory biomarkers in patients who experienced cardiac injury were generally higher than the levels of those without cardiac injury, including interleukin-6, interleukin-2 receptor (IL-2R), procalcitonin, and high-sensitivity C-reactive protein. There were positive correlations between the levels of high-sensitivity troponin I and N-terminal prohormone of brain natriuretic peptide and the levels of inflammatory biomarkers. Logistic regression shows that IL-2R (odds ratio 1.001, 95% confidence interval 1.000–1.002, P=0.045) and comorbidities (odds ratio 4.909, 95% confidence interval 1.231–19.579, P=0.024) are independent risk factors for cardiac injury in patients with severe COVID-19. Conclusion: High levels of inflammatory biomarkers are associated with higher risk of cardiac injury in patients with severe COVID-19. IL-2R and comorbidities are predictors of cardiac injury.

Impact of Interleukin-6 Receptor Blockade With Tocilizumab on Cardiac Injury in Patients With COVID-19: A Retrospective Cohort Study.

Impact of Interleukin-6 Receptor Blockade With Tocilizumab on Cardiac Injury in Patients With COVID-19: A Retrospective Cohort Study.

The Role of Speckle Strain Echocardiography in the Diagnosis of Early Subclinical Cardiac Injury in Cancer Patients-Is There More Than Just Left Ventricle Global Longitudinal Strain?

With the improvement in survival rate, cardiotoxicity has emerged as a significant adverse effect of cancer therapy. Early diagnosis of subclinical cardiac injury may allow the initiation of cardioprotective therapy and preventing the interruption of optimal cancer therapy and the development of irreversible cardiac dysfunction. In this article, we review the role of two-dimensional speckle tracking echocardiography (2D-STE), beyond the common left ventricle global longitudinal strain in the diagnosis of early subclinical cardiac injury in patients treated with cancer therapies.

Mediators of SARS-CoV-2 entry are preferentially enriched in cardiomyocytes

BackgroundThe coronavirus disease 2019 (COVID-19) has spread rapidly around the world. In addition to common respiratory symptoms such as cough and fever, some patients also have cardiac injury, however, the mechanism of cardiac injury is not clear. In this study, we analyzed the RNA expression atlases of angiotensin-converting enzyme 2(ACE2), cathepsin B (CTSB) and cathepsin L (CTSL) in the human embryonic heart at single-cell resolution.ResultsThe results showed that ACE2 was preferentially enriched in cardiomyocytes. Interestingly, serine protease transmembrane serine protease 2 (TMPRSS2) had less expression in cardiomyocytes, but CTSB and CTSL, which belonged to cell protease, could be found to be enriched in cardiomyocytes. The results of enrichment analysis showed that differentially expressed genes (DEGs) in ACE2-positive cardiomyocytes were mainly enriched in the processes of cardiac muscle contraction, regulation of cardiac conduction, mitochondrial respiratory chain, ion channel binding, adrenergic signaling in cardiomyocytes and viral transcription.ConclusionsOur study suggests that both atrial and ventricular cardiomyocytes are potentially susceptible to severe acute respiratory syndrome coronavirus-2(SARS-CoV-2), and SARS-CoV-2 may enter ventricular cardiomyocytes using CTSB/CTSL for S protein priming. This may be the partial cellular mechanism of cardiac injury in patients with COVID-19.

Electrocardiographic Manifestations in Patients with COVID-19: Daegu in South Korea.

As the coronavirus disease 2019 (COVID-19) spreads worldwide, cardiac injury in patients infected with COVID-19 becomes a significant concern. Thus, this study investigates the impact of several electrocardiogram (ECG) parameters and disease severity in COVID-19 patients. Seven medical centers in Daegu admitted 822 patients with COVID-19 between February and April 2020. This study examined 267 patients among them who underwent an ECG test and evaluated their biochemical parameters like C-reactive protein (CRP), log N-terminal pro-B-type Natriuretic Peptide (NT-proBNP), cardiac enzyme, and ECG parameters (heart rate, PR interval, QRS interval, T inversion, QT interval, and Tpe [the interval between peak to end in a T wave]). Those patients were divided into 3 groups of mild (100 patients), moderate (89 patients), and severe (78 patients) according to clinical severity score. The level of CRP, log NT-proBNP, and creatinine kinase-myocardial band were significantly increased in severe patients. Meanwhile, severe patients exhibited prolonged QT intervals (QTc) and Tpe (Tpe-c) compared to mild or moderate patients. Moreover, deceased patients (58; 21.7%) showed increased dispersion of QTc and Tpe-c compared with surviving patients (78.2±41.1 vs. 40.8±24.6 ms and 60.2±37.3 vs. 40.8±24.5 ms, both p<0.05, respectively). The QTc dispersion of more than 56.1 ms could predict the mortality in multivariate analysis (odd ratio, 11.55; 95% confidence interval, 3.746-42.306). COVID-19 infections could involve cardiac injuries, especially cardiac repolarization abnormalities. A prolonged QTc dispersion could be an independent predictable factor of mortality.

Cardiovascular Complications of COVID-19 in Patients With Multiple Sclerosis: A Lesson From Our Experience

Background and Aim: COVID-19 is an emerging threat that could affect the cardiovascular system in the setting of a cytokine storm syndrome. This study examines the cardiac injury associated with COVID-19 in patients with Multiple Sclerosis (MS). Case Presentation: We analyzed 6 cases of MS in association with COVID-19 who underwent cardiac evaluation during their hospitalization. The mean age of our patients was 36.6 years. Two patients had Secondary Progressive MS (SPMS), one patient had Primary Progressive MS (PPMS), and the rest had Relapsing-Remitting MS (RRMS). Our patients were on both immunomodulatory and immunosuppressive Disease-Modifying Therapies (DMTs). None of our patients had a cardiovascular risk factor or developed cardiovascular complications. Their electrocardiogram, echocardiography, and cardiac enzymes were within normal limits. Results: Their mean length of hospitalization was 11.8 days. After a month of follow-up, all patients returned to their baseline neurological status except the one with PPMS and moderate COVID-19, who experienced 0.5 points increase in her expanded disability status scale score. Conclusion: Patients with MS might be at risk of developing severe COVID-19 in which cardiac injury is a crucial complication. There are limited data describing myocarditis associated with COVID-19 in patients with MS. However, our cases revealed no evidence of cardiac injury in patients with MS, even under immunosuppressive DMTs.

Application of Point-of-care Cardiac Ultrasonography in COVID-19 Infection: Lessons Learned from the Early Experience.

The outbreak of the SARS-CoV-2 infection, also known as coronavirus disease 2019 (COVID-19), was formally defined a pandemic by the World Health Organization (WHO) in March 2020, and is still a global health issue. Since there is a high prevalence of acute cardiac injury in patients with COVID-19 infection, point-of-care cardiac ultrasound (PoCCUS) may be used for longitudinal monitoring of patients infected with COVID-19. However, there is still limited experience on the application of PoCCUS in the COVID-19 pandemic. Within the point of care setting in our system, focused cardiac US exams were performed with specific imaging protocols on the basis of suspicion of a specific disease, such as ruling out tamponade or thrombotic complications. Our preliminary experience shows that PoCCUS helps distinguish the causes of dyspnea in febrile patients. The COVID-19 infection may play a role in unmasking or exacerbating underlying chronic cardiovascular conditions, especially in patients with inadequate past history. In hospitalized patients with COVID-19, CURB-65 score for pneumonia severity and raised D-dimer were significantly associated with deep vein thrombosis (DVT). COVID-19 patients with DVT had worse prognosis, and patients with lower leg edema deserve further evaluation by using point-of-care ultrasound for the lower legs and heart. In COVID-19 patients with arrhythmia, PoCCUS used by experienced hands may reveal abnormal right ventricle (RV) functional parameters and lead to a more comprehensive cardiac US study. When there is suspicion of cardiac disease, PoCCUS can be done first, and if information is inadequate, limited transthoracic echocardiography (TTE), and critical care echocardiography (CCE) can be followed. Ultrasound practitioners should follow the standard precautions for COVID-19 as outlined by the Centers for Disease Control and Prevention to prevent transmission of infection, regardless of suspected or confirmed COVID-19.

Risk factors for COVID-19 patients with cardiac injury: pulmonary ventilation dysfunction and oxygen inhalation insufficiency are not the direct causes.

Background: Cardiac injury in patients with coronavirus disease 2019 (COVID-19) has been reported in recent studies. However, reports on the risk factors for cardiac injury and their prognostic value are limited.Results: In total, 15.9% of all cases were defined as cardiac injury in our study. Patients with severe COVID-19 were significantly associated with older age and higher respiratory rates, Sequential Organ Failure Assessment (SOFA) scores, cardiac injury biomarkers and PaO2/FiO2 ratios. Male patients with chest distress and dyspnea were more likely to have severe disease. Patients with cardiac injury were significantly more likely to have a severe condition and have an outcome of death. However, no significant difference was found in respiratory rates, dyspnea or PaO2/FiO2 ratio between patients with or without cardiac injury. In the logistic regression model, pre-existing hypertension and higher SOFA score were independent risk factors for patients with COVID-19 developing cardiac injury.Conclusions: Our study revealed that cardiac injury was an important predictor for patients having a severe or fatal outcome. Patients with pre-existing hypertension and higher SOFA scores upon admission were more likely to develop cardiac injury. Nevertheless, pulmonary ventilation dysfunction and oxygen inhalation insufficiency were not the main causes of cardiac injury in patients with COVID-19.Methods: A total of 113 confirmed cases were included in our study. Severe patients were defined according to American Thoracic Society guidelines for community-acquired pneumonia. Cardiac injury was defined as a serum cTnI above the 99th-percentile of the upper reference limit. Patient characteristics, clinical laboratory data and treatment details were collected and analyzed. The risk factors for patients with and without cardiac injury were analyzed.

Meta-analysis Comparing Outcomes in Patients With and Without Cardiac Injury and Coronavirus Disease 2019 (COVID 19)

Current evidence is limited to small studies describing the association between cardiac injury and outcomes in patients with coronavirus disease 2019 (COVID-19). To address this, we performed a comprehensive meta-analysis of studies in COVID-19 patients to evaluate the association between cardiac injury and all-cause mortality, intensive care unit (ICU) admission, mechanical ventilation, acute respiratory distress syndrome, acute kidney injury and coagulopathy. Further, studies comparing cardiac biomarker levels in survivors versus nonsurvivors were included. A total of 14 studies (3,175 patients) were utilized for the final analysis. Cardiac injury in patients with COVID-19 was associated with higher risk of mortality (risk ratio [RR]:7.79; 95% confidence interval [CI]: 4.69 to 13.01; I2=58%), ICU admission (RR: 4.06; 95% CI: 1.50 to 10.97; I2 = 61%), mechanical ventilation (RR: 5.53; 95% CI: 3.09 to 9.91; I2 = 0%), and developing coagulopathy (RR: 3.86; 95% CI:2.81 to 5.32; I2 = 0%). However, cardiac injury was not associated with increased risk of acute respiratory distress syndrome (RR:3.22; 95% CI:0.72 to 14.47; I2 = 73%) or acute kidney injury (RR: 11.52, 95% CI:0.03 to 4,159.80; I2 = 0%). The levels of hs-cTnI (MD:34.54 pg/ml;95% CI: 24.67 to 44.40 pg/ml; I2 = 88%), myoglobin (MD:186.81 ng/ml; 95% CI: 121.52 to 252.10 ng/ml; I2 = 88%), NT-pro BNP (MD:1183.55 pg/ml; 95% CI: 520.19 to 1846.91 pg/ml: I2 = 96%) and CK-MB (MD:2.49 ng/ml;95% CI: 1.86 to 3.12 ng/ml; I2 = 90%) were significantly elevated in nonsurvivors compared with survivors with COVID-19 infection. The results of this meta-analysis suggest that cardiac injury is associated with higher mortality, ICU admission, mechanical ventilation and coagulopathy in patients with COVID-19.