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1.
Arch Cardiovasc Dis ; 115(6-7): 388-396, 2022.
Article in English | MEDLINE | ID: covidwho-1943941

ABSTRACT

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


Subject(s)
COVID-19 , Heart Injuries , Hospital Mortality , Humans , Lung , Retrospective Studies , SARS-CoV-2 , Tomography, X-Ray Computed/methods
2.
Intensive Care Med ; 48(1): 111-113, 2022 01.
Article in English | MEDLINE | ID: covidwho-1899118
3.
Cell Rep ; 39(11): 110955, 2022 Jun 14.
Article in English | MEDLINE | ID: covidwho-1866959

ABSTRACT

Direct myocardial and vascular injuries due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection-driven inflammation is the leading cause of acute cardiac injury associated with coronavirus disease 2019 (COVID-19). However, in-depth knowledge of the injury characteristics of the heart affected by inflammation is lacking. In this study, using a quantitative spatial proteomics strategy that combines comparative anatomy, laser-capture microdissection, and histological examination, we establish a region-resolved proteome map of the myocardia and microvessels with obvious inflammatory cells from hearts of patients with COVID-19. A series of molecular dysfunctions of myocardia and microvessels is observed in different cardiac regions. The myocardia and microvessels of the left atrial are the most susceptible to virus infection and inflammatory storm, suggesting more attention should be paid to the lesion and treatment of these two parts. These results can guide in improving clinical treatments for cardiovascular diseases associated with COVID-19.


Subject(s)
COVID-19 , Heart Injuries , COVID-19/complications , Humans , Inflammation , Proteome , SARS-CoV-2
4.
Arq Bras Cardiol ; 118(5): 937-945, 2022 05.
Article in English, Portuguese | MEDLINE | ID: covidwho-1865767

ABSTRACT

BACKGROUND: Some patients with COVID-19 present myocardial injury. OBJECTIVE: To detect myocardial injury in critically ill paediatric patients, and to compare cardiac involvement between children with severe acute respiratory syndrome (SARS) and children with multisystemic inflammatory syndrome (MIS-C). METHODS: All COVID-19 children admitted to a referral intensive care unit were prospectively enrolled and had a two-dimensional echocardiogram (2D-TTE) and a cardiac troponin I (cTnI) assay within the first 72 hours. For statistical analysis, two-sided p < 0.05 was considered significant. RESULTS: Thirty-three patients were included, of which 51.5% presented elevated cTnI and/or abnormal 2D-TTE and 36.4% needed cardiovascular support, which was more frequent in patients with both raised cTnI and 2D-TTE abnormalities than in patients with normal exams (83.3% and 33.3%, respectively; p 0.006, 95% CI = 0.15-0.73). The most common 2D-TTE findings were pericardial effusion (15.2%) and mitral/tricuspid regurgitation (15.2%). Signs of cardiac involvement were more common in MIS-C than in SARS. MIS-C patients also presented a higher rate of the need for cardiovascular support (66.7% vs 25%, p 0.03, 95% CI = -0.7 to -0.04) and a more frequent rate of raised cTnI (77.8% vs 20.8%; p 0.002, 95% CI = 0.19 to 0.79). The negative predictive values of cTnI for the detection of 2D-TTE abnormalities were 100% for MIS-C patients and 73.7% for SARS patients. CONCLUSION: signs of cardiac injury were common, mainly in MIS-C patients. 2D-TTE abnormalities were subtle. To perform a cTnI assay upon admission might help providers to discriminate those patients with a more urgent need for a 2D-TTE.


FUNDAMENTO: Alguns pacientes com COVID-19 apresentam injúria miocárdica. OBJETIVO: Detectar a injúria miocárdica em pacientes criticamente doentes, e comparar o envolvimento cardíaco entre crianças com síndrome respiratória aguda grave (SARS) e crianças com síndrome inflamatória multissistêmica (MIS-C). MÉTODOS: Todas as crianças acometidas da COVID-19 admitidas em uma unidade de terapia intensiva de referência foram cadastradas de forma prospectiva e fizeram uma ecografia transtorácica bidimensional (ETT-2D) e um teste de troponina I cardíaca (cTnI) nas primeiras 72 horas. Para a análise estatística, um p <0,05 bilateral foi considerado significativo. RESULTADOS: 33 pacientes foram incluídos, dos quais 51,5% apresentaram cTnI elevada e/ou ETT-2D anormal e 36,4% precisaram de suporte cardiovascular, que foi mais frequente em pacientes com cTnI elevada e anormalidades em ETT-2D do que em pacientes com exames normais (83,3% e 33,3%, respectivamente; p 0,006, 95% IC = 0,15-0,73). Os achados de ETT-2D mais comuns foram efusão pericárdica (15,2%) e regurgitação tricúspide/mitral (15,2%). Sinais de envolvimento cardíaco foram mais comuns na MIS-C que na SARS. Pacientes com MIS-C também apresentaram um índice mais alto de necessidade de suporte cardiovascular (66,7% X 25%, p 0,03, 95% IC = -0,7 a -0,04) e um índice mais frequente de cTnI elevada (77,8% X 20,8%; p 0,002, 95% IC = 0,19 a 0,79). Os valores preditivos negativos de cTnI para detecção de anormalidades de ETT-2D foram 100% para pacientes com MIS-C, e 73,7% para pacientes com SARS. CONCLUSÃO: Sinais de injúria cardíaca foram comuns, especialmente em pacientes com MIS-C. As anormalidades na ETT-2D foram sutis. A realização de um teste de cTnI na admissão pode ajudar os prestadores de assistência de saúde a discriminar os pacientes com uma necessidade mais urgente de uma ETT-2D.


Subject(s)
COVID-19 , Heart Injuries , Biomarkers , Brazil/epidemiology , COVID-19/complications , Child , Critical Illness , Heart Injuries/diagnostic imaging , Humans , Systemic Inflammatory Response Syndrome , Troponin I
5.
PLoS One ; 16(4): e0250815, 2021.
Article in English | MEDLINE | ID: covidwho-1833533

ABSTRACT

BACKGROUND: COVID-19 is a respiratory infectious disease caused by SARS-CoV-2, and cardiovascular damage is commonly observed in affected patients. We sought to investigate the effect of SARS-CoV-2 infection on cardiac injury and hypertension during the current coronavirus pandemic. STUDY DESIGN AND METHODS: The clinical data of 366 hospitalized COVID-19-confirmed patients were analyzed. The clinical signs and laboratory findings were extracted from electronic medical records. Two independent, experienced clinicians reviewed and analyzed the data. RESULTS: Cardiac injury was found in 11.19% (30/268) of enrolled patients. 93.33% (28/30) of cardiac injury cases were in the severe group. The laboratory findings indicated that white blood cells, neutrophils, procalcitonin, C-reactive protein, lactate, and lactic dehydrogenase were positively associated with cardiac injury marker. Compared with healthy controls, the 190 patients without prior hypertension have higher AngⅡ level, of which 16 (8.42%) patients had a rise in blood pressure to the diagnostic criteria of hypertension during hospitalization, with a significantly increased level of the cTnI, procalcitonin, angiotensin-II (AngⅡ) than those normal blood pressure ones. Multivariate analysis indicated that elevated age, cTnI, the history of hypertension, and diabetes were independent predictors for illness severity. The predictive model, based on the four parameters and gender, has a good ability to identify the clinical severity of COVID-19 in hospitalized patients (area under the curve: 0.932, sensitivity: 98.67%, specificity: 75.68%). CONCLUSION: Hypertension, sometimes accompanied by elevated cTnI, may occur in COVID-19 patients and become a sequela. Enhancing Ang II signaling, driven by SARS-CoV-2 infection, might play an important role in the renin-angiotensin system, and consequently lead to the development of hypertension in COVID-19.


Subject(s)
COVID-19/complications , Heart Injuries/epidemiology , Hypertension/epidemiology , Adult , Aged , Aged, 80 and over , COVID-19/metabolism , COVID-19/physiopathology , Comorbidity , Disease Progression , Female , Heart Injuries/virology , Hospitalization , Humans , Hypertension/physiopathology , Hypertension/virology , Male , Medical Records , Middle Aged , Pandemics , Renin-Angiotensin System , SARS-CoV-2/pathogenicity
6.
Int J Biol Sci ; 18(7): 2703-2713, 2022.
Article in English | MEDLINE | ID: covidwho-1811190

ABSTRACT

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


Subject(s)
COVID-19 , Heart Injuries , Myocarditis , Humans , RNA, Viral , SARS-CoV-2
7.
Cardiol Clin ; 40(3): 287-300, 2022 Aug.
Article in English | MEDLINE | ID: covidwho-1767946

ABSTRACT

Myocardial injury is common in patients with COVID-19 and is associated with an adverse prognosis. Cardiac troponin (cTn) is used to detect myocardial injury and assist with risk stratification in this population. SARS-CoV-2 infection can play a role in the pathogenesis of acute myocardial injury due to both direct and indirect damage to the cardiovascular system. Despite the initial concerns about an increased incidence of acute myocardial infarction (MI), most cTn increases are related to chronic myocardial injury due to comorbidities and/or acute nonischemic myocardial injury. This review will discuss the latest findings on this topic.


Subject(s)
COVID-19 , Heart Injuries , Myocardial Infarction , Biomarkers , COVID-19/complications , Heart Injuries/diagnosis , Humans , Myocardial Infarction/diagnosis , Myocardial Infarction/epidemiology , Prognosis , SARS-CoV-2 , Troponin
9.
EBioMedicine ; 76: 103821, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1670420

ABSTRACT

BACKGROUND: Although acute cardiac injury (ACI) is a known COVID-19 complication, whether ACI acquired during COVID-19 recovers is unknown. This study investigated the incidence of persistent ACI and identified clinical predictors of ACI recovery in hospitalized patients with COVID-19 2.5 months post-discharge. METHODS: This retrospective study consisted of 10,696 hospitalized COVID-19 patients from March 11, 2020 to June 3, 2021. Demographics, comorbidities, and laboratory tests were collected at ACI onset, hospital discharge, and 2.5 months post-discharge. ACI was defined as serum troponin-T (TNT) level >99th-percentile upper reference limit (0.014ng/mL) during hospitalization, and recovery was defined as TNT below this threshold 2.5 months post-discharge. Four models were used to predict ACI recovery status. RESULTS: There were 4,248 (39.7%) COVID-19 patients with ACI, with most (93%) developed ACI on or within a day after admission. In-hospital mortality odds ratio of ACI patients was 4.45 [95%CI: 3.92, 5.05, p<0.001] compared to non-ACI patients. Of the 2,880 ACI survivors, 1,114 (38.7%) returned to our hospitals 2.5 months on average post-discharge, of which only 302 (44.9%) out of 673 patients recovered from ACI. There were no significant differences in demographics, race, ethnicity, major commodities, and length of hospital stay between groups. Prediction of ACI recovery post-discharge using the top predictors (troponin, creatinine, lymphocyte, sodium, lactate dehydrogenase, lymphocytes and hematocrit) at discharge yielded 63.73%-75.73% accuracy. INTERPRETATION: Persistent cardiac injury is common among COVID-19 survivors. Readily available patient data accurately predict ACI recovery post-discharge. Early identification of at-risk patients could help prevent long-term cardiovascular complications. FUNDING: None.


Subject(s)
COVID-19/pathology , Heart Injuries/diagnosis , Troponin I/metabolism , Aged , Aged, 80 and over , COVID-19/complications , COVID-19/virology , Female , Heart Injuries/epidemiology , Heart Injuries/etiology , Heart Injuries/mortality , Hospital Mortality , Humans , Incidence , L-Lactate Dehydrogenase/metabolism , Logistic Models , Lymphocyte Count , Male , Middle Aged , New York/epidemiology , Patient Discharge , Retrospective Studies , SARS-CoV-2/isolation & purification
11.
J Am Heart Assoc ; 11(1): e022010, 2022 01 04.
Article in English | MEDLINE | ID: covidwho-1599177

ABSTRACT

Background Myocardial injury in patients with COVID-19 is associated with increased mortality during index hospitalization; however, the relationship to long-term sequelae of SARS-CoV-2 is unknown. This study assessed the relationship between myocardial injury (high-sensitivity cardiac troponin T level) during index hospitalization for COVID-19 and longer-term outcomes. Methods and Results This is a prospective cohort of patients who were hospitalized at a single center between March and May 2020 with SARS-CoV-2. Cardiac biomarkers were systematically collected. Outcomes were adjudicated and stratified on the basis of myocardial injury. The study cohort includes 483 patients who had high-sensitivity cardiac troponin T data during their index hospitalization. During index hospitalization, 91 (18.8%) died, 70 (14.4%) had thrombotic complications, and 126 (25.6%) had cardiovascular complications. By 12 months, 107 (22.2%) died. During index hospitalization, 301 (62.3%) had cardiac injury (high-sensitivity cardiac troponin T≧14 ng/L); these patients had 28.6%, 32.2%, and 33.2% mortality during index hospitalization, at 6 months, and at 12 months, respectively, compared with 4.1%, 4.9%, and 4.9% mortality for those with low-level positive troponin and 0%, 0%, and 0% for those with undetectable troponin. Of 392 (81.2%) patients who survived the index hospitalization, 94 (24%) had at least 1 readmission within 12 months, of whom 61 (65%) had myocardial injury during the index hospitalization. Of 377 (96%) patients who were alive and had follow-up after the index hospitalization, 211 (56%) patients had a documented, detailed clinical assessment at 6 months. A total of 78 of 211 (37.0%) had ongoing COVID-19-related symptoms; 34 of 211 (16.1%) had neurocognitive decline, 8 of 211 (3.8%) had increased supplemental oxygen requirements, and 42 of 211 (19.9%) had worsening functional status. Conclusions Myocardial injury during index hospitalization for COVID-19 was associated with increased mortality and may predict who are more likely to have postacute sequelae of COVID-19. Among patients who survived their index hospitalization, the incremental mortality through 12 months was low, even among troponin-positive patients.


Subject(s)
COVID-19 , Heart Injuries , COVID-19/complications , COVID-19/therapy , Heart Injuries/epidemiology , Hospitalization , Humans , Prospective Studies , Treatment Outcome , Troponin T/blood
13.
JCI Insight ; 7(2)2022 01 25.
Article in English | MEDLINE | ID: covidwho-1571524

ABSTRACT

Acute cardiac injury is prevalent in critical COVID-19 and associated with increased mortality. Its etiology remains debated, as initially presumed causes - myocarditis and cardiac necrosis - have proved uncommon. To elucidate the pathophysiology of COVID-19-associated cardiac injury, we conducted a prospective study of the first 69 consecutive COVID-19 decedents at CUIMC in New York City. Of 6 acute cardiac histopathologic features, presence of microthrombi was the most commonly detected among our cohort. We tested associations of cardiac microthrombi with biomarkers of inflammation, cardiac injury, and fibrinolysis and with in-hospital antiplatelet therapy, therapeutic anticoagulation, and corticosteroid treatment, while adjusting for multiple clinical factors, including COVID-19 therapies. Higher peak erythrocyte sedimentation rate and C-reactive protein were independently associated with increased odds of microthrombi, supporting an immunothrombotic etiology. Using single-nuclei RNA-sequencing analysis on 3 patients with and 4 patients without cardiac microthrombi, we discovered an enrichment of prothrombotic/antifibrinolytic, extracellular matrix remodeling, and immune-potentiating signaling among cardiac fibroblasts in microthrombi-positive, relative to microthrombi-negative, COVID-19 hearts. Non-COVID-19, nonfailing hearts were used as reference controls. Our study identifies a specific transcriptomic signature in cardiac fibroblasts as a salient feature of microthrombi-positive COVID-19 hearts. Our findings warrant further mechanistic study as cardiac fibroblasts may represent a potential therapeutic target for COVID-19-associated cardiac microthrombi.


Subject(s)
COVID-19 , Heart Injuries , RNA-Seq , SARS-CoV-2/metabolism , Thrombosis , Adult , Aged , Aged, 80 and over , COVID-19/genetics , COVID-19/metabolism , COVID-19/pathology , Female , Heart Injuries/genetics , Heart Injuries/metabolism , Heart Injuries/pathology , Humans , Male , Middle Aged , Myocardium/metabolism , Myocardium/pathology , Prospective Studies , Thrombosis/genetics , Thrombosis/metabolism , Thrombosis/pathology
16.
Am J Cardiol ; 164: 123-130, 2022 02 01.
Article in English | MEDLINE | ID: covidwho-1536420

ABSTRACT

Several recent publications have described myopericarditis cases after the coronavirus disease 2019 (COVID-19) vaccination. However, it is uncertain if these cases occurred secondary to the vaccination or more common etiologies of myopericarditis. To help determine whether a correlation exists between COVID-19 vaccination and myopericarditis, the present study compared the gender-specific cumulative incidence of myopericarditis and myocardial injury in a cohort of COVID-19 vaccinated patients at a tertiary care center in 2021 with the cumulative incidence of these conditions in the same subjects exactly 2 years earlier. We found that the age-adjusted incidence rate of myopericarditis in men was higher in the vaccinated than the control population, rate ratio 9.7 (p = 0.04). However, the age-adjusted incidence rate of myopericarditis in women was no different between the vaccinated and control populations, rate ratio 1.28 (p = 0.71). We further found that the rate of myocardial injury was higher in both men and women in 2021 than in 2019 both before and after vaccination, suggesting that some of the apparent increase in the diagnosis of myopericarditis after vaccination may be attributable to factors unrelated to the COVID-19 vaccinations. In conclusion, our study reaffirms the apparent increase in the diagnosis of myopericarditis after COVID-19 vaccination in men but not in women, although this finding may be confounded by increased rates of myocardial injury in 2021. The benefits of COVID-19 vaccination to individual and public health clearly outweigh the small potential increased risk of myopericarditis after vaccination.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , Heart Injuries , Myocarditis , Myocardium/pathology , Pericarditis , Vaccination/adverse effects , Adolescent , Adult , Aged , Cohort Studies , Female , Heart Injuries/diagnosis , Heart Injuries/epidemiology , Heart Injuries/etiology , Humans , Incidence , Male , Middle Aged , Myocarditis/diagnosis , Myocarditis/epidemiology , Myocarditis/etiology , Pericarditis/diagnosis , Pericarditis/epidemiology , Pericarditis/etiology , Sex Factors , Tertiary Care Centers , Troponin/blood , Young Adult
17.
Front Immunol ; 12: 748417, 2021.
Article in English | MEDLINE | ID: covidwho-1528820

ABSTRACT

Rationale: Myocardial injury associates significantly and independently with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 remains unclear, and cardiac involvement by SARS-CoV-2 presents a major challenge worldwide. Objective: This histological and immunohistochemical study sought to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 myocardial injury. Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control group (n=11). Histological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against targets: caspase-1, caspase-9, gasdermin-d, ICAM-1, IL-1ß, IL-4, IL-6, CD163, TNF-α, TGF-ß, MMP-9, type 1 and type 3 collagen. The samples were also assessed for apoptotic cells by TUNEL. Histological analysis showed severe pericardiocyte interstitial edema and higher mast cells counts per high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-1ß, IL-6, MMP-9, TNF-α, and other markers in the hearts of COVID-19 patients. Expression of caspase-9 did not differ from the controls, while gasdermin-d expression was less. The TUNEL assay was positive in all the COVID-19 samples supporting endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 myocardial injury does not seem to relate to primary myocardiocyte involvement but to local inflammation with associated interstitial edema. We found heightened TGF-ß and interstitial collagen expression in COVID-affected hearts, a potential harbinger of chronic myocardial fibrosis. These results suggest a need for continued clinical surveillance of patients for myocardial dysfunction and arrythmias after recovery from the acute phase of COVID-19.


Subject(s)
COVID-19/metabolism , Heart Injuries/metabolism , SARS-CoV-2 , Aged , Apoptosis , Biopsy , COVID-19/pathology , Caspase 1/metabolism , Collagen/metabolism , Cytokines/metabolism , Female , Heart Injuries/pathology , Humans , Immunohistochemistry , Intercellular Adhesion Molecule-1/metabolism , Male , Matrix Metalloproteinase 9/metabolism , Myocardium/metabolism , Myocardium/pathology
18.
Sci Rep ; 11(1): 22389, 2021 11 17.
Article in English | MEDLINE | ID: covidwho-1521768

ABSTRACT

Outbreak of global pandemic Coronavirus disease 2019 (COVID-19) has so far caused countless morbidity and mortality. However, a detailed report on the impact of COVID-19 on hypertension (HTN) and ensuing cardiac injury is unknown. Herein, we have evaluated the association between HTN and cardiac injury in 388 COVID-19 (47.5 ± 15.2 years) including 75 HTN and 313 normotension. Demographic data, cardiac injury markers, other laboratory findings, and comorbidity details were collected and analyzed. Compared to patients without HTN, hypertensive-COVID-19 patients were older, exhibited higher C-reactive protein (CRP), erythrocyte sedimentation rate, and comorbidities such as diabetes, coronary heart disease, cerebrovascular disease and chronic kidney disease. Further, these hypertensive-COVID-19 patients presented more severe disease with longer hospitalization time, and a concomitant higher rate of bilateral pneumonia, electrolyte disorder, hypoproteinemia and acute respiratory distress syndrome. In addition, cardiac injury markers such as creatine kinase (CK), myoglobin, lactic dehydrogenase (LDH), and N-terminal pro brain natriuretic peptide were significantly increased in these patients. Correlation analysis revealed that systolic blood pressure correlated significantly with the levels of CK, and LDH. Further, HTN was associated with increased LDH and CK-MB in COVID- 19 after adjusting essential variables. We also noticed that patients with elevated either high sensitivity-CRP or CRP demonstrated a significant high level of LDH along with a moderate increase in CK (p = 0.07) and CK-MB (p = 0.09). Our investigation suggested that hypertensive patients presented higher risk of cardiac injury and severe disease phenotype in COVID-19, effectively control blood pressure in HTN patients might improve the prognosis of COVID-19 patients.


Subject(s)
COVID-19/complications , Heart Injuries/epidemiology , Hypertension/epidemiology , Adult , Biomarkers/blood , China/epidemiology , Comorbidity , Disease Outbreaks , Female , Heart Diseases/epidemiology , Hospitalization , Humans , Male , Middle Aged , Prognosis , SARS-CoV-2/pathogenicity
19.
Curr Drug Targets ; 22(16): 1832-1843, 2021.
Article in English | MEDLINE | ID: covidwho-1511929

ABSTRACT

ACE2 has long been known as an injury protective protein, which can protect against a variety of organ damage such as the heart, liver, kidney, and lung. Especially in cardiovascular diseases, as a negative regulator of RAAS, ACE2 is an extremely important protective factor that mainly plays a role by converting Ang II to Ang-(1-7). Nevertheless, with the recent outbreak of COVID-19, it is exposed that another identity of ACE2 is the entry receptor for SARS-CoV-2, which previously serves as the entry receptor for SARS. With the in-depth clinical research, it is found that the severity and susceptibility of COVID-19 are related to cardiovascular diseases, and SARS-CoV-2 binding to ACE2 receptor is also potentially associated with heart injury symptoms. Therefore, in this article, we mainly summarize the relationship between ACE2, COVID-19, and cardiovascular diseases/heart injury.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19 , Cardiovascular Diseases , Heart Injuries , COVID-19/pathology , Cardiovascular Diseases/virology , Heart Injuries/virology , Humans
20.
Hamostaseologie ; 41(5): 356-364, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1483185

ABSTRACT

Cardiovascular manifestations are frequent in COVID-19 infection and are predictive of adverse outcomes. Elevated cardiac biomarkers are common findings in patients with cardiovascular comorbidities and severe COVID-19 infection. Troponin, inflammatory and thrombotic markers may also improve risk prediction in COVID-19. In our comprehensive review, we provide an overview of the incidence, potential mechanisms and outcome of acute cardiac injury in COVID-19. Thereby, we discuss coagulation abnormalities in sepsis and altered immune response as contributing factors favoring myocardial injury. We further highlight the role of endothelial damage in the pathophysiological concepts. Finally, observational studies addressing the incidence of myocardial infarction during COVID-19 pandemic are discussed.


Subject(s)
COVID-19/epidemiology , Heart Injuries/epidemiology , Myocardial Infarction/epidemiology , Pandemics , SARS-CoV-2 , Biomarkers/blood , COVID-19/blood , COVID-19/mortality , Comorbidity , Heart Injuries/blood , Heart Injuries/mortality , Humans , Incidence , Models, Cardiovascular , Myocardial Infarction/blood , Myocardial Infarction/mortality , SARS-CoV-2/pathogenicity , Troponin/blood
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