Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 27
Filter
1.
Viruses ; 13(12)2021 12 13.
Article in English | MEDLINE | ID: covidwho-1572665

ABSTRACT

The SARS-CoV-2 pandemic has mobilized many efforts worldwide to curb its impact on morbidity and mortality. Vaccination of the general population has resulted in the administration of more than 6,700,000,000 doses by the end of October 2021, which is the most effective method to prevent hospitalization and death. Among the adverse effects described, myocarditis and pericarditis are low-frequency events (less than 10 per 100,000 people), mainly observed with messenger RNA vaccines. The mechanisms responsible for these effects have not been specified, considering an exacerbated and uncontrolled immune response and an autoimmune response against specific cardiomyocyte proteins. This greater immunogenicity and reactogenicity is clinically manifested in a differential manner in pediatric patients, adults, and the elderly, determining specific characteristics of its presentation for each age group. It generally develops as a condition of mild to moderate severity, whose symptoms and imaging findings are self-limited, resolving favorably in days to weeks and, exceptionally, reporting deaths associated with this complication. The short- and medium-term prognosis is favorable, highlighting the lack of data on long-term evolution, which should be determined in longer follow-ups.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , Cardiomyopathies/etiology , Adolescent , Aged , Cardiomyopathies/epidemiology , Cardiomyopathies/pathology , Hospitalization , Humans , Immunogenicity, Vaccine , Male , Myocarditis/epidemiology , Myocarditis/etiology , Myocarditis/pathology , Pericarditis/epidemiology , Pericarditis/etiology , Pericarditis/pathology , Prognosis , SARS-CoV-2 , Vaccination
7.
Curr Probl Cardiol ; 46(10): 100926, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1293689

ABSTRACT

The effects of COVID-19 on the cardiovascular system remains understudied given the early stage of the pandemic. Several case series and case reports have been published on COVID-19 related cardiomyopathies; however, there is often a lack of baseline echocardiographic data confirming a normal cardiac health prior to infection. Here we examine four patients with preserved left ventricular systolic function on prior echocardiogram who developed de novo cardiomyopathies which following COVID-19 infection. The study comprised of four individuals with an average age of 80.5 years, 75% of which were white males. 50% of cases were suspected to have Takotsubo CM vs. myocarditis while the remaining half were diagnosed as myocarditis. Left ventricular systolic function dropped from a normal range to an average of 30% during COVID-19 infection in these individuals. Moreover, half of the cases later died. In conclusion, the COVID-19 pandemic has demonstrated its ability to cause several serious cardiovascular complications with associated worsening of prognosis. Repeat TTE showed recovery of systolic function in 50% of the patients included. There does not appear to be any correlation between COVID-19 related treatments, age, or level of inflammatory markers in those who recovered systolic function versus those who remained depressed. Given the minimal literature on this topic, it is evident more information is needed to help advance treatment and understanding of COVID-19 induced cardiomyopathies; particularly if the vaccination fails to protect against novel strains of COVID-19 and the virus becomes endemic.


Subject(s)
COVID-19 , Cardiomyopathies , Aged, 80 and over , Cardiomyopathies/diagnosis , Cardiomyopathies/epidemiology , Cardiomyopathies/etiology , Echocardiography , Humans , Male , Pandemics , SARS-CoV-2
8.
Physiol Rev ; 101(4): 1745-1807, 2021 10 01.
Article in English | MEDLINE | ID: covidwho-1216831

ABSTRACT

The prevalence of heart failure is on the rise and imposes a major health threat, in part, due to the rapidly increased prevalence of overweight and obesity. To this point, epidemiological, clinical, and experimental evidence supports the existence of a unique disease entity termed "obesity cardiomyopathy," which develops independent of hypertension, coronary heart disease, and other heart diseases. Our contemporary review evaluates the evidence for this pathological condition, examines putative responsible mechanisms, and discusses therapeutic options for this disorder. Clinical findings have consolidated the presence of left ventricular dysfunction in obesity. Experimental investigations have uncovered pathophysiological changes in myocardial structure and function in genetically predisposed and diet-induced obesity. Indeed, contemporary evidence consolidates a wide array of cellular and molecular mechanisms underlying the etiology of obesity cardiomyopathy including adipose tissue dysfunction, systemic inflammation, metabolic disturbances (insulin resistance, abnormal glucose transport, spillover of free fatty acids, lipotoxicity, and amino acid derangement), altered intracellular especially mitochondrial Ca2+ homeostasis, oxidative stress, autophagy/mitophagy defect, myocardial fibrosis, dampened coronary flow reserve, coronary microvascular disease (microangiopathy), and endothelial impairment. Given the important role of obesity in the increased risk of heart failure, especially that with preserved systolic function and the recent rises in COVID-19-associated cardiovascular mortality, this review should provide compelling evidence for the presence of obesity cardiomyopathy, independent of various comorbid conditions, underlying mechanisms, and offer new insights into potential therapeutic approaches (pharmacological and lifestyle modification) for the clinical management of obesity cardiomyopathy.


Subject(s)
Cardiomyopathies/etiology , Cardiomyopathies/pathology , Obesity/complications , COVID-19/complications , COVID-19/mortality , Cardiomyopathies/mortality , Humans , Obesity/etiology , Obesity/genetics , SARS-CoV-2
9.
Clin Chem ; 67(8): 1080-1089, 2021 08 05.
Article in English | MEDLINE | ID: covidwho-1189445

ABSTRACT

BACKGROUND: Limited data exist on high-sensitivity cardiac troponin (hs-cTn) for risk-stratification in COVID-19. METHODS: We conducted a multicenter, retrospective, observational, US-based study of COVID-19 patients undergoing hs-cTnT. Outcomes included short-term mortality (in-hospital and 30-days post-discharge) and a composite of major adverse events, including respiratory failure requiring mechanical ventilation, cardiac arrest, and shock within the index presentation and/or mortality during the index hospitalization or within 30-days post-discharge. RESULTS: Among 367 COVID-19 patients undergoing hs-cTnT, myocardial injury was identified in 46%. They had a higher risk for mortality (20% vs 12%, P < 0.0001; unadjusted HR 4.44, 95% CI 2.13-9.25, P < 0.001) and major adverse events (35% vs. 11%, P < 0.0001; unadjusted OR 4.29, 95% CI 2.50-7.40, P < 0.0001). Myocardial injury was associated with major adverse events (adjusted OR 3.84, 95% CI 2.00-7.36, P < 0.0001) but not mortality. Baseline (adjusted OR 1.003, 95% CI 1.00-1.007, P = 0.047) and maximum (adjusted OR 1.005, 95% CI 1.001-1.009, P = 0.0012) hs-cTnT were independent predictors of major adverse events. Most (95%) increases were due to myocardial injury, with 5% (n = 8) classified as type 1 or 2 myocardial infarction. A single hs-cTnT <6 ng/L identified 26% of patients without mortality, with a 94.9% (95% CI 87.5-98.6) negative predictive value and 93.1% sensitivity (95% CI 83.3-98.1) for major adverse events in those presenting to the ED. CONCLUSIONS: Myocardial injury is frequent and prognostic in COVID-19. While most hs-cTnT increases are modest and due to myocardial injury, they have important prognostic implications. A single hs-cTnT <6 ng/L at presentation may facilitate the identification of patients with a favorable prognosis.


Subject(s)
COVID-19/diagnosis , Cardiomyopathies/diagnosis , Myocardial Infarction/diagnosis , Troponin T/blood , Biomarkers/blood , COVID-19/complications , COVID-19/epidemiology , Cardiomyopathies/blood , Cardiomyopathies/etiology , Cohort Studies , Female , Humans , Male , Middle Aged , Myocardial Infarction/blood , Myocardial Infarction/etiology , Pandemics , Prognosis , Retrospective Studies , Risk Assessment , SARS-CoV-2
10.
Intern Emerg Med ; 16(7): 1779-1785, 2021 10.
Article in English | MEDLINE | ID: covidwho-1126620

ABSTRACT

BACKGROUND: Lung ultrasound (LU) is a useful tool for monitoring lung involvement in novel coronavirus (COVID) disease, while information on echocardiographic findings in COVID disease is to date scarce and heterogeneous. We hypothesized that lung and cardiac ultrasound examinations, serially and simultaneously performed, could monitor disease severity in COVID-related ARDS. METHODS: We enrolled 47 consecutive patients with COVID-related ARDS (1st March-31st May 2020). Lung and cardiac ultrasounds were performed on admission, at discharged and when clinically needed. RESULTS: Most patients were mechanically ventilated (75%) and veno-venous extracorporeal membrane oxygenation was needed in ten patients (21.2%). The in-ICU mortality rate was 27%%. On admission, not survivors showed a higher LUS score (p = 0.006) and a higher incidence of consolidations (p = 0.003), lower values of LVEF (p = 0.027) and a higher RV/LV ratio (0.008). At discharge, a significant reduction in the incidence of subpleural consolidations (p < 0.001) and, thus, in LUS score (p < 0.001) and an increase in patter A findings (p < 0.001) together with reduced systolic pulmonary arterial pressures were detectable. In not survivors at final examination, an increased in LUS score (p < 0.001), and in RV/LV ratio (p < 0.001) associated with a reduction in TAPSE (p = 0.013) were observed. A significant correlation was observed between LUS and systolic pulmonary arterial pressure (p = 0.04). LUS and RV/LV resulted independent predictors of in-ICU death. CONCLUSIONS: In COVID-related ARDS, the combined lung and cardiac ultrasound proved to be an useful clinical tool in monitoring disease progression and in identifying parameters (LU score and RV/LV ratio) able to risk stratifying these patients.


Subject(s)
COVID-19/diagnostic imaging , Cardiomyopathies/diagnostic imaging , Respiratory Distress Syndrome/diagnostic imaging , COVID-19/complications , Cardiomyopathies/etiology , Humans , Lung/diagnostic imaging , Respiratory Distress Syndrome/etiology , Severity of Illness Index , Ultrasonography/methods
11.
Curr Heart Fail Rep ; 18(3): 163-168, 2021 06.
Article in English | MEDLINE | ID: covidwho-1118277

ABSTRACT

PURPOSE OF REVIEW: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in the coronavirus 2019 (COVID-19) global pandemic. While primarily a respiratory virus, SARS-CoV-2 can cause myocardial injury. The pattern of injury, referred to as acute COVID-19 cardiovascular syndrome (ACovCS), is defined by cardiac troponin leak in the absence of obstructive coronary artery disease. Although the etiology of the injury is unknown, many speculate that a cytokine release syndrome (CRS) may be an important factor. We aim to review recent data concerning markers of cardiac injury in ACovCS and its relation to the CRS. RECENT FINDINGS: Cardiac injury was common in patients hospitalized for COVID-19, with both cardiac troponin and B-type natriuretic peptide (BNP) being elevated in this population. Biomarkers were correlated with illness severity and increased mortality. Cytokines such as IL-6 were more often elevated in patients with ACovCS. Myocarditis evident on cardiac MR following COVID-19 may be associated with cardiac troponin levels. The impact of dexamethasone and remdesivir, two therapies shown to have clinical benefit in COVID-19, on myocardial injury is unknown. Biomarkers of cardiac stress and injury in COVID-19 may be used to stratify risk in the future. Currently, there is no evidence that inhibition of cytokine release will reduce myocardial injury in patients with COVID-19.


Subject(s)
COVID-19 , Cardiomyopathies , Cytokine Release Syndrome/blood , Natriuretic Peptide, Brain/analysis , Troponin/analysis , Biomarkers/analysis , COVID-19/complications , COVID-19/immunology , Cardiomyopathies/blood , Cardiomyopathies/etiology , Humans , SARS-CoV-2
12.
J Cardiovasc Magn Reson ; 23(1): 14, 2021 02 25.
Article in English | MEDLINE | ID: covidwho-1102339

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) induces myocardial injury, either direct myocarditis or indirect injury due to systemic inflammatory response. Myocardial involvement has been proved to be one of the primary manifestations of COVID-19 infection, according to laboratory test, autopsy, and cardiovascular magnetic resonance (CMR). However, the middle-term outcome of cardiac involvement after the patients were discharged from the hospital is yet unknown. The present study aimed to evaluate mid-term cardiac sequelae in recovered COVID-19 patients by CMR METHODS: A total of 47 recovered COVID-19 patients were prospectively recruited and underwent CMR examination. The CMR protocol consisted of black blood fat-suppressed T2 weighted imaging, T2 star mapping, left ventricle (LV) cine imaging, pre- and post-contrast T1 mapping, and late gadolinium enhancement (LGE). LGE were assessed in mixed both recovered COVID-19 patients and healthy controls. The LV and right ventricle (RV) function and LV mass were assessed and compared with healthy controls. RESULTS: A total of 44 recovered COVID-19 patients and 31 healthy controls were studied. LGE was found in 13 (30%) of COVID-19 patients. All LGE lesions were located in the mid myocardium and/or sub-epicardium with a scattered distribution. Further analysis showed that LGE-positive patients had significantly decreased LV peak global circumferential strain (GCS), RV peak GCS, RV peak global longitudinal strain (GLS) as compared to non-LGE patients (p < 0.05), while no difference was found between the non-LGE patients and healthy controls. CONCLUSION: Myocardium injury existed in 30% of COVID-19 patients. These patients have depressed LV GCS and peak RV strains at the 3-month follow-up. CMR can monitor the COVID-19-induced myocarditis progression, and CMR strain analysis is a sensitive tool to evaluate the recovery of LV and RV dysfunction.


Subject(s)
COVID-19/complications , Cardiomyopathies/diagnostic imaging , Cardiomyopathies/etiology , Magnetic Resonance Imaging/methods , COVID-19/pathology , Female , Follow-Up Studies , Heart/diagnostic imaging , Humans , Male , Middle Aged , Myocardium/pathology , Prospective Studies , SARS-CoV-2
13.
Am J Obstet Gynecol MFM ; 2(2): 100113, 2020 05.
Article in English | MEDLINE | ID: covidwho-1064728

ABSTRACT

At our institution, 2 of the initial 7 pregnant patients with confirmed coronavirus disease 2019 severe infection (28.6%; 95% CI, 8.2%-64.1%) developed cardiac dysfunction with moderately reduced left ventricular ejection fractions of 40%-45% and hypokinesis. Viral myocarditis and cardiomyopathy have also been reported in nonpregnant coronavirus disease 2019 patients. A case series of nonpregnant patients with coronavirus disease 2019 found that 33% of those in intensive care developed cardiomyopathy. More data are needed to ascertain the incidence of cardiomyopathy from coronavirus disease 2019 in pregnancy, in all pregnant women with coronavirus disease 2019, and those with severe disease (eg, pneumonia). We suggest an echocardiogram in pregnant women with coronavirus disease 2019 pneumonia, in particular those necessitating oxygen, or those who are critically ill, and we recommend the use of handheld, point-of-care devices where possible to minimize contamination of staff and traditional large echocardiogram machines.


Subject(s)
COVID-19/therapy , Cardiomyopathies/therapy , Cesarean Section , Heart Failure/therapy , Pregnancy Complications, Cardiovascular/therapy , Pregnancy Complications, Infectious/therapy , Respiration, Artificial , Adult , Anti-Arrhythmia Agents/therapeutic use , Antibodies, Monoclonal, Humanized/therapeutic use , Anticonvulsants/therapeutic use , Blood Gas Analysis , COVID-19/complications , COVID-19/diagnosis , COVID-19/physiopathology , COVID-19 Nucleic Acid Testing , Cardiomyopathies/diagnosis , Cardiomyopathies/etiology , Cardiomyopathies/physiopathology , Diabetes, Gestational , Diuretics/therapeutic use , Echocardiography , Enzyme Inhibitors/therapeutic use , Female , Fever , Furosemide/therapeutic use , Heart Arrest/etiology , Heart Arrest/therapy , Heart Failure/diagnosis , Heart Failure/etiology , Heart Failure/physiopathology , Humans , Hydroxychloroquine/therapeutic use , Hypoxia/etiology , Hypoxia/therapy , Intubation, Intratracheal , Magnesium Sulfate/therapeutic use , Metoprolol/therapeutic use , Middle Aged , Obesity, Maternal/complications , Oxygen Inhalation Therapy , Point-of-Care Systems , Pre-Eclampsia/drug therapy , Pre-Eclampsia/physiopathology , Pregnancy , Pregnancy Complications, Cardiovascular/diagnosis , Pregnancy Complications, Cardiovascular/physiopathology , Pregnancy Complications, Infectious/diagnosis , Pregnancy Complications, Infectious/physiopathology , Return of Spontaneous Circulation , SARS-CoV-2 , Severity of Illness Index , Stroke Volume , Tachycardia/drug therapy , Tachycardia/physiopathology , Tachycardia, Supraventricular/drug therapy , Tachycardia, Supraventricular/etiology
14.
ESC Heart Fail ; 8(1): 37-46, 2021 02.
Article in English | MEDLINE | ID: covidwho-1064350

ABSTRACT

AIMS: COVID-19, a respiratory viral disease causing severe pneumonia, also affects the heart and other organs. Whether its cardiac involvement is a specific feature consisting of myocarditis, or simply due to microvascular injury and systemic inflammation, is yet unclear and presently debated. Because myocardial injury is also common in other kinds of pneumonias, we investigated and compared such occurrence in severe pneumonias due to COVID-19 and other causes. METHODS AND RESULTS: We analysed data from 156 critically ill patients requiring mechanical ventilation in four European tertiary hospitals, including all n = 76 COVID-19 patients with severe disease course requiring at least ventilatory support, matched to n = 76 from a retrospective consecutive patient cohort of severe pneumonias of other origin (matched for age, gender, and type of ventilator therapy). When compared to the non-COVID-19, mortality (COVID-19 = 38.2% vs. non-COVID-19 = 51.3%, P = 0.142) and impairment of systolic function were not significantly different. Surprisingly, myocardial injury was even more frequent in non-COVID-19 (96.4% vs. 78.1% P = 0.004). Although inflammatory activity [C-reactive protein (CRP) and interleukin-6] was indifferent, d-dimer and thromboembolic incidence (COVID-19 = 23.7% vs. non-COVID-19 = 5.3%, P = 0.002) driven by pulmonary embolism rates (COVID-19 = 17.1% vs. non-COVID-19 = 2.6%, P = 0.005) were higher. CONCLUSIONS: Myocardial injury was frequent in severe COVID-19 requiring mechanical ventilation, but still less frequent than in similarly severe pneumonias of other origin, indicating that cardiac involvement may not be a specific feature of COVID-19. While mortality was also similar, COVID-19 is characterized with increased thrombogenicity and high pulmonary embolism rates.


Subject(s)
COVID-19/complications , Cardiomyopathies/etiology , Acute Disease , Aged , COVID-19/mortality , COVID-19/therapy , Cardiomyopathies/mortality , Case-Control Studies , Female , Humans , Intensive Care Units/statistics & numerical data , Length of Stay/statistics & numerical data , Male , Myocarditis/etiology , Myocarditis/mortality , Pneumonia/complications , Respiration, Artificial , Retrospective Studies , Tertiary Care Centers
15.
BMC Infect Dis ; 21(1): 33, 2021 Jan 07.
Article in English | MEDLINE | ID: covidwho-1035153

ABSTRACT

BACKGROUND: Septic cardiomyopathy has been observed in association with influenza, indicating that not only bacteria but also other infective agents can cause this condition. There has been no systematic study as to whether Treponema pallidum infection induces septic cardiomyopathy, and we are the first to report this possibility. CASE PRESENTATION: We report two cases of a 48-year-old man and a 57-year-old man who were diagnosed with syphilis-related septic cardiomyopathy. The diagnosis of cardiomyopathy was made based on elevation of cardiogenic markers and decrease in ejection fraction evaluated by echocardiography. Screen for infective pathogens was negative except for syphilis, which supported our diagnosis. The two patients recovered following effective anti-syphilis treatment and advanced life support technology. Syphilis serology became negative after treatment. CONCLUSION: Syphilis has the potential to cause septic cardiomyopathy. Clinicians should consider Treponema pallidum in cases of septic cardiomyopathy with unknown pathogens. However, the specific pathophysiological mechanism of syphilis-associated septic cardiomyopathy has not been elucidated, and more specific studies are needed.


Subject(s)
Bacteremia/etiology , Cardiomyopathies/etiology , Syphilis/complications , Anti-Bacterial Agents/therapeutic use , Bacteremia/complications , Bacteremia/drug therapy , Biomarkers/blood , Cardiomyopathies/diagnosis , Cardiomyopathies/microbiology , Echocardiography , Humans , Imipenem/therapeutic use , Male , Middle Aged , Syphilis/diagnosis , Syphilis/drug therapy , Syphilis Serodiagnosis , Treponema pallidum/immunology
16.
BMJ Open ; 11(1): e046575, 2021 01 08.
Article in English | MEDLINE | ID: covidwho-1015692

ABSTRACT

INTRODUCTION: Acute myocardial injury in patients with COVID-19 infection has been recognised as one important complication associated with in-hospital mortality. The potential dose-response effect of cardiac troponin (cTn) concentrations on adverse clinical outcomes has not been systematically studied. Hence, we will conduct a comprehensive dose-response meta-analysis to quantitatively evaluate the relationship between elevated cTn concentrations and in-hospital adverse clinical outcomes in patients with COVID-19. METHODS: We will search PubMed, EMBASE, Cochrane Library and ISI Knowledge via Web of Science databases, as well as preprint databases (medRxiv and bioRxiv), from inception to October 2021, to identify all retrospective and prospective cohorts and randomised controlled studies using related keywords. The primary outcome will be all-cause mortality during hospitalisation. The secondary outcome will be major adverse event (MAE). To conduct a dose-response meta-analysis of the potential linear or restricted cubic spline regression relationship between elevated cTn concentrations and all-cause mortality or MAE, studies with three or more categories of cTn concentrations will be included. Univariable or multivariable meta-regression and subgroup analyses will be conducted to compare elevated and non-elevated categories of cTn concentration. Sensitivity analyses will be used to assess the robustness of our results by removing each included study at one time to obtain and evaluate the remaining overall estimates of all-cause mortality or MAE. ETHICS AND DISSEMINATION: In accordance with the Institutional Review Board/Independent Ethics Committee of Fuwai Hospital, ethical approval was waived for this systematic review protocol. This meta-analysis will be disseminated through a peer-reviewing process for journal publication and conference communication. PROSPERO REGISTRATION NUMBER: CRD42020216059.


Subject(s)
COVID-19/blood , Cardiomyopathies/blood , Cardiomyopathies/etiology , Research Design , Systematic Reviews as Topic/methods , Troponin C/blood , COVID-19/mortality , Cardiomyopathies/mortality , Hospital Mortality , Humans , Predictive Value of Tests , Prognosis
18.
Am J Clin Pathol ; 155(6): 793-801, 2021 05 18.
Article in English | MEDLINE | ID: covidwho-975194

ABSTRACT

OBJECTIVES: To present an index case and review the histologic and electron microscopic findings in chloroquine (CQ) and hydroxychloroquine (HCQ) myopathy, focusing primarily on cardiomyopathy. CQ and HCQ are antimalarial drugs with disease-modifying activity in rheumatic diseases (DMARD) and now are among the most widely used DMARDs. Although they are rare, severe adverse effects caused mainly by deposition of intracellular metabolites in both cardiac and skeletal muscle have been described. Currently, both CQ and HCQ have been proposed to have efficacy for patients with coronavirus disease 2019, and several large centers in the United States and other countries have started clinical trials. METHODS: A case of HCQ cardiotoxicity diagnosed on an endomyocardial biopsy is presented. A review of the pathology archives was performed to identify additional cases of CQ or HCQ myopathy, and histologic changes were recorded. A brief literature review with an emphasis on pathologic findings in myopathies was performed. RESULTS: Including the index case, 4 cases of CQ or HCQ myopathy were identified. Light microscopic findings included vacuolated myopathy, and electron microscopic findings included myeloid bodies and curvilinear inclusion bodies. CONCLUSION: CQ and HCQ myopathy can present following long-term administration of the drug. The pathologic findings are nonspecific and overlap with other vacuolated myopathies, necessitating careful correlation of the histologic changes with the patient's medical history.


Subject(s)
Antimalarials/adverse effects , COVID-19/drug therapy , Cardiomyopathies/etiology , Chloroquine/adverse effects , Hydroxychloroquine/adverse effects , Antimalarials/therapeutic use , Antiviral Agents/adverse effects , Antiviral Agents/therapeutic use , COVID-19/diagnosis , Chloroquine/pharmacology , Humans , Hydroxychloroquine/pharmacology
19.
J Clin Lab Anal ; 35(1): e23654, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-932443

ABSTRACT

BACKGROUND: Geriatric patients with coronavirus disease (COVID-19) are at high risk of developing cardiac injury. Identifying the factors that affect high-sensitivity cardiac troponin I may indicate the cause of cardiac injury in elderly patients, and this could hopefully assist in protecting heart function in this patient population. METHODS: One hundred and eighty inpatients who were admitted for COVID-19 were screened. Patients older than 60 years were included in this study, and the clinical characteristics and laboratory results of the cohort were analyzed. The correlation between cardiac injury and clinical/laboratory variables was statistically analyzed, and further logistic regression was performed to determine how these variables influence cardiac injury in geriatric patients. RESULTS: Age (p < 0.001) significantly correlated with cardiac injury, whereas sex (p = 0.372) and coexisting diseases did not. Rising procalcitonin (p = 0.001), interleukin-2 receptor (p < 0.001), interleukin 6 (p = 0.001), interleukin 10 (p < 0.001), tumor necrosis factor α (p = 0.001), high-sensitivity C-reactive protein (p = 0.001), D-dimer (p < 0.001), white blood cells (p < 0.001), neutrophils (p = 0.001), declining lymphocytes (p < 0.001), and natural killer cells (p = 0.005) were associated with cardiac injury and showed predictive ability in the multivariate logistic regression. CONCLUSION: Our results suggest that age and inflammatory factors influence cardiac injury in elderly patients. Interfering with inflammation in this patient population may potentially confer cardiac protection.


Subject(s)
COVID-19/complications , Cardiomyopathies/virology , Aged , Aged, 80 and over , COVID-19/blood , Cardiomyopathies/etiology , Creatine Kinase/blood , Humans , Inflammation Mediators/blood , Killer Cells, Natural , L-Lactate Dehydrogenase/blood , Male , Middle Aged , Myocarditis/etiology , Myocarditis/virology , Natriuretic Peptide, Brain/blood , Peptide Fragments/blood , Risk Factors , Troponin T/blood
20.
Life Sci ; 262: 118510, 2020 Dec 01.
Article in English | MEDLINE | ID: covidwho-800007

ABSTRACT

SARS-CoV-2 is responsible for the 2019 coronavirus disease (COVID-19), a global pandemic that began in March 2020 and is currently in progress. To date, COVID-19 has caused about 935,000 deaths in more than 200 countries. The respiratory system is most affected by injuries caused by COVID-19, but other organs may be involved, including the cardiovascular system. SARS-CoV-2 penetrates host cells through the angiotensin 2 conversion enzyme (ACE-2). ACE-2 is expressed not only in the lungs, but also in other organs, including the cardiovascular system. Several studies have found that a good percentage of patients with severe COVID-19 have cardiac lesions, including myocardial fibrosis, edema and pericarditis. Pathological remodeling of the extracellular matrix caused by viral infection leads to myocardial fibrotic lesions. These fibrotic scars can cause cardiac dysfunction, reducing the ejection fraction caused by the presence of stiffened myocardial matrix, or cardiac arrhythmias that cause an alteration in the electrical conduction system of the heart. These cardiac dysfunctions can cause death. It is therefore essential to identify cardiac involvement early in order to act with appropriate therapeutic treatments. In this review, we describe what is known about cardiac injury from COVID-19, highlighting effective pharmacological therapeutic solutions to combat cardiac injury, particularly cardiac fibrosis, caused by COVID-19.


Subject(s)
COVID-19/complications , COVID-19/drug therapy , Cardiomyopathies/drug therapy , Cardiomyopathies/etiology , SARS-CoV-2/pathogenicity , Angiotensin-Converting Enzyme 2/physiology , COVID-19/physiopathology , Humans , Pandemics , SARS-CoV-2/drug effects
SELECTION OF CITATIONS
SEARCH DETAIL