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European Heart Journal. Acute... Sep 2020Coronavirus disease 2019 (COVID-19) is a global pandemic impacting 213 countries/territories and more than 5,934,936 patients worldwide. Cardiac injury has been reported... (Meta-Analysis)
Meta-Analysis
Cardiac injury is associated with severe outcome and death in patients with Coronavirus disease 2019 (COVID-19) infection: A systematic review and meta-analysis of observational studies.
Coronavirus disease 2019 (COVID-19) is a global pandemic impacting 213 countries/territories and more than 5,934,936 patients worldwide. Cardiac injury has been reported to occur in severe and death cases. This meta-analysis was done to summarize available findings on the association between cardiac injury and severity of COVID-19 infection. Online databases including Scopus, PubMed, Web of Science, Cochrane Library and Google Scholar were searched to detect relevant publications up to 20 May 2020, using relevant keywords. To pool data, a fixed- or random-effects model was used depending on the heterogeneity between studies. In total, 22 studies with 3684 COVID-19 infected patients (severe cases=1095 and death cases=365) were included in this study. Higher serum levels of lactate dehydrogenase (weighted mean difference (WMD) =108.86 U/L, 95% confidence interval (CI)=75.93-141.79, <0.001) and creatine kinase-MB (WMD=2.60 U/L, 95% CI=1.32-3.88, <0.001) were associated with a significant increase in the severity of COVID-19 infection. Furthermore, higher serum levels of lactate dehydrogenase (WMD=213.44 U/L, 95% CI=129.97-296.92, <0.001), cardiac troponin I (WMD=26.35 pg/mL, 95% CI=14.54-38.15, <0.001), creatine kinase (WMD=48.10 U/L, 95% CI=0.27-95.94, = 0.049) and myoglobin (WMD=159.77 ng/mL, 95% CI=99.54-220.01, <0.001) were associated with a significant increase in the mortality of COVID-19 infection. Cardiac injury, as assessed by serum analysis (lactate dehydrogenase, cardiac troponin I, creatine kinase (-MB) and myoglobin), was associated with severe outcome and death from COVID-19 infection.
Topics: Betacoronavirus; Biomarkers; COVID-19; Coronavirus Infections; Creatine Kinase, MB Form; Heart Diseases; Humans; Myocardium; Observational Studies as Topic; Pandemics; Pneumonia, Viral; SARS-CoV-2; Troponin I
PubMed: 32567326
DOI: 10.1177/2048872620937165 -
BMC Cardiovascular Disorders Dec 2021The majority of studies evaluating the effect of myocardial injury on the survival of COVID-19 patients have been performed outside of the United States (U.S.). These... (Meta-Analysis)
Meta-Analysis
INTRODUCTION
The majority of studies evaluating the effect of myocardial injury on the survival of COVID-19 patients have been performed outside of the United States (U.S.). These studies have often utilized definitions of myocardial injury that are not guideline-based and thus, not applicable to the U.S.
METHODS
The current study is a two-part investigation of the effect of myocardial injury on the clinical outcome of patients hospitalized with COVID-19. The first part is a retrospective analysis of 268 patients admitted to our healthcare system in Toledo, Ohio, U.S.; the second part is a systematic review and meta-analysis of all similar studies performed within the U.S.
RESULTS
In our retrospective analysis, patients with myocardial injury were older (mean age 73 vs. 59 years, P 0.001), more likely to have hypertension (86% vs. 67%, P 0.005), underlying cardiovascular disease (57% vs. 24%, P 0.001), and chronic kidney disease (26% vs. 10%, P 0.004). Myocardial injury was also associated with a lower likelihood of discharge to home (35% vs. 69%, P 0.001), and a higher likelihood of death (33% vs. 10%, P 0.001), acute kidney injury (74% vs. 30%, P 0.001), and circulatory shock (33% vs. 12%, P 0.001). Our meta-analysis included 12,577 patients from 8 U.S. states and 55 hospitals who were hospitalized with COVID-19, with the finding that myocardial injury was significantly associated with increased mortality (HR 2.43, CI 2.28-3.6, P 0.0005). The prevalence of myocardial injury ranged from 9.2 to 51%, with a mean prevalence of 27.2%.
CONCLUSION
Hospitalized COVID-19 patients in the U.S. have a high prevalence of myocardial injury, which was associated with poorer survival and outcomes.
Topics: Aged; COVID-19; Cardiovascular Diseases; Female; Hospitalization; Humans; Male; Middle Aged; Myocardial Infarction; Ohio; Prognosis; Renal Insufficiency, Chronic; Retrospective Studies; SARS-CoV-2; Troponin I
PubMed: 34972516
DOI: 10.1186/s12872-021-02450-3 -
The Canadian Journal of Cardiology Mar 2023Chest pain is a common cause for emergency department (ED) presentations. After myocardial infarction (MI) has been ruled out by means of electrocardiography and... (Review)
Review
BACKGROUND
Chest pain is a common cause for emergency department (ED) presentations. After myocardial infarction (MI) has been ruled out by means of electrocardiography and troponin testing, decisions around anatomic or functional testing may be informed by clinical risk scores. We conducted a systematic review to synthesize evidence of the prognostic performance of chest pain risk scores among ED patients who have had MI ruled out by means of a high-sensitivity troponin assay.
METHODS
We queried multiple databases from inception to May 17, 2022. We included studies that quantified risk of 30-day major adverse cardiac events (MACE), at different cutoffs of clinical risk scores, among adult patients who had MI ruled out by means of a high-sensitivity troponin assay. Prognostic performance of each score was synthesized and described, but meta-analysis was not possible.
RESULTS
Six studies met inclusion criteria. Short-term MACE risk among patients who had MI ruled out by means of high-sensitivity cardiac troponin assays was very low. The HEART score, with a cutoff of 3 or less, predicted a very low risk of MACE among the greatest proportion of patients. Other scores had lower sensitivity or classified fewer patients as low risk.
CONCLUSIONS
The HEART score with a cutoff value of 3 or less accurately identified the greatest number of patients at low risk of 30-day MACE. However, MACE risk among patients who have MI ruled out by means of high-sensitivity troponin testing is sufficiently low that clinical risk stratification or noninvasive testing may be of little additional value in identifying patients with coronary disease.
Topics: Adult; Humans; Myocardial Infarction; Chest Pain; Risk Factors; Troponin; Emergency Service, Hospital; Electrocardiography; Risk Assessment; Acute Coronary Syndrome
PubMed: 36641050
DOI: 10.1016/j.cjca.2022.12.028 -
Medicine Dec 2016Interest in the use of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) has expanded from diagnosis of acute myocardial infarction to risk assessment for... (Meta-Analysis)
Meta-Analysis
Interest in the use of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) has expanded from diagnosis of acute myocardial infarction to risk assessment for morbidity and mortality. Although cTnT and cTnI were shown to have equivalent diagnostic performance in the setting of suspected acute myocardial infarction, potential prognostic differences are largely unexplored.The aim of this study is to quantify and compare the relationship between cTnT and cTnI, and cardiovascular and all-cause mortality in the general population.Medline, Embase, and the Cochrane Library (from inception through October 2016) were searched for prospective observational cohort studies reporting on the prognostic value of basal high-sensitive cTnT and/or cTnI levels on cardiovascular and all-cause mortality in the general population. Data on study characteristics, participants' characteristics, outcome parameters, and quality [according to the Effective Public Health Practice Project (EPHPP) "Quality Assessment Tool For Quantitative Studies] were retrieved. Hazard ratios per standard deviation increase in basal cardiac troponin level (HR per 1-SD; retrieved from the included articles or estimated) were pooled using a random-effects model.On a total of 2585 reviewed citations, 11 studies, with data on 65,019 participants, were included in the meta-analysis. Random effects pooling showed significant associations between basal cardiac troponin levels and HR for cardiovascular and all-cause mortality [HR per 1-SD 1.29 (95% confidence interval, 95% CI, 1.20-1.38) and HR per 1-SD 1.18 (95% CI, 1.11-1.26), respectively]. Stratified analyses showed higher HRs for cTnT than cTnI [cardiovascular mortality: cTnT HR per 1-SD 1.37 (95% CI, 1.23-1.52); and cTnI HR per 1-SD 1.21 (95% CI, 1.16-1.26); all-cause mortality: cTnT HR per 1-SD 1.31 (955 CI, 1.13-1.53); and cTnI HR per 1-SD 1.14 (95% CI, 1.06-1.22)]. These differences were significant (P < 0.01) in meta-regression analyses for cardiovascular mortality but did not reach statistical significance for all-cause mortality.Elevated, basal cTnT, and cTnI show robust associations with an increased risk of cardiovascular and all-cause mortality during follow-up in the general population.Systematic review registration number PROSPERO CRD42014006964.
Topics: Biomarkers; Cardiovascular Diseases; Humans; Mortality; Predictive Value of Tests; Prognosis; Risk Factors; Troponin I; Troponin T
PubMed: 28033267
DOI: 10.1097/MD.0000000000005703 -
European Heart Journal. Acute... Feb 2020The purpose of this study was to determine (a) the ability of serial high-sensitivity cardiac troponin T measurements to rule out acute myocardial infarction and (b) the... (Meta-Analysis)
Meta-Analysis
Serial high-sensitivity cardiac troponin T measurements to rule out acute myocardial infarction and a single high baseline measurement for swift rule-in: A systematic review and meta-analysis.
AIMS
The purpose of this study was to determine (a) the ability of serial high-sensitivity cardiac troponin T measurements to rule out acute myocardial infarction and (b) the ability of a single high baseline high-sensitivity cardiac troponin T measurement to rule in acute myocardial infarction in patients presenting to the emergency department with acute chest pain.
METHODS AND RESULTS
Embase, Medline, Cochrane, Web of Science and Google scholar were searched for prospective cohort studies that evaluated parameters of diagnostic accuracy of serial high-sensitivity cardiac troponin T to rule out acute myocardial infarction and a single baseline high-sensitivity cardiac troponin T value>50 ng/l to rule in acute myocardial infarction. The search yielded 21 studies for the systematic review, of which 14 were included in the meta-analysis, with a total of 11,929 patients and an overall prevalence of acute myocardial infarction of 13.0%. For rule-out, six studies presented the sensitivity of serial measurements <14 ng/l. This cut-off classified 60.1% of patients as rule-out and the summary sensitivity was 96.7% (95% confidence interval: 92.3-99.3). Three studies presented the sensitivity of a one-hour algorithm with a baseline high-sensitivity cardiac troponin T value<12 ng/l and delta 1 hour <3 ng/l. This algorithm classified 60.2% of patients as rule-out and the summary sensitivity was 98.9% (96.4-100). For rule-in, six studies reported the specificity of baseline high-sensitivity cardiac troponin T value>50 ng/l. The summary specificity was 94.6% (91.5-97.1).
CONCLUSION
Serial high-sensitivity cardiac troponin T measurement strategies to rule out acute myocardial infarction perform well, and a single baseline high-sensitivity cardiac troponin T value>50 ng/l to rule in acute myocardial infarction has a high specificity.
Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Algorithms; Chest Pain; Emergency Service, Hospital; Female; Humans; Male; Middle Aged; Myocardial Infarction; Prevalence; Prospective Studies; Sensitivity and Specificity; Troponin T
PubMed: 30618277
DOI: 10.1177/2048872618819421 -
The Western Journal of Emergency... Oct 2021The diagnosis of non-ST-elevated myocardial infarction (NSTEMI) depends on a combination of history, electrocardiogram, and cardiac biomarkers. The most sensitive and...
INTRODUCTION
The diagnosis of non-ST-elevated myocardial infarction (NSTEMI) depends on a combination of history, electrocardiogram, and cardiac biomarkers. The most sensitive and specific biomarkers for cardiac injury are the troponin assays. Many hospitals continue to automatically order less sensitive and less specific biomarkers such as creatine kinase (CK) alongside cardiac troponin (cTn) for workup of patients with chest pain. The objective of this systematic review was to identify whether CK testing is useful in the workup of patients with NSTEMI symptoms.
METHODS
We undertook a systematic review to ascertain whether CK ordered as part of the workup for NSTEMI was useful in screening patients with cardiac chest pain. The MEDLINE, Embase, and Cochrane databases were searched from January 1995-September 2020. Additional papers were added after consultation with experts. We screened a total of 2,865 papers, of which eight were included in the final analysis. These papers all compared CK and cTn for NSTEMI diagnosis.
RESULTS
In each of the eight papers included in the analysis, cTn showed a greater sensitivity and specificity than CK in the diagnosis of NSTEMI. Furthermore, none of the articles published reliable evidence that CK is useful in NSTEMI diagnosis when troponin was negative.
CONCLUSION
There is no evidence to continue to use CK as part of the workup of NSTEMI acute coronary syndrome in undifferentiated chest pain patients. We conclude that CK should not be used to screen patients presenting to the emergency department with chest pain.
Topics: Biomarkers; Chest Pain; Creatine Kinase; Electrocardiography; Humans; Non-ST Elevated Myocardial Infarction; Troponin; Troponin T
PubMed: 34787553
DOI: 10.5811/westjem.2020.11.47709 -
European Journal of Trauma and... Aug 2021Myocardial contusion can be a life-threatening condition in patients who sustained blunt thoracic trauma. The diagnostic approach remains a subject of debate. The aim of... (Meta-Analysis)
Meta-Analysis
PURPOSE
Myocardial contusion can be a life-threatening condition in patients who sustained blunt thoracic trauma. The diagnostic approach remains a subject of debate. The aim of this study was to determine the sensitivity and specificity of echocardiography, electrocardiography, troponins T and I (TnT and TnI), and creatine kinase muscle/brain (CK-MB) for identifying patients with a myocardial contusion following blunt thoracic trauma.
METHODS
Sensitivity and specificity were first determined in a 10-year retrospective cohort study and second by a systematic literature review with meta-analysis.
RESULTS
Of the 117 patients in the retrospective study, 44 (38%) were considered positive for myocardial contusion. Chest X-ray, chest CT scan, electrocardiograph, and echocardiography had poor sensitivity (< 15%) but good specificity (≥ 90%). Sensitivity to cardiac biomarkers measured at presentation ranged from 59% for TnT to 77% for hs-TnT, specificity ranged from 63% for CK-MB to 100% for TnT. The systematic literature review yielded 28 studies, with 14.5% out of 7242 patients reported as positive for myocardial contusion. The pooled sensitivity of electrocardiography, troponin I, and CK-MB was between 62 and 71%, versus only 45% for echocardiography and 38% for troponin T. The pooled specificity ranged from 63% for CK-MB to 85% for troponin T and 88% for echocardiography.
CONCLUSION
The best diagnostic approach for myocardial contusion is a combination of electrocardiography and measurement of cardiac biomarkers. If abnormalities are found, telemonitoring is necessary for the early detection of life-threatening arrhythmias. Chest X-ray and CT scan may show other thoracic injuries but provide no information on myocardial contusion.
Topics: Biomarkers; Electrocardiography; Humans; Myocardial Contusions; Retrospective Studies; Sensitivity and Specificity; Thoracic Injuries; Troponin T
PubMed: 31982920
DOI: 10.1007/s00068-020-01305-4 -
Clinical Cardiology Nov 2013Use of high-sensitivity troponin (hs-Tn) assays can detect small levels of myocardial damage previously undetectable with conventional troponin (c-Tn) assays. However,... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Use of high-sensitivity troponin (hs-Tn) assays can detect small levels of myocardial damage previously undetectable with conventional troponin (c-Tn) assays. However, prognostic utility of these hs-Tn assays in prediction of mortality remains unclear in the presence of nonelevated c-Tn levels on admission. A systematic review and meta-analysis was performed to assess mortality risk of patients with hs-Tn elevations in the setting of normal c-Tn levels.
HYPOTHESIS
Patients with hs-Tn elevations with normal c-Tn levels on admission blood samples, drawn to rule out acute coronary syndrome (ACS), have a higher mortality risk than those without hs-Tn or c-Tn elevations.
METHODS
A search was made of the PubMed, CENTRAL, EMBASE, CINAHL, EBSCO, and Web of Science databases. Studies evaluating patients with suspected ACS that reported mortality rates for those with elevated hs-Tn levels but normal c-Tn levels on admission were included. A random-effects model was used to pool event rates, and data were reported in odds ratios (95% confidence interval).
RESULTS
Four studies (N = 2033, mean age 64-75 years, 49%-70% male) revealed that nearly 32% of suspected ACS patients with normal c-Tn levels on admission had elevated hs-Tn levels. Elevated hs-Tn levels conferred a significantly higher risk of all-cause mortality vs normal hs-Tn levels (odds ratio: 4.35, 95% confidence interval: 2.81-6.73, P < 0.01), with negligible heterogeneity (I(2) = 0%).
CONCLUSIONS
Elevation of hs-Tn levels predicted a higher risk of mortality in patients with suspected ACS and may aid in the early identification of higher-risk patients in this setting. Future studies are needed to investigate further optimal management strategies.
Topics: Aged; Biomarkers; Chi-Square Distribution; Female; Heart Diseases; Humans; Male; Middle Aged; Myocardium; Odds Ratio; Patient Admission; Predictive Value of Tests; Prognosis; Risk Assessment; Risk Factors; Troponin; Up-Regulation
PubMed: 24037966
DOI: 10.1002/clc.22196 -
European Heart Journal Mar 2013Myocardial infarction (MI) is a key endpoint in randomized controlled trials (RCTs), but heterogeneous definitions limit comparisons across RCTs or meta-analyses. The... (Review)
Review
Myocardial infarction (MI) is a key endpoint in randomized controlled trials (RCTs), but heterogeneous definitions limit comparisons across RCTs or meta-analyses. The 2000 European Society of Cardiology/American College of Cardiology MI redefinition and the 2007 universal MI definition consensus documents made recommendations to address this issue. In cardiovascular randomized trials, we evaluated the impact of implementation of three key recommendations from these reports-troponin use to define MI; separate reporting of spontaneous and procedure-related MI; and infarct size reporting. We searched ClinicalTrials.gov and MEDLINE databases for cardiovascular RCTs with more than 500 patients in which enrolment began between September 2000 and July 2012 and that listed MI in the primary endpoint. We searched English-language publications with primary results or design papers. Of 3222 studies screened, 96 (3.0%) met our criteria. We extracted enrolment start date, number of patients and MI events, follow-up duration, and coronary revascularization rate. Data extraction quality was assessed by duplicated extractions. Of 96 RCTs, 80 had a primary results publication, comprising 608 091 patients and 43 621 endpoint MIs. Myocardial infarction represented 45.3% (95% confidence interval, 40.2-50.4) of events in the primary composite endpoint. Troponin defined MI in 57% (53/93) of trials with an MI definition available. Of these RCTs, three used troponin only if creatine kinase-MB was unavailable, six used troponin to define peri-procedural MI, seven specified the 99th percentile as the MI decision limit, and three reported spontaneous and procedure-related MI separately. None reported biomarker-based infarct size, but five reported MI as multiples of the assay upper limit of normal. Although MI is a major component of cardiovascular RCT primary endpoints, standardized MI reporting and implementation of consensus document recommendations for MI definition are limited. Developing appropriate strategies for uniform implementation is required.
Topics: Biomarkers; Endpoint Determination; Guideline Adherence; Humans; Myocardial Infarction; Myocardial Reperfusion; Practice Guidelines as Topic; Randomized Controlled Trials as Topic; Terminology as Topic; Troponin
PubMed: 23355654
DOI: 10.1093/eurheartj/eht003 -
Scientific Reports Feb 2021Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with evidence suggesting they represent a heterogeneous population. This study... (Meta-Analysis)
Meta-Analysis
Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with evidence suggesting they represent a heterogeneous population. This study summarises the prognostic role of all proteins characterised in CAFs with immunohistochemistry in non-small cell lung cancer thus far. The functions of these proteins in cellular processes crucial to CAFs are also analysed. Five databases were searched to extract survival outcomes from published studies and statistical techniques, including a novel method, used to capture missing values from the literature. A total of 26 proteins were identified, 21 of which were combined into 7 common cellular processes key to CAFs. Quality assessments for sensitivity analyses were carried out for each study using the REMARK criteria whilst publication bias was assessed using funnel plots. Random effects models consistently identified the expression of podoplanin (Overall Survival (OS)/Disease-specific Survival (DSS), univariate analysis HR 2.25, 95% CIs 1.80-2.82) and α-SMA (OS/DSS, univariate analysis HR 2.11, 95% CIs 1.18-3.77) in CAFs as highly prognostic regardless of outcome measure or analysis method. Moreover, proteins involved in maintaining and generating the CAF phenotype (α-SMA, TGF-β and p-Smad2) proved highly significant after sensitivity analysis (HR 2.74, 95% CIs 1.74-4.33) supporting attempts at targeting this pathway for therapeutic benefit.
Topics: Actins; Biomarkers, Tumor; Cancer-Associated Fibroblasts; Carcinoma, Non-Small-Cell Lung; Fibroblasts; Genetic Heterogeneity; Humans; Lung Neoplasms; Phenotype; Prognosis; Smad2 Protein; Transforming Growth Factor beta; Tumor Microenvironment
PubMed: 33580106
DOI: 10.1038/s41598-021-81796-2