OBJECTIVE: To evaluate the accuracy of cardiac troponin (cTn) levels in the diagnosis of acute myocardial infarction (AMI) in patients with chronic kidney disease (CKD) and explore a potential strategy for improving the diagnostic accuracy. METHODS: We retrospectively analyzed the data from patients with high-risk chest pain admitted in Zhujiang Hospital from January, 2018 to December, 2020, including 126 patients with and 272 patients without CKD, and 122 patients diagnosed to have AMI and 276 patients without AMI. The baseline clinical data of the patients and blood test results within 12 h after admission were collected. RESULTS: In patients without AMI, cTnT level was significantly higher in those with co-morbid CKD than in those without CKD (<i>Pi> < 0.001), and showed a moderate negative correlation with eGFR (<i>ri>_s=- 0.501, <i>Pi> < 0.001), while cTnI level did not differ significantly between the two groups (<i>Pi>=0.72). In patients with CKD, the optimal cutoff level was 0.177 μg/L for cTnT and 0.415 ng/mL for cTnI for diagnosis of AMI, for which cTnI had a higher specificity than cTnT. The diagnostic model combining both cTnT and cTnI levels [<i>Pi>=e^Y/(1+ e^Y), Y=6.928 (cTnT)-0.5 (cTnI)-1.491] had a higher AUC value than cTn level alone. CONCLUSION In CKD patients, the cutoff level of cTn is increased for diagnosing AMI, and cTnI has a higher diagnostic specificity than cTnT. The combination of cTnT and cTnI levels may further improve diagnostic efficacy for AMI.
Humans ; Retrospective Studies ; Myocardial Infarction/diagnosis* ; Comorbidity ; Troponin T ; Troponin I ; Renal Insufficiency, Chronic/diagnosis* ; Biomarkers

BACKGROUND: The relationship between the elevation of cardiac troponin and the increase of mortality and hospitalization rate in patients with heart failure with reduced ejection fraction is clear. This study investigated the association between the extent of elevated levels of high-sensitivity cardiac troponin I (hs-cTnI) and the prognosis in heart failure with preserved ejection fraction patients. METHODS: A retrospective cohort study consecutively enrolled 470 patients with heart failure with preserved ejection fraction from September 2014 to August 2017. According to the level of hs-cTnI, the patients were divided into the elevated level group (hs-cTnI >0.034 ng/mL in male and hs-cTnI >0.016 ng/mL in female) and the normal level group. All of the patients were followed up once every 6 months. Adverse cardiovascular events were cardiogenic death and heart failure hospitalization. RESULTS: The mean follow-up period was 36.2 ± 7.9 months. Cardiogenic mortality (18.6% [26/140] vs. 1.5% [5/330], P <0.001) and heart failure (HF) hospitalization rate (74.3% [104/140] vs. 43.6% [144/330], P <0.001) were significantly higher in the elevated level group. The Cox regression analysis showed that the elevated level of hs-cTnI was a predictor of cardiogenic death (hazard ratio [HR]: 5.578, 95% confidence interval [CI]: 2.995-10.386, P <0.001) and HF hospitalization (HR: 3.254, 95% CI: 2.698-3.923, P <0.001). The receiver operating characteristic curve demonstrated that a sensitivity of 72.6% and specificity of 88.8% for correct prediction of adverse cardiovascular events when a level of hs-cTnI of 0.1305 ng/mL in male and a sensitivity of 70.6% and specificity of 90.2% when a level of hs-cTnI of 0.0755 ng/mL in female were used as the cut-off value. CONCLUSION Significant elevation of hs-cTnI (≥0.1305 ng/mL in male and ≥0.0755 ng/mL in female) is an effective indicator of the increased risk of cardiogenic death and HF hospitalization in heart failure with preserved ejection fraction patients.
Humans ; Male ; Female ; Troponin I ; Stroke Volume ; Retrospective Studies ; Biomarkers ; Heart Failure ; Prognosis

OBJECTIVE: To investigate the clinical significance of early troponin I (TnI) level in the prognosis of severe heat stroke. METHODS: Clinical data of 131 patients with severe heat stroke in the intensive care unit (ICU) of the Affiliated Changzhou NO.2 People's Hospital of Nanjing Medical University (study dataset) and ICU 67 patients with severe heat stroke in Jintan First People's Hospital of Changzhou (validation dataset) were retrospectively analyzed from June 2013 to September 2022. The patients were divided into survival group and death group according to 30-day outcomes. TnI was collected within 24 hours after admission to the emergency department. Cox regression analysis was performed to analyze the risk factors of severe heat stroke death. Spearman correlation test was used to analyze the correlation between TnI and heart rate, and peripheral systolic blood pressure. The receiver operator characteristic curve (ROC curve) was drawn to evaluate the predictive value of TnI for death in patients with severe heat stroke. Decision curve analysis (DCA) was conducted to assess the clinical net benefit rate of TnI prediction. Grouping by TnI cut-off value, Kaplan-Meier survival curve was used to analyze 30-day cumulative survival. Sensitivity analysis included modified Possion regression, E-value, and subgroup forest map was used to evaluate the mortality risk of TnI in different populations. External dataset was used to verify the predictive value of TnI. RESULTS: The death group had significantly higher TnI compared to the survival group [μg/L: 0.623 (0.196, 1.510) vs. 0.084 (0.019, 0.285), P < 0.01]. Multivariate Cox regression analysis after adjusting for confounding factors showed that TnI was an independent risk factor for death [hazard ratio (HR) = 1.885, 95% confidence interval (95%CI) was 1.528-2.325,P < 0.001]. Spearman correlation test showed that TnI was positively correlated with heart rate (r = 0.537, P < 0.001) and negatively correlated with peripheral systolic blood pressure (r = -0.611, P < 0.001). ROC curve showed that the area under the curve (AUC) of the TnI (0.817) was better than that of the acute physiology and chronic health evaluation II (APACHE II, 0.756). The DCA curve showed that the range of clinical net benefit rate of TnI (6.21%-20.00%) was higher than that of APACHE II score (5.14%-20.00%). Kaplan-Meier survival curve showed that patients in the low-risk group (TnI ≤ 0.106) had a significantly higher 30-day survival rate than that in the high-risk group (TnI > 0.106) group (Log-Rank test: χ² = 17.350, P < 0.001). Modified Possion regression with adjustment for confounding factors showed that TnI was still an independent risk factor for death in patients with severe heat stroke [relative risk (RR) = 1.425, 95%CI was 1.284-1.583, P < 0.001]. The E-value was 2.215. The subgroup forest plot showed that the risk factors of TnI were obvious in male patients and patients ≤ 60 years old (male: HR = 1.731, 95%CI was 1.402-2.138, P < 0.001; ≤ 60 years old: HR = 1.651, 95%CI was 1.362-2.012, P < 0.001). In the validation dataset, ROC curve analysis showed that the AUC (0.836) of TnI predicting the prognosis of severe heat stroke was still higher than the APACHE II score (0.763). CONCLUSIONS Early elevation of TnI is a high-risk factor for death in patients with severe heat stroke, and it has a good predictive value for death.
Humans ; Male ; Middle Aged ; Troponin I ; Retrospective Studies ; Clinical Relevance ; ROC Curve ; Prognosis ; Intensive Care Units ; Heat Stroke/diagnosis* ; Sepsis

OBJECTIVE: To examine the effect of Shenmai Injection (SMJ) on ferroptosis during myocardial ischemia reperfusion (I/R) injury in rats and the underlying mechanism. METHODS: A total of 120 SPF-grade adult male SD rats, weighing 220-250 g were randomly divided into different groups according to a random number table. Myocardial I/R model was established by occluding the left anterior descending artery for 30 min followed by 120 min of reperfusion. SMJ was injected intraperitoneally at the onset of 120 min of reperfusion, and erastin (an agonist of ferroptosis), ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) and ML385 (an inhibitor of nuclear factor erythroid-2 related factor 2 (Nrf2)) were administered intraperitoneally separately 30 min before myocardial ischemia as different pretreatments. Cardiac function before ischemia, after ischemia and after reperfusion was analysed. Pathological changes in the myocardium and the ultrastructure of cardiomyocytes were observed, and the myocardial infarction area was measured. Additionally, the concentration of Fe²⁺ in heart tissues and the levels of creatine kinase-MB (CK-MB), troponin I (cTnl), malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were measured using assay kits, and the expressions of Nrf2, glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) were examined by Western blot. RESULTS: Compared with the sham group, I/R significantly injured heart tissues, as evidenced by the disordered, ruptured and oedematous myocardial fibres; the increases in infarct size, serum CK-MB, cTnI and MDA levels, and myocardial Fe²⁺ concentrations; and the decreases in SOD activity (P<0.05). These results were accompanied by ultrastructural alterations to the mitochondria, increased expression of ACSL4 and inhibited the activation of Nrf2/GPX4 signalling (P<0.05). Compared with I/R group, pretreatment with 9 mL/kg SMJ and 2 mg/kg Fer-1 significantly reduced myocardial I/R injury, Fe²⁺ concentrations and ACSL4 expression and attenuated mitochondrial impairment, while 14 mg/kg erastin exacerbated myocardial I/R injury (P<0.05). In addition, cardioprotection provided by 9 mL/kg SMJ was completely reversed by ML385, as evidenced by the increased myocardial infarct size, CK-MB, cTnI, MDA and Fe²⁺ concentrations, and the decreased SOD activity (P<0.05). CONCLUSIONS Ferroptosis is involved in myocardial I/R injury. Pretreatment with SMJ alleviated myocardial I/R injury by activating Nrf2/GPX4 signalling-mediated ferroptosis, thereby providing a strategy for the prevention and treatment of ischemic heart diseases.
Animals ; Male ; Rats ; Coenzyme A ; Creatine Kinase ; Ferroptosis ; Ligases ; Malondialdehyde ; Myocardial Infarction/drug therapy* ; Myocardial Ischemia/drug therapy* ; Myocardial Reperfusion Injury/pathology* ; Myocytes, Cardiac/metabolism* ; NF-E2-Related Factor 2/metabolism* ; Phospholipid Hydroperoxide Glutathione Peroxidase ; Rats, Sprague-Dawley ; Superoxide Dismutase/metabolism* ; Troponin I

INTRODUCTION: A vast number of COVID-19 cases have been reported worldwide since the initial outbreak in China, and the disease has since become a global pandemic. Knowledge on this predominantly respiratory illness is evolving with studies suggesting myocardial injury reflected by elevated cardiac enzymes portending to more severe disease. CT scoring indices provide visual, semi-quantitative assessment of lung involvement and have aided in determining extent of COVID-19 pneumonia but, none have been validated for prognostication. Establishing a relationship between these non-invasive diagnostic parameters could provide timely identification and proper allocation of limited medical resources to patients in need of more aggressive therapy. METHODS AND RESULTS: A total of 50 COVID-19 patients were retrospectively enrolled and their clinical parameters collected from an electronic medical database. There was a total of 31 patients with troponin I-HS with chest CT scan done and another 42 patients for NT-proBNP and chest CT. The levels of both cardiac biomarkers in patients with clinically severe COVID pneumonia were higher than those with mild and moderate disease. Rank-order analysis showed that both troponin I-HS (moderate, p=0.0003174) and NT-proBNP (moderate, p=0.006255) correlated positively with CT severity scores. Furthermore, there is a significant relationship between mortality and septic shock with both Troponin I-HS (p<0.001; p=0.002) and NT-proBNP (p=0.004; p=0.031). CONCLUSION The cardiac markers troponin I-HS and NT-proBNP increased significantly at more severe CT scores and more notably, these biomarkers predicted the development of septic shock and mortality in COVID-19 pneumonia.
COVID-19 ; NT-proBNP ; pro-brain natriuretic peptide (1-76) ; Troponin I

BACKGROUND

Atrial fibrillation (AF) after coronary artery bypass graft (CABG) surgery may lead to prolonged hospital stay and increased morbidity and mortality. Identifying people at risk may help in the management and improve the outcome of patients undergoing this procedure.

The aims of this were to determine the incidence of AF in patients who underwent CABG surgery in ManilaMed-Medical Center Manila and whether certain factors were associated with developing AF in patients who underwent the procedure.

This was a single-center, retrospective, cross-sectional study wherein adult patients who underwent CABG, without previous AF, were included.

Among patients included in the study, 29 developed AF, with an incidence of 27.62%. Patients who had AF after CABG were, on average, older (65.79 vs 59.29 years, P = 0.002); had dyslipidemia (72% vs 47%, P = 0.021), a higher average left atrial volume index (LAVI) (26.72 vs. 23.45, P = 0.038), an LAVI greater than 34 mL/m2 (24% vs 3%, P = 0.002), and an episode of previous stroke (28% vs 11%, P = 0.038); and had been taking diuretics (28% vs 9%, P = 0.027) but had a lower prevalence of having diabetes (41% vs 66%, P = 0.023).

Atrial fibrillation remains to be a frequent arrhythmia after CABG occurring in 28% of patients who had CABG. It may occur in older patients, patients with dyslipidemia, patients with a large left atrium, patients who had a previous stroke, and patients taking diuretics. On the other hand, the odds of a diabetic patient developing AF after CABG are low.

Objective: To evaluate the cardiovascular damage of patients with COVID-19, and determine the correlation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP） and cardiac troponin-I (cTnI） with the severity of COVID-19, and the impact of concomitant cardiovascular disease on severity of COVID-19 was also evaluated. Methods: A cross-sectional study was designed on 150 consecutive patients with COVID-19 in the fever clinic of Tongji Hospital in Wuhan from January 19 to February 13 in 2020, including 126 mild cases and 24 cases in critical care. Both univariate and multivariate logistic regression were used to analyze the correlation of past medical history including hypertension, diabetes and coronary heart disease (CHD）, as well as the levels of serum NT-proBNP and cTnI to the disease severity of COVID-19 patients. Results: Age, hypersensitive C-reactive protein(hs-CRP) and serum creatinine levels of the patients were higher in critical care cases than in mild cases(all <i>Pi><0.05). Prevalence of male, elevated NT-proBNP and cTnI, hypertension and coronary heart disease were significantly higher in critical cases care patients than in the mild cases(all <i>Pi><0.05). Univariate logistic regression analysis showed that age, male, elevated NT-proBNP, elevated cTnI, elevated hs-CRP, elevated serum creatinine, hypertension, and CHD were significantly correlated with critical disease status(all <i>Pi><0.05). Multivariate logistic regression analysis showed that elevated cTnI(<i>ORi>=26.909，95%<i>CIi> 4.086-177.226，<i>Pi>=0.001) and CHD (<i>ORi>=16.609，95%<i>CIi> 2.288-120.577，<i>Pi>=0.005) were the independent risk factors of critical disease status. Conclusions: COVID-19 can significantly affect the heart function and lead to myocardial injury. The past medical history of CHD and increased level of cTnI are 2 independent determinants of clinical disease status in patients with COVID-19.
Betacoronavirus ; Biomarkers/blood* ; COVID-19 ; Cardiovascular Diseases/virology* ; China ; Coronavirus Infections/pathology* ; Cross-Sectional Studies ; Female ; Humans ; Male ; Myocardium/pathology* ; Natriuretic Peptide, Brain/blood* ; Pandemics ; Peptide Fragments ; Pneumonia, Viral/pathology* ; Prognosis ; SARS-CoV-2 ; Troponin I/blood*

OBJECTIVE: Although a left ventricular (LV) diastolic dysfunction is an important prognostic factor in myocardial dysfunction in septic shock, emergency departments (EDs) have limited capability of performing echocardiography. Cardiac troponin is a specific marker of a myocardial injury. On the other hand, little is known about the LV diastolic dysfunction in septic shock patients. This study examined the associations between troponin-I (TnI) level and LV diastolic dysfunction. METHODS: A 5-year retrospective cohort study was conducted between January 2011 and December 2015, including adult septic shock patients who were treated with protocol-driven resuscitation bundle therapy and had the TnI tested at the ED. The LV diastolic dysfunction was defined as E/e′ratios above 15 in echocardiography. RESULTS: Of the 442 septic shock patients with an abnormal TnI (≥0.04 ng/mL) at admission, echocardiography was performed on 255 patients and 81 patients (31.8%) showed a LV diastolic dysfunction. The TnI level at ED admission was higher in the LV diastolic dysfunction group compared to the non-dysfunction group (0.08 [0.03–0.25] ng/mL vs. 0.14 [0.05–0.43] ng/mL, P=0.035). On the other hand, according to multivariate logistic regression and chronic kidney disease (odds ratio, 1.74; 95% confidence interval, 1.02–2.99) was the only factor associated with a LV diastolic dysfunction. Receiver operating characteristic analysis revealed the area under the curve of the initial TnI to be only 0.589 (P=0.038) and no correlation was observed between the initial TnI and E/e′(r=0.079, P=0.199). CONCLUSION: A LV diastolic dysfunction occurred in approximately quarter of septic shock patients with TnI elevation, but the TnI test showed a weak association with diastolic dysfunction. Further studies will be needed to identify the predictors for a diastolic dysfunction in septic shock patients.
Adult ; Biomarkers ; Cardiomyopathies ; Cohort Studies ; Critical Illness ; Echocardiography ; Emergency Service, Hospital ; Hand ; Humans ; Logistic Models ; Renal Insufficiency, Chronic ; Resuscitation ; Retrospective Studies ; ROC Curve ; Shock, Septic ; Troponin I ; Troponin

BACKGROUND AND OBJECTIVES: Microvascular damage due to distal embolization during percutaneous coronary intervention (PCI) is an important cause of periprocedural myocardial infarction. We assessed the lipid-core plaque using near-infrared spectroscopy (NIRS) and microvascular dysfunction invasively with the index of microcirculatory resistance (IMR) and evaluated their relationship. METHODS: This study is pilot retrospective observational study. We analyzed 39 patients who performed NIRS before and after PCI, while fractional flow reserve, thermo-dilution coronary flow reserve (CFR) and IMR were measured after PCI. The maximum value of lipid core burden index (LCBI) for any of the 4-mm segments at the culprit lesion (culprit LCBI(4mm)) was calculated at the culprit lesion. We divided the patients into 2 groups using a cutoff of culprit LCBI(4mm) ≥500. RESULTS: Mean pre-PCI LCBI was 333±196 and mean post-PCI IMR was 20±14 U. Post-PCI IMR was higher (15.6±7.3 vs. 42.6±17.6 U, p<0.001) and post-PCI CFR was lower (3.7±2.2 vs. 2.1±1.0, p=0.029) in the high LCBI group. Pre-PCI LCBI was positively correlated with post-PCI IMR (ρ=0.358, p=0.025) and negatively correlated with post-PCI CFR (ρ=−0.494, p=0.001). The incidence of microvascular dysfunction (IMR ≥25 U) was higher in the high LCBI group (9.4% vs. 85.7%, p<0.001). However, there were no significant differences in the incidences of creatine Kinase-MB (9.4% vs. 14.3%, p=0.563) and troponin-I elevation (12.5% vs. 14.3%, p=1.000). CONCLUSIONS: A large lipid-core plaque at the ‘culprit’ lesion is observed higher incidence of post-PCI microvascular dysfunction after PCI. Prospective study with adequate subject numbers will be needed.
Coronary Artery Disease ; Creatine ; Humans ; Incidence ; Microvessels ; Myocardial Infarction ; Observational Study ; Percutaneous Coronary Intervention ; Prospective Studies ; Retrospective Studies ; Spectroscopy, Near-Infrared ; Troponin I

Acute myocardial infarction is one of the most common causes of unexpected deaths, but there are limitations to its diagnosis in postmortem inspection. In this study, we aimed to investigate the usefulness of cardiac marker analysis for the diagnosis of acute myocardial infarction in postmortem inspection. This study was conducted on 30 postmortem inspection cases conducted by the National Forensic Service from 2016 to 2018. Tests for three myocardial enzymes (myoglobin, creatinine kinase-MB, and cardiac troponin I) were performed in each case, and the relationships between enzyme levels, cause of death, and factors affecting the postmortem tests were analyzed. Cardiac enzyme concentrations were not significantly different between the heart disease group and other disease groups, and the false-positive rate was increased due to postmortem changes. Therefore, we can conclude that it is not appropriate to use cardiac enzyme analysis for the diagnosis of acute myocardial infarction in postmortem inspection.
Cause of Death ; Creatinine ; Diagnosis ; Heart Diseases ; Myocardial Infarction ; Postmortem Changes ; Troponin ; Troponin I