Elevated cTnI Research Articles

Quantitation of cardiac troponin I in cancer patients treated with immune checkpoint inhibitors: a case-control study.

Immune checkpoint inhibitors (ICIs) cause a variety of toxicities, including immune-related adverse events (irAEs), but there are no biomarkers to predict theirdevelopment. Guidelines recommend measuring circulating cardiac troponin I (cTnI) during ICI therapy to detect related cardiotoxicities. Moreover, elevated cTnI has also been associated with worse outcomes in non-cardiac patients, including cancer. Thus here, we investigated whether cTnI levels were higher in patients with irAEs. The study consisted of three groups; 21 cancer patients undergoing ICI immunotherapies who presented with irAEs, four patients without irAEs, and 20 healthy controls. Patient samples were assessed at baseline (n=25), during ICI treatment (n=25, median=6weeks of treatment) and at toxicity (n=6, median=13weeks of treatment). Inaddition to blood high sensitivity cardiac troponin I (hs-cTnI), anti-thyroglobulin (TG) andanti-thyroid peroxidase (TPO) antibodies were also quantitated to detect thyroid dysfunction, constituting the second leading toxicity (23.8%) after pneumonitis (28.6%). Four patients with irAEs (n=4/21; 19%) and one without irAEs (n=1/4; 25%) showed higher hs-cTnI levels at any time-point; the remaining had physiological levels. None of these patients developed cardiotoxicity. Concurrent elevated levels of anti-thyroid antibodies and hs-cTnI were detected in one patient with thyroid dysfunction (n=1/5, 20%). However, these antibodies were also elevated in three patients (n=3/16, 19%) with non-thyroid irAEs and in up to 40% of healthy controls. hs-cTnI was not elevated in patients with irAEs, but larger studies are needed to confirm these observations.

Preoperative cardiac troponin I as a predictor of postoperative cardiac events in patients with end stage renal disease undergoing non-cardiac surgery

We investigated if elevated cardiac troponin I (cTnI) serum levels before non-cardiac surgery were predictors of postoperative cardiac events in patients with end stage renal disease (ESRD) undergoing dialysis. In total, 703 consecutive patients with ESRD undergoing dialysis who underwent non-cardiac surgery were enrolled. Preoperative cTnI serum levels were measured at least once in all patients. The primary endpoint was defined as a composite of cardiac death, myocardial infarction (MI), and pulmonary edema during hospitalization or within 30 days after surgery in patients with a hospitalization longer than 30 days after surgery. Postoperative cardiac events occurred in 48 (6.8%) out of 703 patients (cardiac death 1, MI 18, and pulmonary edema 33). Diabetes mellitus (DM), previous ischemic heart disease, and congestive heart failure were more common in patients with postoperative cardiac events. Peak cTnI serum levels were higher in patients with postoperative cardiac event (180 ± 420 ng/L vs. 80 ± 190 ng/L, p = 0.008), and also elevated peak cTnI levels > 45 ng/L were more common in patients with postoperative cardiac events (66.8% vs. 30.5%, p < 0.001). Multivariate logistic regression analysis showed that DM (odds ratio [OR] 2.509, 95% confidence interval [CI] 1.178–5.345, p = 0.017) and serum peak cTnI levels ≥ 45 ng/L (OR 3.167, 95% CI 1.557–6.444, p = 0.001) were independent predictors for the primary outcome of cardiac death/MI/pulmonary edema. Moreover, cTnI levels ≥ 45 ng/L had an incremental prognostic value to the revised cardiac risk index (RCRI) (Chi-square = 23, p < 0.001), and to the combined RCRI and left ventricular ejection fraction (Chi-square = 12, p = 0.001). Elevated preoperative cTnI levels are predictors of postoperative cardiac events including cardiac death, MI, and pulmonary edema in patients with ESRD undergoing non-cardiac surgery.

Prognostic value of cardiac troponin in dialysis patients with paroxysmal supraventricular tachycardia.

A rise in cardiac troponin I (cTnI) is common in supraventricular tachycardia (SVT). While troponin elevation in SVT is thought to be a predictor of future adverse events in patients with prior coronary artery disease, the prognostic significance of cTnI in end-stage kidney disease (ESKD) patients with SVT are not known. We aimed to examine the prognostic significance of cTnI in ESKD patients presenting with SVT in the emergency department. This was a retrospective, multiple-center observational study utilizing regularly collected electronic medical records. We screened electronic medical records of all dialysis patients presenting to the emergency departments in 5 hospitals over 12 years with SVT. These patients were divided into whether cTnI was tested, and were further stratified into the cTnI-positive and cTnI-negative groups. The primary outcome of the study was the 3-year risk of major adverse cardiovascular events (MACE). Sixty-two patients were qualified for inclusion. Fifty-seven patients (91.9%) were tested for cTnI, and 5 patients were not. Patients with the cTnI test were older (P = .03) and had a longer length of hospital stay (P < .001). Forty-seven patients (82.5%) had a positive result, and 10 (17.5%) had a negative result. A history of hypertension (P = .013) and decreased left ventricular ejection fraction (P = .048) were the independent predictors of cTnI elevation. After a mean follow-up period of 20.6 ± 14.7 months, there were no differences in 3-year MACE between patients with or without elevated cTnI levels in Kaplan-Meier analysis (P = .34). A history of coronary artery disease was the only independent predictor of 3-year MACE (P = .017). Through the subgroup analysis, a history of coronary artery disease (HR 2.73; CI 1.01-7.41; P = .049) remained an independent risk factor for 3-year MACE in patients with elevated cTnI levels. A large proportion (82.5%) of troponin elevation was observed in ESKD patients with SVT, but it had a poor correlation with MACE.

Prognostic significance of troponin increment after percutaneous coronary intervention: A retrospective study.

ObjectiveThe prognostic significance of troponin elevation following percutaneous coronary intervention (PCI) remains debated. This study aimed to evaluate the association between different thresholds of post-PCI cardiac troponin I (cTnI) and mortality.MethodsFrom January 2012 to July 2017, 5,218 consecutive patients undergoing elective PCI with pre-PCI cTnI < 99th percentile of the upper reference limit (URL) were included. Levels of cTnI were measured before PCI and every 8 h for 24 h after procedural. The outcomes were 3-year cardiac mortality.ResultsPatients had a mean age of 66.2 years, 27.6% were women, 67.0% had hypertension, and 26.2% had diabetes mellitus. During the 3 years of follow-up, cardiac death occurred in 0.86%, 1.46%, 1.69%, 2.36%, and 2.86% of patients with cTnI < 1, ≥ 1 to < 5, ≥ 5 to < 35, ≥ 35 to < 70, and ≥ 70 times URL. The cardiac mortality rate was moderately increased with higher peak cTnI values, but the Kaplan–Meier curve demonstrated no significant association between any increment of cTnI and either cardiac or non-cardiac mortality. Isolated cTnI increment of ≥ 5 × URL, ≥ 35 × URL, and ≥ 70 × URL was occurred in 1,379 (26.4%), 197 (3.8%), and 70 (1.3%) patients, respectively. In multivariate Cox regression analysis and Fine-Gray model, none of the above cTnI thresholds was significantly associated with an increased risk of cardiac death.ConclusionIn patients who underwent elective PCI, post-PCI cTnI elevation is not independently associated with cardiac mortality.

Cardiovascular adverse events induced by immune checkpoint inhibitors: A real world study from 2018 to 2022.

BackgroundThe reported rate of cardiovascular adverse events (CAE) caused by immune checkpoint inhibitors (ICI) is low but potentially fatal. Assess the risk of CAE in cancer patients and compare the incidence of CAE between Chinese developed ICIs and imported ICIs.MethodsA retrospective analysis was performed on cancer patients treated with ICI for at least four cycles in the Second Affiliated Hospital of Dalian Medical University from January 2018 to March 2022. Baseline characteristics, physiological and biochemical values, electrocardiographic and echocardiographic findings were compared between patients with and without CAE.ResultsAmong 495 patients treated with ICIs, CAEs occurred in 64 patients (12.93%). The median time to the event was 105 days (61–202). The patients with low neutrophil-to-lymphocyte ratio (L-NLR) were significantly associated with the risk of developing CAE (hazard ratio HR 3.64, 95% confidence ratio CI 1.86–7.15, P = 0.000). Patients with higher comorbidity burden significantly increased the risk of developing CAE (HR 1.30, 95% CI 1.05–1.61, P = 0.014). Those who received a combination of ICI and vascular endothelial growth factor receptor (VEGFR) inhibitors (HR 2.57, 95% CI 1.37–4.84, P = 0.003) or thoracic radiation therapy (HR 32.93, 95% CI 8.81–123.14, P = 0.000) were at a significantly increased risk of developing CAE. Compared to baseline values, creatine kinase is -oenzymes (CK-MB) (95% CI -9.73 to -2.20, P = 0.003) and cardiac troponin I (cTnI) (95% CI -1.06 to -0.06, P = 0.028) were elevated, and the QTc interval prolonged (95% CI -27.07 to -6.49, P = 0.002). Using nivolumab as a control, there was no difference in CAE risk among the eight ICIs investigated. However, the results of the propensity matching showed that programmed death-ligand 1 (PD-L1) inhibitors had lower CAE occurrence compared with programmed cell death protein 1 (PD-1) inhibitors (adjusted HR = 0.38, P = 0.045).ConclusionPatients who received concurrent VEGFR inhibitors and ICIs had a history of thoracic radiation therapy, L-NLR, and higher comorbidity burden had an increased risk of CAEs. Elevated cTnI, CK-MB, and QTc, can be used to monitor CAEs. There was no significant difference in CAE risks between Chinese domestic and imported ICIs. PD-L1 inhibitors had lower CAE occurrence than PD-1 inhibitors.

Evaluation Value and Clinical Significance of Cardiac Troponin Level and Pediatric Sequential Organ Failure Score in the Definition of Sepsis 3.0 in Critically Ill Children.

Objective A case-control study was conducted to explore the value and clinical significance of troponin level and pediatric sequential organ failure score in the evaluation of sepsis 3.0 definition in critically ill children. Methods 180 children with sepsis who were admitted to the ICU from March 2019 to June 2021 were enrolled in our hospital as the research objects. In addition, 100 children with general infection did not meet the diagnostic criteria of systemic inflammatory response syndrome (SIRS) as controls. The creatine kinase MB (CK-MB) and cardiac troponin I (cTnI) data at the 1st and 24-72 h after admission to pediatric intensive care unit (PICU) were enrolled as the observation indexes of myocardial enzymology. In the meantime, the relevant literature was reviewed to obtain the indicators related to sepsis death. The data of the first examination in the medical history data were enrolled for analysis. According to the definition of sepsis 3.0 in critically ill children, they were assigned into sepsis and nonsepsis group. According to the survival outcome of discharge and 30 days after discharge, the patients were assigned into the death subgroup and survival subgroup and were assigned into the sequential organ failure assessment (SOFA) score ≥ 2 subgroup and< 2 subgroup according to SOFA score. COX proportional hazard regression was used to analyze the relationship between CK-MB, cTnI, and SOFA scores and prognosis. ROC curve was adopted to analyze the value of CK-MB, cTnI, and SOFA scores in the evaluation of critical sepsis in children. Results Univariate analysis indicated that the prognosis of children with sepsis was correlated with abnormal levels of CK-MB and cTnI, SOFA score, oxygenation index < 200, mean arterial pressure, and Glasgow coma scale (GCS), and the difference was statistically significant (P < 0.05). The results of COX regression analysis indicated that the variables that were remarkably associated with death from sepsis in children were CK-MB, elevated cTnI levels, and SOFA score ≥ 2, and serum cTnI and/or CK-MB levels and SOFA score were remarkably higher correlation (r = 0.453, P < 0.05). In terms of the myocardial enzyme levels in the sepsis group and the nonsepsis group, the levels of CK-MB and (or) cTnI augmented in 121/180 cases (67.22%) in the sepsis group and in 19/100 cases (19.00%) in the nonsepsis group. The levels of CK-MB and (or) cTnI were augmented, and the difference was statistically significant (P < 0.05). The levels of CK-MB and cTnI in the sepsis group at admission to ICU and 24 to 72 hours after admission were remarkably higher compared to the nonsepsis group. The levels of CK-MB and cTnI at 24-72 h were higher compared to ICU. The myocardial enzyme levels of different SOFA scores and survival outcome subgroups in the sepsis group were compared. The subgroup with SFOA score ≥ 2 points had remarkably higher levels of CK-MB and (or) cTnI than the subgroup with <2 points. The survival subgroup of CK-MB and cTnI level was remarkably higher compared to the death subgroup, the CK-MB and cTnI levels in each subgroup at 224-72 hours were remarkably higher compared to the ICU, and the difference was statistically significant (P < 0.05). Kaplan-Meier method and log-rank test indicated that the survival rates of groups 1 to 4 at 30 days were 33.23%, 78.71%, 40.03%, and 100.00%, respectively. The average survival time and their 95% CI were 12.82 d (10.52~ 16.26 d), 22.34 d (18.76~ 25.81 d), 14.65 d (11.62~ 16.38 d), and 30 d (30.00~ 30.00 d), respectively. Pairwise comparison indicated that the survival time of children in group 1 was the shortest, and that in group 4 was the longest. The results of ROC curve research showed that the CK-MB, cTnI, and SOFA scores and AUC for the combination test were 0.778 (95% CI 0.642–0.914), 0.736 (95% CI 0.602–0.890), 0.848 (95% CI 0.733–0.963), and 0.934 (95% CI 0.854–0.999), respectively. The AUC of combined diagnosis was remarkably higher compared to single factor prediction, and the difference was statistically significant (P < 0.05). Predictive value showed the joint test > SOFA score > CK − MB > cTnI. Conclusion Troponin level and pediatric SOFA score can be adopted as effective indicators to assess the severity and prognosis of patients with sepsis and can guide the formulation of a reasonable treatment plan.

Elevated Cardiac Troponin I following Asymptomatic Intradialytic Hypotension: A Pilot Study with a 2-Year Follow-Up.

Background Intradialytic hypotension (IDH) has been recognized as a serious and frequent complication during hemodialysis (HD) of end-stage renal disease (ESRD) patients, but the effect of asymptomatic IDH on cardiac troponin I (cTnI) levels is not definitively elucidated. Methods 70 asymptomatic HD patients with negative predialysis cTnI were included. They were on maintenance HD thrice weekly. All patients were monitored during the HD session for hemodynamic changes and symptoms related to IDH. Patients were followed for two years, and their outcomes are noted as an acute coronary syndrome (ACS), cardiac death, no ACS, noncardiac death, and kidney transplant. Results Compared with the baseline blood pressure values, there was a drop in systolic blood pressure for all subjects, but according to the 2007 European Best Practice Guidelines on hemodynamic instability, asymptomatic IDH was defined in 27 (38.6%) patients. The results demonstrated a significant correlation (r = 0.492) (p < 0.05) between asymptomatic IDH and elevated postdialysis levels of cTnI. In 2-year follow-up of patients, ACS and cardiac death happened more in patients with elevated cTnI. Conclusion The results of our study suggest that asymptomatic IDH affects cTnI levels. Given that cTnI is a marker of myocardial damage and a predictor of cardiovascular mortality in ESRD patients, these findings recommend that considering the asymptomatic decrease in blood pressure levels during HD is very important and critical.

Elevated cardiac troponin I and short-term mortality in patients with acute type A aortic dissection.

To explore the association between elevated cardiac troponin I (cTnI) on 30-day mortality in patients with acute type A aortic dissection (ATAAD). A total of 1321 consecutive patients who were admitted to the emergency department of Fuwai Hospital from January 2016 to December 2020 were enrolled. Patients had computed tomography-confirmed ATAAD and were measured serum cTnI on admission. Patients were divided into the troponin-positive (cTnI > 0.02 ng/mL) or the troponin-negative group (cTnI ≤ 0.02 ng/mL). Troponin was detected by PATHFAST instrument produced by Medins Co., Ltd., and the reference range of normal value is 0-0.02 ng/mL. A total of 522 out of 1321 patients (39.5%) in our study had elevated cTnI, who had higher 30-day mortality rate compared with the troponin-negative group (44.4% vs. 19.4% P < 0.0001). Multivariate logistic regression results showed that elevated cTnI was an independent risk indicator for 30-day mortality (odds ratio: 2.582; 95% confidence interval: 1.357-4.914; P = 0.0039). The addition of elevated cTnI level to a clinical-based risk prediction model resulted in significant incremental prognostic value (AUC difference: 0.0261). Elevated cTnI is common in patients with ATAAD, and is associated with increased 30-day mortality risk.

Prevalence, Determinants and Clinical Significance of Cardiac Troponin-I Elevation among Individuals with Hypertensive Emergency: A Prospective Observational Study.

Cardiac troponin-I (cTnI) elevation release during hypertensive emergencies (HEs) is a frequent epiphenomenon that may tangle management of individuals being treated for HEs. The primary objective of this study was to determine the prevalence, determinants, and clinical significance of cTnI elevation and secondary objective was to find out the prognostic significance of cTnI elevation in patients admitted for HE in the emergency department (ED) of a tertiary care hospital. The investigator has employed the quantitative research approach with a prospective observational descriptive design. The population of this study comprised of 205 adults, which included both males and females, who were more than or 18 years of age. The subjects were selected by non-probability purposive sampling technique. The study was conducted from August 2015 to December 2016 (16 months). Ethical permission was obtained from the Institutional Ethics Committee (IEC), Max Super Speciality Hospital, Saket, New Delhi and well-informed written consents were taken from the subjects. The analysis of data was done with the help of SPSS, version 17.0. Out of 205 patients in the study, cTnI elevation was found in 102 patients (49.8%). Moreover, there was increased duration of stay in the hospital in patient with elevated cTnI level with mean duration stay 1.55 ± 0.82 (p <0.001). In addition, cTnI elevation was associated with increased mortality, 11 out of 102 in an elevated cTnI group (10.8%) with p <0.002. It was found that cTnI elevation in individuals affected by various clinical factors. The authors highlighted a high frequency of mortality among the individuals presented with HE with elevated cTnI level, whereas the presence of cTnI was associated with greater odds of death. Gupta K, Kiran M, Chhabra S, Mehta M, Kumar N. Prevalence, Determinants and Clinical Significance of Cardiac Troponin-I Elevation among Individuals with Hypertensive Emergency: A Prospective Observational Study. Indian J Crit Care Med 2022;26(7):786-790.

The role of myocarditis in the acute phase of Kawasaki as a predictor of the future coronary aneurysm: a case–control study

BackgroundThis study aimed to evaluate the relationship between cardiac troponin I and T (cTnI, cTnT) and creatine kinase (CK)-MB during the acute phase of Kawasaki disease (KD) and the development of coronary artery involvement (CAI).ResultsNinety children diagnosed with KD and 38 attending ambulatory clinics as controls were enrolled in this study. Serum levels of cardiac enzymes were measured in all case and control groups. Serial echocardiograms were performed in KD patients during the acute, subacute and convalescence phases. Thirty-six percent of patients had CAI during the acute phase of KD; this rate was 21% and 18% in the echocardiography in the sub-acute and convalescent-phase, respectively. Elevated serum cTnI and cTnT levels were seen in 15.5% and 10% of KD patients, respectively, but not in the controls (P < 0.01). Patients with abnormal echocardiography had significantly higher levels of CK-MB but cTnI and cTnT. Cardiac troponins have high specificity, and CK-MB had a high sensitivity for predicting CAI in KD.ConclusionSubclinical myocarditis occurs during KD, and serum cardiac troponin levels are significantly elevated, but cardiac biomarkers cannot predict CAI in the future.

The Prognostic Value of Cardiac Troponin I in Patients with or without Three-Vessel Disease Undergoing Complete Percutaneous Coronary Intervention.

Postprocedural cardiac troponin I (cTnI) elevation commonly occurs in patients undergoing percutaneous coronary intervention (PCI); however, its prognostic value remains controversial. This study aimed to investigate the prognostic value of peak postprocedural cTnI in cardiac patients with or without three-vessel disease (TVD) undergoing complete PCI. A total of 1237 consecutive patients (77% males, mean age 58 ± 10 years) with normal baseline cTnI levels were enrolled, 439 patients (77% males, 59 ± 10 years) with TVD, and 798 patients (77% males, 57 ± 10 years) with single- or double-vessel disease (non-TVD). The primary outcome was the occurrence of major adverse cardiovascular events (MACE), defined as a composite of non-fatal MI, non-fatal stroke, unplanned revascularization, re-hospitalization due to heart failure or severe arrhythmias, and all-cause death. During the median follow-up of 5.3 years, a total of 169 patients (13.7%) developed MACE, including 73 (16.6%) in the TVD group and 96 (12.0%) in the non-TVD group (p = 0.024). After adjustment, the multivariate Cox analysis showed that hypertension (HR 1.50; 95% CI: 1.01–2.20; p = 0.042), TVD (HR 1.44; 95% CI: 1.03–2.02; p = 0.033), and cTnI ≥ 70× URL (HR 2.47; 95% CI: 1.28–4.78, p = 0.007) were independently associated with increased MACE during long-term follow-up. Further subgroup analyses showed that cTnI ≥ 70× URL was an independent predictor of MACE in TVD patients (HR 3.32, 95% CI: 1.51–7.34, p = 0.003), but not in non-TVD patients (HR 1.01, 95%CI: 0.24–4.32, p = 0.991). In conclusion, elevation of post-PCI cTnI ≥ 70× URL is independently associated with a high risk of MACE during long-term follow-up in patients with TVD, but not in those with non-TVD.

The highest troponin I level during admission is associated with mortality in blunt cardiac injury patients

BackgroundCardiac troponin I (cTnI) levels are usually measured in primary evaluations of blunt cardiac injury (BCI) patients. We evaluated the associations of cTnI levels with the outcomes of BCI patients at different times. MethodsFrom 2015 to 2019, blunt chest trauma patients with elevated cTnI levels were compared with patients without elevated cTnI levels using propensity score matching (PSM) to minimize selection bias. The cTnI levels at different times in the survivors and nonsurvivors were compared. ResultsA total of 2,287 blunt chest trauma patients were included, and 57 (2.5%) of the patients had BCIs. PSM showed that patients with and without elevated cTnI levels had similar mortality rates (13.0% vs. 11.1%, p-value = 0.317], hospital lengths of stay (LOSs) [17.3 (14.4) vs. 15.5 (22.2) days, p-value = 0.699] and intensive care unit (ICU) LOSs [7.7 (12.1) vs. 6.4 (15.4) days, p-value = 0.072]. Among the BCI patients, nonsurvivors had a significantly higher highest cTnI level during the observation period than survivors. Additionally, patients who needed surgical intervention had significantly higher highest cTnI levels than patients who did not. ConclusionsAn elevated cTnI level is insufficient for the evaluation of BCI and the determination of the need for further treatment. The highest cTnI level during the observation period may be related to mortality and the need for surgery in BCI patients.

Elevated Admission Cardiac Troponin I Predicts Adverse Outcomes of Acute Type B Aortic Dissection after Endovascular Treatment.

BackgroundThere is a lack of evidence about the predictive role of serum cardiac troponin I (cTnI) on the long-term adverse outcomes of acute type B aortic dissection (aTBAD) patients after thoracic endovascular aortic repair (TEVAR). In this study, we identified whether cTnI was an independent risk factor of 5-year adverse outcomes for aTBAD patients after TEVAR.MethodsWe reviewed consecutive aTBAD patients without previous heart disease who were admitted for TEVAR. The total study population was divided into the cTnI(+) group (≥0.03 ng/mL) and the cTnI(−) group (<0.03 ng/mL) according to the time-dependent receiver operating characteristic curve analysis. The differences in clinical characteristics, operative details and clinical outcomes were compared between the two groups.ResultsThere was no difference in age and male prevalence between the two groups. Compared with the cTnI(−) group, the incidence of chronic kidney disease was higher in patients with cTnI ≥0.03 ng/mL. In addition, the cTnI(+) group presented with more frequent premature beats and non-myocardial-infarction ST-T segment changes. In terms of laboratory examinations, white blood cell counts, neutrophil counts, serum D-dimer and serum fibrin degradation products showed an increase in the cTnI(+) group, while lymphocyte and platelet counts showed a decrease in these patients. Patients with elevated cTnI suffered from increased risks of 5-year aortic-related adverse events (hazard ratio, HR = 1.822, 95% confidence interval, CI: 1.094–3.035; p = 0.021) and all-cause mortality (HR = 4.009, 95% CI: 2.175–7.388; p < 0.001).ConclusionAmong aTBAD patients without previous heart disease, preoperative elevated cTnI identified patients at an increased risk of long-term adverse outcomes after TEVAR.

CLINICAL IMPLICATIONS OF CARDIAC TROPONIN-I IN PATIENTS WITH HYPERTENSIVE CRISIS VISITING THE EMERGENCY DEPARTMENTS

Objective: Cardiac troponin-I (cTnI) is the representative marker of myocardial injury. Elevation of cTnI is frequently accompanied in patients with hypertensive crisis, but there are few studies on its prognostic significance in hypertensive crisis. The aim of this study was to determine whether cTnI could predict the all-cause mortality in patients with hypertensive crisis visiting the emergency department (ED). Design and method: In this observational study, we enrolled patients aged &gt; = 18 years who visited an ED between 2016 and 2019 for hypertensive crisis, which was defined as systolic blood pressure &gt; = 180 mmHg and/or diastolic blood pressure &gt; = 110 mmHg. Among the 6,467 patient, 3,938 patients who performed assay for cTnI were finally analyzed. Results: Among the 3,938 patients, 596 (15.1%) patients had cTnI levels above the 99th percentile upper reference limit (elevated cTnI, &gt; 0.04 ng/mL) and 600 (15.2%) patients had cTnI levels between the detection limit (&gt; = 0.01 ng/mL) and the 99th percentile upper reference limit (borderline cTnI). The 3-year all-cause mortality in elevated cTnI group, borderline cTnI groups, and normal cTnI groups were 41.6%, 36.5%, and 12.8%, respectively. After adjusting for confounding variables, patients with elevated cTnI (adjusted hazard ratio [HR] 2.01; 95% confidence interval [CI], 1.61–2.52) and patients with borderline cTnI (adjusted HR 1.64; 95% CI, 1.32–2.04) showed significantly higher risk of 3-year all-cause mortality than patients with normal cTnI. Conclusions: In patients with hypertensive crisis, cTnI levels provide useful prognostic information and permit the early identification of patients with an increased risk of death. Moreover, borderline cTnI was also significantly associated with higher risk of all-cause mortality. More intensive treatment and follow-up strategies are needed for patients with hypertensive crisis with elevated cTnI.

Prognostic Value of Cardiac Troponin I in Patients with Ventricular Tachyarrhythmias.

Besides the diagnostic role in acute myocardial infarction, cardiac troponin I levels (cTNI) may be increased in various other clinical conditions, including heart failure, valvular heart disease and sepsis. However, limited data are available regarding the prognostic role of cTNI in the setting of ventricular tachyarrhythmias. Therefore, the present study sought to assess the prognostic impact of cTNI in patients with ventricular tachyarrhythmias (i.e., ventricular tachycardia (VT) and fibrillation (VF)) on admission. A large retrospective registry was used, including all consecutive patients presenting with ventricular tachyarrhythmias from 2002 to 2015. The prognostic impact of elevated cTNI levels was investigated for 30-day all-cause mortality (i.e., primary endpoint) using Kaplan–Meier, receiver operating characteristic (ROC), multivariable Cox regression analyses and propensity score matching. From a total of 1104 patients with ventricular tachyarrhythmias and available cTNI levels on admission, 46% were admitted with VT and 54% with VF. At 30 days, high cTNI was associated with the primary endpoint (40% vs. 22%; log rank p = 0.001; HR = 2.004; 95% CI 1.603–2.505; p = 0.001), which was still evident after multivariable adjustment and propensity score matching (30% vs. 18%; log rank p = 0.003; HR = 1.729; 95% CI 1.184–2.525; p = 0.005). Significant discrimination of the primary endpoint was especially evident in VT patients (area under the curve (AUC) 0.734; 95% CI 0.645–0.823; p = 0.001). In contrast, secondary endpoints, including all-cause mortality at 30 months and a composite arrhythmic endpoint, were not affected by cTNI levels. The risk of cardiac rehospitalization was lower in patients with high cTNI, which was no longer observed after propensity score matching. In conclusion, high cTNI levels were associated with increased risk of all-cause mortality at 30 days in patients presenting with ventricular tachyarrhythmias.

A comparison of modelled serum cTnT and cTnI kinetics after 60 min swimming

Post-exercise elevations of cardiac troponin T (cTnT) and I (cTnI) are often used in isolation but interpreted interchangeably. Research suggests, however, that post-exercise cTn kinetic might differ with each isoform. In this cross-sectional observational study, we collected blood samples before, immediately after (5 minutes), and at 1-, 3-, 6-, 12-, and 24-hour post-exercise in a mixed cohort of 56 participants after a distance-trial of 60 min continuous swimming (age range from 14 to 22, 57.1% female). Cardiac troponin kinetics were modelled using Bayesian mixed-effects models to estimate time to peak (TTP) and peak concentration (PC) for each isoform, while controlling for participants sex, tanner stage and average relative heart rate during the test. Exercise induced an elevation of cTnT and cTnI in 93% and 75% of the participants, respectively. Cardiac troponin T peaked earlier, at 2.9 h (CI: 2.6 – 3.2 h) post-exercise, whereas cTnI peaked later, at 4.5 h (CI: 4.2 – 4.9 h). Peak concentrations for cTnT and cTnI were 2.5 ng/L, CI: 0 – 11.2 ng/L and 2.16 ng/L, CI: 0 – 22.7 ng/L, respectively. Additionally, we did not observe a systematic effect of sex and maturational status mediating cTn responses.

Elevated troponin I levels on admission predict long-term mortality in patients with acute cerebral infarction following thrombolysis

Background/objectiveCardiac diseases are frequently accompanied by elevated levels of biomarkers, among which, troponin is commonly investigated. The levels of plasma cardiac troponin I (cTnI), which has been shown to predict short-term mortality, are elevated in patients with acute cerebral infarction (ACI). However, few studies have assessed the association between cTnI concentration and long-term mortality in patients with ACI following thrombolysis.MethodsPatients with ACI admitted between January 1, 2014, and December 31, 2016, were registered. Data on demographics and outcomes with elevated cTnI levels were also collected.ResultsA total of 145 patients with ACI were recruited; 97 (66%), 30 (20%), and 18 (12%) patients had cTnI concentrations < 0.030 (group 1), 0.030–0.10 (group 2), and > 0.10 μg/L (group 3), respectively. cTnI elevation was associated with older age, atrial fibrillation, congestive heart failure, renal insufficiency, coronary artery disease, stroke severity (National Institutes of Health Stroke Scale score), and prior smoking history at admission. After adjusting for comorbidities and severity at 3 months after ACI, cTnI elevation on admission was significantly associated with ascending 5-year mortality (hazard ratio, 1.80; 95% confidence interval, 1.22–2.65).ConclusionsEven after adjusting for several possible confounders, cTnI elevation in patients with ACI treated with rt-PA was associated with a 1.80-fold increased risk of 5-year mortality.

Signs of Cardiac Injury in Critically Ill Paediatric Patients with COVID-19: a Single-Center Experience in Brazil.

ResumoFundamento 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.

Exploring the predictors and prognostic significance of exercise-induced cardiac troponin release in master athletes following a 28 km mountain race. The Vamvakou research project

ABSTRACT Background/objective Aetiology and significance of exercise-induced troponin release remains a contentious issue. We investigated the effect of a 28 km mountain run on cardiac troponin I (cTnI), in relation to training, performance, nutritional, biochemical and echocardiography variables, in a group of 25 recreational male master athletes. Material and methods A comprehensive list of variables related with nutrition, training, performance and echocardiography, was collected pre- and post-race. Twenty-four months later, outcomes regarding cardiovascular events were obtained. Results Serum cTnI values were increased after the race, with mean values rising from 7.2 ± 2.2 (before) to 80.0 ± 33.2 ng/L (post race), (p < 0.001) and 23/25(92%) exceeding Upper Reference limit (50 ng/L). Echocardiography did not reveal significant alterations, or correlations with cTnI values. The percentage difference in hs-cTnI concentrations pre- and post-race correlated positively with age, race-induced changes of selected muscle damage indices, resistance training volume and negatively with endurance capacity and training volume (r: −0.727 to 0.725, p < 0.05). All athletes reported no cardiovascular event during the 24-month period post-race. Conclusion cTnI elevation induced by a 28 km mountain running race was not correlated with echocardiographic, nutritional parameters and was less pronounced in athletes with larger endurance training history, in contrast with resistance training and age.

The Use of Panax Ginseng to Reduce the Cardiotoxicity of Doxorubicin and Study its Effect on Modulating Oxidative Stress, Inflammatory, and Apoptosis Pathways

BACKGROUND: Doxorubicin (DOX) is a broad-spectrum anti-cancer drug that is used to treat a variety of cancers, including blood cancers such as leukemia and solid tissue cancers. However, its use some time limited because of its cardiotoxicity. OBJECTIVE: The objective of the study was to determine the cardioprotective effect of ginseng in the case of cardiotoxicity caused by doxorubicin therapy. Methods: Thirty experimental animals (male Sprague Wistar rats) were used in this research and they were separated into three groups: Rats in Group I (n# = 10) were given distilled water plus normal saline, rats in Group II (n# = 10) were given distilled water plus doxorubicin, and rats in Group III (n# = 10) were given Panax ginseng plus doxorubicin. Serum concentration, malondialdehyde (MDA), glutathione reductase (GSH), lipid peroxidase (LPO), TNF (ng/L), cardiac troponin (ng/L), brain natriuretic peptide BNP(g/L), and caspase-3 (pmol/L) levels were measured in all groups. RESULTS: Doxorubicin caused substantial cardiotoxicity as a result of a significant increase in the elevation of cTnI to 40.09 ± 6.67 (ng/L). In addition, MDA, LPO, TNF-α, and caspase-3 levels were increased in doxorubicin group compared to the control group p &lt; 0.05. Panax ginseng reduced cardiac troponin (cTnI) However, its effect on reduction of BNP levels insignificantly compared to the doxorubicin group p = 0.06. Panax ginseng reduced LPO and MDA and raised the antioxidant potential biomarker GSH significantly compared to the doxorubicin group p &lt; 0.05. Panax ginseng significantly reduced inflammatory (TNF-α) and apoptotic (caspase-3) biomarkers when compared to the doxorubicin group. CONCLUSIONS: According to the findings of this study, Panax ginseng suppresses reactive oxygen species and inflammatory and apoptotic pathways in experimental rats, thereby preventing doxorubicin-induced cardiovascular events.