Increase In cTnI Research Articles

The Role of Triglyceride/HDL Ratio, Triglyceride-Glucose Index, and Pan-Immune-Inflammation Value in the Differential Diagnosis of Acute Coronary Syndrome and Predicting Mortality.

Objectives: We aimed to evaluate the predictive importance of various clinical and laboratory parameters in the differential diagnosis of Acute Coronary Syndrome (ACS). Understanding these predictors is critical for improving diagnostic accuracy, guiding therapeutic decisions, and ultimately enhancing patient outcomes. Methods: The study included a total of 427 patients diagnosed with ACS, comprising 142 with unstable angina, 142 with non-ST elevation myocardial infarction (NSTEMI), and 143 with ST elevation myocardial infarction (STEMI). The data were collected from medical records of patients treated at a tertiary care hospital between January 2020 and December 2024. In addition to other biochemical parameters, triglyceride/HDL ratio (THR), triglyceride-glucose index (TGI), and Pan-Immune-Inflammation Value (PIV) were calculated and compared. Results: THR, TGI, PIV, and mortality rate were statistically higher in the STEMI group (p = 0.034, p = 0.031, p = 0.022, p = 0.045, respectively). The risk factors were found to be significantly associated with STEMI in the multiple logistic regression analysis and included age, total cholesterol, triglycerides, diabetes mellitus, smoking, cTnI, LVEF, THR, TGI, and PIV. High THR increases the risk of STEMI (AUC = 0.67, 95% CI: 0.62-0.72, p = 0.020). High THR increases the risk of mortality in ACS patients (AUC = 0.70, 95% CI: 0.65-0.75, p = 0.004). THRs above 3.5 are associated with higher risk. Sensitivity is 75% and specificity is 60%. High TGI increases the risk of mortality in ACS patients (AUC = 0.73, 95% CI: 0.68-0.78, p = 0.007). TGIs above 8.5 are associated with higher risk. Sensitivity is 78% and specificity is 63%. High PIVs increase the risk of mortality in ACS patients (AUC = 0.75, 95% CI: 0.70-0.80, p = 0.009). PIVs above 370 are associated with higher risk. Sensitivity is 80% and specificity is 65%. The combination of TGI, THR, PIV, and cTnI has the highest predictive capability over individual parameters for STEMI and mortality. Conclusions: We found that age, total cholesterol, triglycerides, cTnI, THR, TGI, and PIV increase, low LVEF, presence of diabetes mellitus, and smoking have predictive values for STEMI and mortality in patients with ACS. Unlike the studies in the literature, this is the first study in which cTnI, THR, TGI, and PIV values were evaluated together in ACS and mortality prediction.

Ability of the coronary angiography-derived index of microcirculatory resistance to predict microvascular obstruction in patients with ST-segment elevation.

The coronary angiography-derived index of microvascular resistance (caIMR) correlates well with the index of microcirculatory resistance (IMR), which predicts microvascular obstruction (MVO). However, the relationship between caIMR and MVO remains unclear. To evaluate the predictive ability of caIMR of MVO after ST-segment elevation myocardial infarction (STEMI). CaIMR was calculated using computational flow and pressure simulation in patients with STEMI in whom MVO status had been assessed by cardiac magnetic resonance (CMR) after successful primary percutaneous intervention at Peking University First Hospital between December 2016 and August 2019. The clinical, biochemical, echocardiographic, and CMR characteristics were assessed according to MVO status. The predictive value of the clinical parameters and caIMR was evaluated. Fifty-three eligible patients were divided into an MVO group (n = 32) and a no-MVO group (n = 21). The caIMR tended to be higher in the MVO group (41.6 U vs. 30.1 U; p = 0.136). CaIMR and peak cardiac troponin-I (cTNI) were independent predictors of MVO (per 1-U increment in caIMR: odds ratio [OR] 1.044, 95% confidence interval [CI] 1.004-1.086, p = 0.030; per 1 ng/L increase in peak cTNI: OR 1.018, 95% CI 1.003-1.033, p = 0.022). In receiver-operating characteristic curve analysis, when a cut-off value of 45.17 U was used, caIMR had some ability to predict MVO (area under the curve 0.622, 95% CI 0.478-0.752, p = 0.127). CaIMR and peak cTNI were independent predictors of short-term MVO in patients with STEMI who had undergone successful primary percutaneous coronary intervention and may help to identify those at high risk of MVO.

Predictive Value of Post-operative Cardiac Troponin I and Lactate Levels After Ventricular Septal Defect Closure

Objectives: Although the mortality rate of primary ventricular septal defect (VSD) closure surgery has been reduced to <0.5% in many centers, low cardiac output syndrome and multi-organ failure syndrome development in the post-operative period are still the most common causes of mortality and morbidity. The use of biochemical markers in the early period can be used as effective predictors for reducing mortality and morbidity. In this study, the effect of post-operative serum lactate and cardiac troponin I (cTNI) levels on hospital mortality in patients who underwent primary closure of VSD was investigated retrospectively. Methods: The effect of lactate and cTNI values on hospital mortality in 52 patients who underwent surgical repair for VSD was investigated. Serum lactate levels of all patients in the first 6 h after the operation; on the first post-operative day, cTNI values were examined retrospectively. Serum lactate levels exceeding 3.5 mmol/ lt and cTNI values exceeding 35 ng/mL were determined as the cut-off points. Results: Serum lactate level and cTNI increase were found to be statistically different in the mortality group (p<0.05). It was shown that increased cTNI was associated with weight, left ventricular end-diastolic diameter, and cardiopulmonary bypass time (p<0.05). Serum lactate levels were 4.1±0.5 mmol/lt in the non-mortality group and 15.3±8.3 mmol/lt in the mortality group, and the difference was statistically significant (p<0.05). Hospital mortality was observed in 6 patients. Conclusion: In patients undergoing VSD closure surgery, serum lactate levels measured in the first 6 h postoperatively and cTNI levels measured on the first post-operative day are associated with hospital mortality. Concomitant elevations of lactate and cTNI values in patients after VSD closure should suggest to take caution and early supportive treatments to reduce mortality.

Preclinical cardiovascular safety assessment of pharmacology-toxicology relationship for a set of novel kinase inhibitors.

Cardiovascular toxicity is one of the more common causes of attrition in preclinical and clinical drug development. Preclinical cardiovascular safety assessment involves numerous in vitro and in vivo endpoints which are being continually reviewed and improved to lower the incidence of cardiovascular toxicity that manifests only after the initiation of clinical trials. An example of notable preclinical toxicity is necrosis in the papillary muscle of the left ventricle in dogs that is induced by exaggerated pharmacological effects of vasodilators or positive inotropic/vasodilating off-target drug effects. Two distinct, small-molecule inhibitors that target an intracellular kinase, Compound A and Compound B, were profiled in 2-week dose-range finding and 4-week toxicity studies. Serum cardiac troponin (cTnI) was evaluated after a single dose and after 2-week and 4-week repeat dose studies with each kinase inhibitor. Acute effects on hemodynamic (heart rate, blood pressures, left ventricular contractility) and electrocardiographic (QTcV, PR, QRS intervals) endpoints by each inhibitor were assessed in an anesthetized dog cardiovascular model. Cardiovascular degeneration/necrosis with and without fibrosis was observed in dogs and correlated to increases in serum cTnI in repeat-dose toxicity studies. At the same doses used in toxicologic assessments, both kinase inhibitors produced sustained increases in heart rate, left ventricular contractility, and cardiac output, and decreases in mean arterial pressure. Cardiac pathology findings associated with these 2 kinase inhibitors were accompanied not only by cardiac troponin elevations but also associated with hemodynamic changes, highlighting the importance of the link of the physiologic-toxicologic interplay in cardiovascular safety assessment.

Cardiac Troponin and Treatment Effects of Omecamtiv Mecarbil: Results From the GALACTIC-HF Study

BackgroundOmecamtiv mecarbil improves outcomes in patients with heart failure and reduced ejection fraction (HFrEF). We examined the relationship between baseline troponin, change in troponin over time, and the treatment effect of omecamtiv mecarbil in patients enrolled in the Global Approach to Lowering Adverse Cardiac Outcomes through Improving Contractility in Heart Failure (GALACTIC-HF) trial (NCT02929329). MethodsGALACTIC-HF was a double-blind, placebo-controlled trial that randomized 8256 patients with symptomatic HFrEF to omecamtiv mecarbil or placebo. High sensitivity troponin I (cTnI) was measured serially at a core laboratory. We analyzed the relationship between both baseline cTnI and change in cTnI concentrations with clinical outcomes and the treatment effect of omecamtiv mecarbil. ResultsHigher baseline cTnI concentrations were associated with a risk of adverse outcomes (hazard ratio for the primary endpoint of time to first HF event or CV death = 1.30; 95% CI 1.28, 1.33, p < 0.001 per doubling of baseline cTnI). Although the incidence of safety outcomes was higher in patients with higher baseline cTnI, there was no difference between treatment groups. Treatment with omecamtiv mecarbil led to a modest increase in cTnI that was related to plasma concentrations of omecamtiv mecarbil and peaked at 6 weeks. An increase in troponin from baseline to week 6 was associated with an increased risk of the primary endpoint (p < 0.001) which was similar regardless of treatment assignment (p value for interaction = 0.2). ConclusionsIn a cohort of patients with HFrEF, baseline cTnI concentrations were strongly associated with adverse clinical outcomes. Although cTnI concentrations were increased in patients treated with omecamtiv mecarbil, we did not find a differential effect of omecamtiv mecarbil on either safety or efficacy based on baseline cTnI status or change in cTnI.

Cardiac troponin I release after transcatheter closure of atrial septal defects is associated with supraventricular arrhythmias on early follow-up.

Atrial septal defects (ASD) are prevalent congenital heart anomalies found in the adult population. Percutaneous ASD closure has become a routine clinical practice. Elevation of postprocedural transient cardiac biomarkers and exacerbation of supraventricular arrhythmias have been reported in the subject literature. To explore the relationship between cardiac troponin I (cTnI) elevation and supraventricular ectopy (SVE) following percutaneous closure of secundum atrial septal defect (ASD) in adult patients. 600 consecutive patients who underwent successful transcatheter ASD secundum closure were analyzed. Serum levels of cTnI were measured before and within 72 h of device implantation. 24-hour Holter monitoring was performed before the procedure, at 1 month, and at 6 months of follow-up. SVE burden increased 1 month after the procedure (median 1021.00; min.-max. 11.00-29 862.00) compared to baseline values (median 146.00; min.-max. 0-1865.00; p < 0.01). 61.7% of patients demonstrated a cTnI rise exceeding 50% of the upper reference limit within 24 h of the procedure. A statistically significant positive correlation between SVE burden 1 month after the procedure and periprocedural cTnI increase (p < 0.05, r = 0.41) was observed, while cTnI levels significantly correlated with procedure and fluoroscopy time (p < 0.001), device size (p < 0.001) and maximal ASD diameter (p < 0.001). A significant increase of cTnI is noted frequently after transcatheter ASD closure and seems to predict exacerbation in SVE burden on short-term follow up. The independent risk factors of cTnI rise are prolonged procedure duration and larger device sizes.

Mechanistic study of electroacupuncture preconditioning in alleviating myocardial ischemia-reperfusion injury in rats: involvement of mTOR/ROS signaling pathway to inhibit ferroptosis

Purpose The objective of this study was to investigate the mechanism of electroacupuncture pretreatment in reducing myocardial ischemia-reperfusion injury in rats. Materials and methods The comparison of HR among the different groups did not yield statistically significant differences (p > 0.05). Additionally, the trend of HR change at different time points within each group was not statistically significant (p > 0.05). In contrast, the comparison of SBP among the different groups showed statistically significant differences (p < 0.05). Furthermore, the trend of SBP change at different time points within each group exhibited significant differences (p < 0.05). Results Compared to the Sham group, rats in the I/R group and EA control group showed a significant decrease in EF, FS, SOD, p-mTOR/mTOR, GPX4, and FTH1, and an increase in CK-MB, cTnI, LDH, iron, ROS, MDA, ACSL4, and NCOA4 (p < 0.05). Compared to EA control group, rats in the EA group exhibited a significant increase in EF, FS, SOD, p-mTOR/mTOR, GPX4, and FTH1, and a decrease in CK-MB, cTnI, LDH, iron, ROS, MDA, ACSL4, and NCOA4 (p < 0.05). Compared to the EA group, rats in the EA + RAP group showed a significant decrease in EF, FS, SOD, p-mTOR/mTOR, GPX4, and FTH1, and an increase in CK-MB, cTnI, LDH, iron, ROS, MDA, ACSL4, and NCOA4 (p < 0.05). Conclusions Electroacupuncture preconditioning confers protective effects against myocardial ischemia-reperfusion injury in rats. Its mechanism may involve the activation of the mTOR/ROS signaling pathway by electroacupuncture to inhibit ferroptosis.

Relation between high-sensitivity troponin I serum levels and myocardial ischemia in patients with suspected chronic coronary syndrome: The RESET-MI study

BackgroundPrevious studies showed that exercise may increase cardiac troponin serum levels; whether the occurrence of myocardial ischemia influences the changes of exercise-induced troponin raise, however, remains debatable. MethodsWe prospectively enrolled consecutive patients undergoing for the first time an elective stress myocardial perfusion scintigraphy (MPS) because of clinical suspicion of obstructive coronary artery disease (CAD). Patients were divided into 3 groups based on the evidence and degree of stress-induced myocardial ischemia at MPS: 1) group 1, no myocardial ischemia (≤4 %); 2) group 2, mild myocardial ischemia (5–10 %); 3) group 3, moderate-to-severe myocardial ischemia (≥10 %). High-sensitivity cardiac troponin I (cTnI) was measured immediately before (T0) and 1 hour (T1) and 4 h (T2) after the stress test. ResultsOne hundred-seven patients (71 males; age 65.6 ± 9.4 years) were enrolled in the study. Serum hs-cTnI concentrations (logarithmic values) significantly increased after MPS, compared to baseline, in the whole population, from 1.47±1.26 ng/L at T0, to 1.68±1.12 ng/L at T1 (p<0.001) and 2.15±1.02 ng/L at T2 (p<0.001 vs. both T0 and T1). The increase in hs-cTnI did not significantly differ between the 3 groups (p = 0.44). The heart rate achieved during the test was the strongest determinant of cTnI increase (p < 0.001) after the stress test. ConclusionsIn patients with suspected CAD, stress MPS induces an increase of cTnI that is independent of the induction and extension/severity of myocardial ischemia and is mainly related to myocardial work, as indicated by the heart rate achieved during the test.

The specificity of cardiac troponin elevations for myocardial infarction declines with age

Abstract Background Cardiac troponin T (cTnT) and I (cTnI) are the gold standard biomarkers of myocardial infarction (MI). Studies have shown that the concentration of cTn increases with age among healthy individuals, but the clinical impact of this is unclear. Further, there seem to be a difference in the increases in cTnI and in cTnT - the latter being more sensitive to increasing age. Purpose To investigate the impact of age on the diagnostic ability of cTnT and cTnI for myocardial infarction. Methods This nationwide cohort study includes patients admitted with cTn measurements from 2009-2022 using one of five cTn assays: Roche high-sensitivity cTnT (hs-cTnT), Abbott Alinity high sensitivity cTnI (hs-cTnI), Siemens Vista Hs-cTnI, Siemens Atellica hs-cTnI and Beckman-Coulter hs-cTnI. We selected the peak concentration of cTn on admission and grouped patients into those who had cTnI and those who had cTnT measured which were divided into age groups of &amp;lt;40 years, 40-50 years, 50-60 years, 60-70 years, 70-80 years, 80-90 years and &amp;gt;90 years. The primary outcome was a diagnosis of MI during admission. Receiver operating characteristics (ROC) were used for the concentration of cTn normalized to the assays 99th percentile, and we explored the specificity of elevations of each assay above the 99th percentile. Results A total of 350,428 patients were included in this study with a median age of 67 years (IQR 52-77); 188,382 (54%) were males and 48,262 (14%) had a history of ischemic heart disease prior to the admission. When grouping for type of cTn used, more patients were treated when hs-cTnT (240,660, 69%) was used compared with hs-cTnI (109,768, 31%). The patient treated using hs-cTnT were slightly older than patients treated with hs-cTnI, 67 years (IQR 53-77) vs 65 years (53-77) p&amp;lt;0.001. During the admission 29,023 patients (8.3%) had a MI. Figure 1 panel A shows the ROC curve of hs-cTnT and hs-cTnI for each age group. Both biomarkers showed a decline in the area under the curve (AUC) with increasing age. Figure 1 panel B shows the AUC for each age group. Hs-cTnI had a higher AUC for all age groups and seemed to decrease less with age. Figure 2 shows the specificity for the 99th percentile of each assay for the age groups. There were substantial differences in the specificity at the 99th percentile between cTn assays, with the cTnT assay being the least specific for all age groups, while the two Siemens assays had the highest specificity. An elevation above the 99th percentile of the cTnT assay had a specificity of 3% in the group of patients &amp;gt;90 years old. Conclusion The specificity of elevation of cTn for MI declined with increasing age for all assays. This decline seemed to be largest for the cTnT assay were an elevation above the 99th percentile among patients &amp;gt;90 years old had a specificity of 3% for MI.Figure 1Figure 2

Relation between high-sensitivity troponin i serum levels and myocardial ischemia in patients with suspected chronic coronary syndrome: the RESET-MI study

Abstract Background Previous studies showed that exercise may increase cardiac troponin serum levels; however, whether exercise-induced myocardial ischemia influences the exercise-induced increase of troponin levels remains debatable. Methods We prospectively enrolled consecutive patients undergoing an elective stress myocardial perfusion scintigraphy (MPS) because of a clinical suspicion of obstructive coronary artery disease (CAD). Patients were divided into 3 groups according to the evidence and degree of stress-induced myocardial ischemia at MPS: 1) Group 1, no ischemia (≤4% of myocardium); 2) Group 2, mild ischemia (5-10%); 3) Group 3, moderate-to-severe myocardial ischemia (≥10%). High-sensitivity cardiac troponin I (cTnI) was measured immediately before (T0) and 1 hour (T1) and 4 hours (T2) after the stress test. A successive evaluation of patients was performed at 24 months. Results One-hundred consecutive patients (64 males; age 65.5±9.5 years) were enrolled in the study. An exercise stress test and a dipyridamole stress test were performed in 81 and 19 patients, respectively. Serum hs-cTnI concentrations significantly increased after stress test, compared to baseline, in the whole population, from (median, interquartile range) 3.9 (2.5-6.1) ng/L at T0, to 4.2 (2.8-7.3) ng/L at T1 (p&amp;lt;0.001) and 6.7 (3.8-14.1) ng/L at T2 (p&amp;lt;0.001 vs. both T0 and T1). The increase in hs-cTnI did not significantly differ between the 3 groups (p=0.35; Figure). The increase was significant after both exercise (+54.5%) and dipyridamole (+18.2%), although the increase was greater after exercise (p=0.002). Heart rate achieved during the test was the strongest determinant of cTnI increase after the stress test (p &amp;lt; 0.001). Conclusions In patients with suspected CAD, stress MPS induces an increase of cTnI that is independent of the induction and severity of myocardial ischemia and is mainly related to myocardial work, as indicated by heart rate achieved during the stress test.Figure

Cardiac Biomarker Responses to Acute Exercise in Show Jumping Horses.

Cardiac biomarkers are useful to identify cardiac muscle variations in human and equine medicine. The aim of this study was to investigate the acute effect of a bout of show jumping training on serum activity of cardiac and muscular biomarkers in healthy athletic horses to include cardiac troponin (cTnI), myoglobin (MB), aspartate amino transferase (AST), alanine amino transferase (ALT), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH). Serum samples were collected from seven Italian Saddle horses (three geldings and four mares; 10 ± 3 years; mean body weight 480 ±70 kg), regularly trained for show jumping at rest, immediately after exercise (show jumping simulate trial) and during the recovery period (30 and 60 min after exercise). ANOVA was applied to all parameters, and Pearson correlation coefficient t (r) evaluated. Immediately after exercise there was an increase in cTnI (P < .01), MB (P < .01), and CPK (P < .005); a positive correlation between cTnI and AST and between AST and LDH; and a negative correlation between cTnI and ALT and between ALT and CPK. Thirty minutes after exercise, there was a positive correlation between AST and ALT and between AST and LDH, while 60 mintues after exercise, there was a positive correlation between MB and LDH and a negative correlation between AST and CPK. The results obtained demonstrate the cardiac and muscular response to short-term intense exercise show jumping exercise.

Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice

BackgroundThe toxic effect of doxorubicin on the heart limits its clinical usage in cancer therapy. This work intended to investigate, for the first time, the efficacy of rifampicin administration against doxorubicin-induction of cardiotoxicity in mice. Forty adult male albino mice were distributed into four sets: Control, Doxorubicin, Doxorubicin + Rifampicin 0.107, and Doxorubicin + Rifampicin 0.214, with n = 10 for each. Heart histopathology and biochemical assays for heart function tests [creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), cardiac troponin I (cTnI), atrial natriuretic peptide (ANP), and vascular endothelial growth factor (VEGF)], oxidative stress [malondialdehyde (MDA) and superoxide dismutase (SOD)], and minerals [phosphorus, sodium, potassium, and calcium] were done.ResultsDoxorubicin-induced cardiotoxicity using a total dose of 15 mg/kg was confirmed histologically. Cardiomyocytes showed congestion, necrosis, edema, and inflammatory cell infiltration. Biochemically, elevations in LDH, CK, and AST activities, p < 0.001, as well as increases in cTnI and ANP levels, p < 0.001, increased oxidative stress (MDA, p < 0.001), high minerals (Na, K, p < 0.001, P, p < 0.01, and Ca, p < 0.05), with reduced VEGF concentration, p < 0.001, and low antioxidant (SOD, p < 0.001) were observed in the Doxorubicin group compared to control. Co-treatment with rifampicin significantly (p < 0.001) reduced the increased oxidative stress, high Na and K, increased LDH, CK, AST, cTnI, and ANP, and elevated the low SOD toward the normal ranges. Our histological data supported our biochemical data; rifampicin dose 0.214 mg/kg showed better improvements than dose 0107.ConclusionsOur results demonstrated that rifampicin could help protect the body against doxorubicin-induced cardiotoxicity through its antioxidative effect.

Abstract P2001: Deficiency Of Claudin-5 Leads To Myocardial Atrophy And Dilation In Mouse Heart With Severe Mitochondrial Dysfunction And Electrical Dissociation

Background: Cardiac overexpression of Claudin-5 (Cldn5) exerts protection against myocardial ischemia and reperfusion injury. However, whether cardiac deficiency of Cldn5 affects cardiac function is still unclear. Here we investigated the role of Cldn5 in mouse heart by means of cardiac Cldn5 knockdown to better understand the intracellular function of Cldn5 in cardio-protection. Methods and Results: Cldn5 shRNA adeno-associated virus (AAV) was used to knockdown Cldn5 in the left ventricle of male C57BL/6J mice by intramyocardial injection. Four weeks post AAV injection, echocardiography and electrocardiography were performed to measure cardiac function. We found 25% of mice died in Cldn5 shRNA AAV injection group. The residual mice were terminated followed by left ventricles isolation for proteomics analysis, cytokine analysis, WGA staining, Masson-trichrome staining and transmission electron microscope (TEM) observation. The signal pathway markers of apoptosis, autophagy and lipid peroxidation were also detected by western blot. The protein level of Cldn5 in left ventricles was decreased by 75% in shRNA AAV injection group accompanied by changes of bcl-2, bax, LC3II, p62, Cox2 and GPX4. The fraction shortening of the heart was decreased by 23.5% with ventricular dilation and ST elevation. We also observed the increase of IL-1beta, TNF alpha, BNP, CT and cTnI in myocardium. WGA staining showed the area of cross section of single cardiomyocyte was decreased and Masson staining showed the collagen deposition was increased in myocardium. The TEM indicated Cldn5 knockdown induced mitochondrial fission and depletion. Finally, the proteomics analysis demonstrated that Cldn5 knockdown severely disturbed ATP metabolic regulation, mitochondrial permeability transition pore opening, calcium ion transport, cardiac contraction, endoplasmic reticulum stress response and antioxidant activity in the AAV injected myocardium. Conclusion: We demonstrated for the first time the deficiency of Cldn5 in myocardium caused myocardial atrophy and dilation with deteriorative heart function. The mechanism of Cldn5 deficiency-induced cardiac dysfunction is associated with severe mitochondrial dysfunction and excitation-contraction coupling.

Exercise-induced myocardial T1 increase and right ventricular dysfunction in recreational cyclists: a CMR study

PurposeAlthough cardiac troponin I (cTnI) increase following strenuous exercise has been observed, the development of exercise-induced myocardial edema remains unclear. Cardiac magnetic resonance (CMR) native T1/T2 mapping is sensitive to the pathological increase of myocardial water content. Therefore, we evaluated exercise-induced acute myocardial changes in recreational cyclists by incorporating biomarkers, echocardiography and CMR.MethodsNineteen male recreational participants (age: 48 ± 5 years) cycled the ‘L’étape du tour de France” (EDT) 2021’ (175 km, 3600 altimeters). One week before the race, a maximal graded cycling test was conducted to determine individual heart rate (HR) training zones. One day before and 3–6 h post-exercise 3 T CMR and echocardiography were performed to assess myocardial native T1/T2 relaxation times and cardiac function, and blood samples were collected. All participants were asked to cycle 2 h around their anaerobic gas exchange threshold (HR zone 4).ResultsEighteen participants completed the EDT stage in 537 ± 58 min, including 154 ± 61 min of cycling time in HR zone 4. Post-race right ventricular (RV) dysfunction with reduced strain and increased volumes (p < 0.05) and borderline significant left ventricular global longitudinal strain reduction (p = 0.05) were observed. Post-exercise cTnI (0.75 ± 5.1 ng/l to 69.9 ± 41.6 ng/l; p < 0.001) and T1 relaxation times (1133 ± 48 ms to 1182 ± 46 ms, p < 0.001) increased significantly with no significant change in T2 (p = 0.474). cTnI release correlated with increase in T1 relaxation time (p = 0.002; r = 0.703), post-race RV dysfunction (p < 0.05; r = 0.562) and longer cycling in HR zone 4 (p < 0.05; r = 0.607).ConclusionStrenuous exercise causes early post-race cTnI increase, increased T1 relaxation time and RV dysfunction in recreational cyclists, which showed interdependent correlation. The long-term clinical significance of these changes needs further investigation.Trial registration numbers and dateNCT 04940650 06/18/2021. NCT 05138003 06/18/2021.

Predictive Value of Perioperative Cardiac Troponin I in Patients Undergone Liver Transplantation: A Retrospective Cohort Study.

To examine the change rule and clinical significance of cardiac troponin I (cTnI) in the perioperative period of liver transplantation in adults, as well as its association with 28-day mortality. This was a retrospective cohort study: patients who underwent elective orthotopic liver transplantation (OLT) in Beijing Chao-Yang Hospital between June 2015 and June 2020 were selected, and plasma cTnI values were collected through the electronic medical record system within 7 days after surgery. Furthermore, the baseline clinical data of these patients were collected, and the change curve of cTnI values following liver transplantation was plotted. Using univariate and multivariate logistic regression models, the relationship between the level of postoperative cTnI and short-term mortality was investigated. The primary study endpoint was mortality within 28 days after surgery. We included 414 patients who had undergone liver transplantation in this study, 48 of whom died within 28 days after surgery. cTnI, a specific marker of myocardial injury, could predict that the postoperative cardiovascular complications were higher in the death group and significantly affect the short-term prognosis of patients; however, its prognostic cut-off value was approximately 0.545 ng/mL (13×URL), indicating that a minor elevation of cTnI after liver transplantation did not significantly affect the prognosis. Moreover, a comparison of the baseline data and postoperative ICU management scores of the two groups revealed that diabetes, maximum value of cTnI >0.545 ng/mL within 7 days, and the need for postoperative renal replacement therapy (RRT) were independent prognostic factors of death within 28 days after liver transplantation. Within 7 days after surgery, an increase in cTnI to the maximum value of 0.545 ng/mL (13×URL) could have a significant impact on the short-term prognosis of patients. Diabetes and postoperative RRT were two independent prognostic factors for liver transplantation perioperative mortality.

Patterns of Cardiac Troponin I Concentrations as Risk Predictors of Cardiovascular Disease and Death: The Trøndelag Health Study

BackgroundConcentrations of cardiac troponin predict risk of cardiovascular disease and death in the general population. There is limited evidence on changing patterns of cardiac troponin in the years preceding cardiovascular events. MethodsWe analyzed cardiac troponin I (cTnI) with a high-sensitivity assay in 3272 participants in the Trøndelag Health (HUNT) Study at study visit 4 (2017-2019). Of these, 3198 had measurement of cTnI at study visit 2 (1995-1997), 2661 at study visit 3, and 2587 at all 3 study visits. We assessed the trajectories of cTnI concentrations in the years prior to cardiovascular events using a generalized linear mixed model, with adjustment for age, sex, cardiovascular risk factors, and comorbidities. ResultsAt HUNT4 baseline, median age was 64.8 (range 39.4-101.3) years, and 55% were women. Study participants who were admitted because of heart failure or died from cardiovascular cause on follow-up had a steeper increase in cTnI compared with study participants with no events (P < .001). The average yearly change in cTnI was 0.235 (95% confidence interval, 0.192-0.289) ng/L for study participants with heart failure or cardiovascular death, and −0.022 (95% confidence interval, −0.022 to −0.023) ng/L for study participants with no events. Study participants who experienced myocardial infarction, ischemic stroke, or noncardiovascular mortality exhibited similar cTnI patterns. ConclusionsFatal and nonfatal cardiovascular events are preceded by slowly increasing concentrations of cardiac troponin, independently of established cardiovascular risk factors. Our results support the use of cTnI measurements to identify at-risk subjects who progress to subclinical and later overt cardiovascular disease.

Prolonged infusion of bivalirudin after elective percutaneous coronary intervention protects against procedural myocardial injury (a COBER study)—a randomized trial

Procedural myocardial injury (PMI), which is the most common complication of elective percutaneous coronary intervention (ePCI), is associated with future adverse cardiac events. In this randomized pilot trial, we assessed the effects of prolonged use of the anti-coagulant bivalirudin on PMI after ePCI. Patients undergoing ePCI were randomized into the following two groups: the bivalirudin use during operation group (BUDO, 0.75 mg/kg bolus plus 1.75 mg/kg/h) and the bivalirudin use during and after operation for 4 h (BUDAO, 0.75 mg/kg bolus plus 1.75 mg/kg/h). Blood samples were collected before and 24 h after ePCI (per 8 h). The primary outcome, PMI, was defined as an increase in post-ePCI cardiac troponin I (cTnI) levels of > 1 × 99th% upper reference limit (URL) when the pre-PCI cTnI was normal or a rise in cTnI of > 20% of the baseline value when it was above the 99th percentile URL, but it was stable or falling. Major PMI (MPMI) was defined as a post-ePCI cTnI increase of > 5 × 99th% URL. A total of 330 patients were included (n = 165 per group). The incidences of PMI and MPMI were not significantly higher in the BUDO group than in the BUDAO group (PMI: 115 [69.70%] vs. 102 [61.82%], P = 0.164; MPMI: 81 [49.09%] vs. 70 [42.42%], P = 0.269). However, the absolute change in cTnI levels (calculated as the peak value 24 h post-PCI minus the pre-PCI value) was notably larger in the BUDO group (0.13 [0.03, 1.95]) than in the BUDAO group (0.07 [0.01, 0.61]) (P = 0.045). Moreover, the incidence of bleeding events was similar between the two groups (BUDO: 0 [0.00%]; BUDAO: 2 [1.21%], P = 0.498). Prolonged infusion of bivalirudin for 4 h after ePCI reduces PMI severity without increasing the risk of bleeding.ClinicalTrials.gov.Number: NCT04120961, 09/10/2019.

Comparison of the predictive value of the modified CADILLAC, GRACE and TIMI risk scores for the risk of short-term death in patients with acute ST segment elevation myocardial infarction after percutaneous coronary intervention

To establish a modified controlled abciximab and device investigation to lower late angioplasty complication (CADILLAC) score, and to compare the predictive value of modified CADILLAC score, the global registry of acute coronary event (GRACE) score and the thrombolysis in myocardial infarction (TIMI) score in predicting the risk of short-term death after percutaneous coronary intervention (PCI) in patients with acute ST segment elevation myocardial infarction (STEMI). A retrospective study was conducted. The clinical data of 169 STEMI patients under going PCI admitted to the department of cardiology of Guizhou Provincial People's Hospital from September 2019 to December 2020 through emergency chest pain fast track were enrolled. A multivariate Logistic regression analysis was used to screen the factors closely related to the mortality risk within 30 days of STEMI, and a modified CADILLAC scoring system was established by referring to CADILLAC scoring settings. The score of modified CADILLAC, GRACE and TIMI scores of patients were calculated after admission, and the number of deaths due to cardiovascular disease (CVD) within 30 days after onset was recorded. The receiver operating characteristic curve (ROC curve) was used to evaluate the predictive value of three scoring systems on the risk of death within 30 days after PCI in patients with STEMI. In 169 STEMI patients, 16 patients died of CVD within 30 days after PCI, and the actual case mortality was 9.47%. Multivariate Logistic regression analysis showed that age > 75 years old, cardiac function Killip ≥ Grade III, ventricular arrhythmia, ST segment elevation ≥ 0.2 mV, cardiac troponin I (cTnI) increase, systolic blood pressure (SBP) < 90 mmHg (1 mmHg ≈ 0.133 kPa) were all independent predictors of death after PCI in STEMI patients. The improved CADILLAC scoring system was constructed based on the above predictive factors combined with left ventricular ejection fraction (LVEF) less than 0.40. The GRACE, TIMI and modified CADILLAC scores of dead patients were significantly higher than those of survival patients (GRACE score: 197.60±31.83 vs. 149.81±36.72, TIMI score: 11.21±2.13 vs. 7.27±1.97, modified CADILLAC score: 12.60±2.52 vs. 6.96±2.17, all P < 0.05). The higher the risk stratification of the three scores, the higher the mortality of patients with CVD within 30 days after PCI [the mortality of patients with low, medium and high risk in GRACE score were 2.41% (2/83), 9.61% (5/52) and 26.47% (9/34); the mortality of patients with low, medium and high risk in TIMI score were 3.12% (3/96), 12.82% (5/39) and 23.53% (8/34); and the mortality of patients with low, medium and high risk in modified CADILLAC score were 3.19% (3/94), 7.69% (4/52) and 39.13% (9/23), respectively, all P < 0.01]. The area under the ROC curve (AUC) of the GRACE, TIMI and the modified CADILLAC scores predicting the risk of death 30 days after PCI in STEMI patients were 0.855 [95% confidence interval (95%CI) was 0.702-0.923], 0.725 (95%CI was 0.666-0.812) and 0.882 (95%CI was 0.732-0.936), respectively, all P = 0.000; the sensitivity of its prediction accuracy were 81.59%, 78.65% and 89.26%, and the specificity were 78.62%, 57.12% and 75.54%, respectively. The GRACE and the modified CADILLAC scores have predictive value for the short-term mortality risk of STEMI patients after PCI, and the modified CADILLAC score is more accurate. But the TIMI score has a poor predictive effect on the short-term mortality risk of STEMI patients after PCI.

691 RELATION BETWEEN HIGH-SENSITIVITY TROPONIN I SERUM LEVELS AND MYOCARDIAL ISCHEMIA IN PATIENTS WITH SUSPECTED CHRONIC CORONARY SYNDROME: THE RESET-MI STUDY

Abstract Background Although the detection of a rise and/or fall pattern of cardiac troponin (cTn) serum levels in presence of a clinical context of acute myocardial ischemia, represents the main criterion for the diagnosis of acute myocardial infarction (AMI), troponins may increase in various conditions of myocardial injury different from ischemic myocardial necrosis or simply following myocardial ischemia, in the absence of cell necrosis. Some studies found that troponins also increase after physical exertion and other types of stressful stimuli in the absence of obstructive CAD and myocardial ischemia. No previous study, however, investigated the relation between cTn serum levels and the extent of myocardial ischemia in patients with a suspect of CCS. Methods We prospectively enrolled consecutive patients undergoing an elective stress myocardial perfusion scintigraphy (MPS) because of a clinical suspicion of obstructive coronary artery disease (CAD). Patients were divided into 3 groups based on the evidence and degree of stress-induced MI at MPS: 1) group 1, no MI (≤4%); 2) group 2, mild MI (5-10%); 3) group 3, moderate-to-severe MI (≥10%). High sensitivity (hs)-cTnI was measured immediately before (T0) and 1 hour (T1) and 4 hours (T2) after the stress test. A successive evaluation of patients was performed at 24 months. Results One-hundred consecutive patients (64 males; age 65.5±9.5 years) were enrolled in the study. Serum hs-cTnI concentrations significantly increased after MPS, compared to baseline, in the whole population, from (median, interquartile range) 3.9 (2.5-6.1) ng/L at T0, to 4.2 (2.8-7.3) ng/L at T1 (p&amp;lt;0.001) and 6.7 (3.8-14.1) ng/L at T2 (p&amp;lt;0.001 vs. both T0 and T1). The increase in hs-cTnI did not significantly differ between the 3 groups (p=0.35). Heart rate achieved during the test was the strongest determinant of cTnI increase (p &amp;lt; 0.001). No major adverse cardiac event occurred during follow-up. Only 12 patients (12%) underwent coronary revascularization, whereas angina episodes were reported by 23 patients (23%). There were no significant differences in hs-cTnI increase after the stress test between patients with clinical events at follow-up compared with those who did not report myocardial revascularization or angina recurrence (p=0.21). Conclusions In patients with suspected CAD, stress MPS induces an increase of cTnI that is independent of the induction and the extent of myocardial ischemia and is mainly related to myocardial work, as indicated by HR achieved during the test.

Cardiac troponins: Mechanisms of release and role in healthy and diseased subjects.

The cardiac troponins (cTns), cardiac troponin C (cTnC), cTnT, and cTnI are key elements of myocardial apparatus, fixed as protein complex on the thin filament of sarcomere and are involved in the regulation of excitation-contraction coupling of cardiomyocytes in the presence of Ca2+ . Circulating cTnT and cTnI (cTns) increase following cardiac tissue necrosis, and they are consolidated biomarkers of acute myocardial infarction (AMI). However, the use of high sensitivity (hs)-immunoassay tests for cTnT and cTnI has made it possible to identify a multitude of other clinical conditions associated with increased circulating levels of cTns. cTns can be measured also in the peripheral circulation of healthy subjects or athletes, suggesting that different mechanisms are involved in the release of cTns in the blood independently of cardiac cell necrosis. In this review, the molecular/cellular mechanisms involved in cTns release in blood and the exploitation of cTnI and cTnT as biomarkers of cardiac adverse events, in addition to cardiac necrosis, are discussed.