Elevated cTnI Research Articles

Assessment of left ventricular systolic function in hypertrophic cardiomyopathy patients with myocardial injury: a study based on layer-specific speckle tracking echocardiaography.

We conducted this study to investigate left ventricle (LV) systolic function in endocardial, mid-myocardial, and epicardial layers by two-dimensional (2D) speckle tracking echocardiography (STE) in hypertrophic cardiomyopathy (HCM) patients with myocardial injury indexed by elevated serum cardiac troponin I (cTnI). Twenty-nine HCM patients with myocardial injury, thirty-five HCM patients without myocardial injury, and ninty-one healthy controls were enrolled in this study. Serum cTnI > 0.026ng/mL was defined as myocardial injury. LV longitudinal and circumferential strain (LS and CS) were assessed in endocardial, mid-myocardial and epicardial layers. Layer-specific LS and CS differed significantly (all P < 0.001) among all three groups in all three layers, in a descending order from healthy controls to HCM patients without myocardial injury to HCM patients with myocardial injury. Layer-specific LS and CS were decreased the most in HCM patients with myocardial injury indexed by elevated seum cTnI (all P < 0.05). In HCM patients with myocardial injury, layer-specific LS and CS were significantly lower in the segments with greater hypertrophy (segmental thickness ≥ 15mm) (all P < 0.001) except for endocardial CS (P > 0.05). Layer-specific evaluation of LV strain may improve understanding of impaired LV systolic function in HCM patients with myocardial injury, thus preventing further damage.

Nanoformulated Ajwa (Phoenix Dactylifera) Bioactive Compounds Improve the Safety of Doxorubicin without Compromising its Anticancer Efficacy in Breast Cancer.

One of the major causes of women’s death in the world is breast cancer. Consequently, numerous regimens for the control of this severe disease have been created. The chemotherapeutic agent doxorubicin (DOX) is frequently used to treat breast cancer, but DOX can also cause cardiotoxic effects that lead to heart failure. Therefore, many research studies have been done to find a natural product that effectively potentiates or does not interfere with DOX’s anticancer effect and protects against its cardiotoxicity. We studied the impact of combined nanoformulated Ajwa (Phoenix dactylifera) selected bioactive compounds (BAC) rutin (R) and quercetin (Q) in nude mice breast cancer xenografts on DOX-mediated anticancer efficacy. We also studied if this Ajwa BAC could safeguard against DOX-mediated cardiomyopathies by evaluating plasma cardiac troponin-I (cTn-I) levels and cardiac histopathology. Nanoformulated Ajwa BAC effectively alleviated weight loss induced by DOX in mice and significantly decreased the elevated cTn-I. Furthermore, 5 mg RQ-NPs/kg of nude mice that subcutaneously daily injected for 11 days, attenuated the histopathological alterations induced in cardiac muscles due to DOX without any interference with the anticancer effects of DOX against breast cancer.

Evaluation of N-terminal prohormone of brain natriuretic peptide and cardiac troponin-I levels in cats with systolic anterior motion of the mitral valve in the absence of left ventricular hypertrophy

ObjectivesTo identify the prevalence of systolic anterior motion of the mitral valve (SAM) in apparently healthy cats in the absence of left ventricular hypertrophy (LVH) and examine the relationship between specific cardiac biomarker concentrations and echocardiographic parameters in these individuals. Animalseighty client-owned cats. Materials and methodsretrospective study; inclusion criteria were the presence of SAM on conscious echocardiography and concurrent measurement of plasma N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and serum cardiac troponin-I (cTnI). Cats were excluded if they had LVH, left atrial enlargement or systemic disease. The percentages of cats with NT-proBNP and cTnI concentrations above the normal reference range were calculated. The correlation between each biomarker concentration and left ventricular myocardial wall thickness, left atrial size and maximum left ventricular outflow tract velocity was evaluated. ResultsThirty-four of 80 patients with SAM showed no evidence of cardiac remodelling (LVH or left atrial enlargement). Of these patients, 30 of 34 had elevated NT-proBNP, and cTnI was elevated in 13 of 27 (48.1%) cats where this biomarker was measured in association with the NT-proBNP assay. A positive correlation was observed between concentration of plasma NT-proBNP and maximum left ventricular outflow tract velocity (rs = 0.67, p<0.0001). No significant correlations were found between the concentration of biomarkers and the remaining echocardiographic parameters. ConclusionsSAM is frequently observed in cats even in the absence of cardiac remodelling, and these individuals often demonstrate elevated plasma NT-proBNP and serum cTnI concentrations. Plasma NT-proBNP elevation is correlated with the severity of the left ventricular outflow obstruction caused by SAM.

Associations between estimated glomerular filtration rate and cardiac biomarkers

BackgroundChronic kidney disease (CKD) is associated with an increased cardiovascular disease (CVD) mortality risk. Elevation of cardiac biomarkers in patients with renal dysfunction is ambiguous in the diagnosis of CVD. The purpose of this study was to investigate the associations between estimated glomerular filtration rate (eGFR) and cardiac biomarkers, and the influence of renal dysfunction on the cardiac biomarkers.MethodsWe examined the cross‐sectional associations of eGFR with cardiac troponin I (cTnI), creatine kinase (CK), CK‐MB, lactic dehydrogenase (LDH), hydroxybutyrate dehydrogenase (HBDH), and brain natriuretic peptide (BNP) in 812 adults and 215 child. Spearman correlation and logistic regression analysis were performed to evaluate the associations.ResultsFor adults, lower eGFR CKD‐EPI had significantly higher cTnI, CK‐MB, LDH, HBDH, and BNP. There were negative correlations between eGFRCKD‐EPI and cTnI, CK‐MB, LDH, HBDH, and BNP. After adjustment for potential confounders, as compared with eGFRCKD‐EPI ≥ 90 mL/min/1.73 m2, eGFRCKD‐EPI < 60 mL/min/1.73 m2 remained associated with a 2.83 (1.08‐7.41) [ratio (95% CI)] times higher cTnI and a 6.50 (2.32‐18.22) [ratio (95% CI)] times higher HBDH. For child, lower eGFRSchwartz had significant higher CK and CK‐MB. There were negative correlations between eGFRSchwartz and CK, and eGFRSchwartz and CK‐MB. After adjustment for potential confounders, as compared with eGFRSchwartz ≥ 90 mL/min/1.73 m2, eGFRSchwartz < 90 mL/min/1.73 m2 revealed no significant higher CVD biomarkers.ConclusionReduced eGFR is associated with elevated cTnI and HBDH among adults without clinically evident CVD, but not child.

Cardiac-cerebral-renal associations in pediatric traumatic brain injury: Preliminary findings

ObjectiveThe clinical epidemiology of organ outcomes in pediatric traumatic brain injury (TBI) has not been examined. We describe associated markers of cerebral, cardiac and renal injury after pediatric TBI. DesignProspective observational study. PatientsChildren 0–18 years who were hospitalized with TBI. MeasurementsMeasures of myocardial (at least one elevated plasma troponin [cTnI] ≥ 0.4 ng/ml) and multiorgan (hemodynamic variables, cerebral perfusion, and renal) function were examined within the first ten days of hospital admission and within 24 h of each other. Main ResultsData from 28 children who were 11[IQR 10.3] years, male (64.3%), with isolated TBI (67.9%), injury severity score (ISS) 25[10], and admission Glasgow coma score (GCS) 11[9] were examined. Overall, 50% (14 children) had elevated cTnI, including those with isolated TBI (57.9%; 11/19), polytrauma (33.3%; 3/9), mild TBI (57.1% 8/14), and severe TBI (42.9%; 6/11). Elevated cTnI occurred within the first six days of admission and across all age groups, in both sexes, and regardless of TBI lesion type, GCS, and ISS. Age-adjusted admission tachycardia was associated with cTnI elevation (AUC 0.82; p < 0.001). Reduced urine output occurred more commonly in patients with isolated TBI (27.3% elevated cTnI vs. 0% normal cTnI). ConclusionsMyocardial injury commonly occurs during the first six days after pediatric TBI irrespective of injury severity, age, sex, TBI lesion type, or polytrauma. Age-adjusted tachycardia may be a clinical indicator of myocardial injury, and elevated troponin may be associated with cardio-cerebro-renal dysfunction.

Epinephrine Exacerbates Myocyte Injury in a Porcine Model of Cardiac Arrest

ObjectiveAlthough circulating cardiac troponin (cTn) concentrations are often elevated in patients following resuscitation from cardiac arrest (CA), this finding is commonly attributed to myocyte injury caused by ongoing myocardial infarction (MI) and/or defibrillation during resuscitation. To determine whether measurable cTn elevations occur independently of these factors, we employed serial sampling of systemic and coronary venous blood to quantify cTn release in a porcine model of CA devoid of ongoing MI or multiple defibrillation attempts. In light of recent concerns regarding potential detrimental effects of epinephrine (EPI) in CA, cTn levels were compared in animals that were resuscitated with vs. without exogenous EPI.MethodsSwine (n=41) were subjected to 7 min CA via electrical induction of ventricular fibrillation (VF) followed by cardiopulmonary resuscitation (CPR) with manual chest compressions and mechanical ventilation for up to 20 min. Biphasic defibrillation (200 J) was performed 1 min after the start of CPR and a subset of animals (n=10) received intravenous EPI (0.015 mg/kg) 1 min later. After return of spontaneous circulation (ROSC; defined as unassisted systolic blood pressure &gt;80 mmHg for 1 min), animals were followed for up to 4 hours with serial blood sampling from the jugular vein and coronary sinus for assessment of cTnI via a porcine‐specific ELISA.ResultsAmong the entire cohort, 1.2±0.1 defibrillator shocks were required to terminate VF, ROSC was achieved 175±7 seconds after the initiation of CPR, and 15 animals (38%) survived for the entire 4‐hour recovery period (2/10 with EPI, 13/31 without EPI). Despite the absence of ongoing MI or prolonged resuscitation efforts, a significant 5‐fold rise in coronary sinus (from 106±17 to 526±74 ng/L, p&lt;0.01) and systemic (from 67±14 to 350±54 ng/L, p&lt;0.01) cTnI concentrations was observed 15 min post‐ROSC (trans‐coronary cTnI gradient from 39±7 to 176±29 ng/L, p&lt;0.01). Widening of the trans‐coronary cTnI gradient continued throughout the recovery period, reaching 795±164 ng/L 4 hours post‐ROSC and leading to a 16‐fold increase in circulating cTnI concentrations at this timepoint (1087±208 ng/L, p&lt;0.01 vs. baseline). Exogenous EPI exacerbated myocyte injury, as EPI‐treated animals exhibited a significantly higher trans‐coronary cTnI gradient 30 min post‐ROSC that persisted throughout the recovery period and led to significantly higher circulating cTnI concentrations vs. animals resuscitated without EPI at each timepoint (Figure ).ConclusionsThese results demonstrate that resuscitation from CA is associated with measurable elevations in cTnI as early as 15 min post‐ROSC, even in the absence of ongoing MI or prolonged CPR with multiple defibrillator shocks. Thus, assessment of circulating cTnI following resuscitation from CA is unlikely to accurately identify patients suffering from an acute coronary syndrome. Administration of exogenous EPI during resuscitation exacerbates the extent of myocyte injury, which may contribute to poor long‐term outcomes.Support or Funding InformationFunding SourcesNIH, AHA, ZOLL Foundation, Pro‐Al Medico Technologies, Inc., UB CAT, NCATS, and the Dept. of Veterans Affairs.Figure 1

Association of major adverse cardiovascular events and cardiac troponin-I levels following percutaneous coronary intervention: a three-year follow-up study at a single center.

Major adverse cardiovascular events occurrences of patients with different cardiac troponin-I (cTnI) levels following percutaneous coronary intervention (PCI) remained controversial. The prognostic relevance and risk factors of PCI-related myocardial infarction (MI) were not very clear as well. Our study included 249 coronary artery disease patients without preoperative cTnI elevation who successfully accepted PCI from 2013 to 2014. A three-year follow-up was conducted for each patient. The patients were divided into PCI-related MI group and non-PCI-related MI group. Risk factors of PCI-related MI were first explored. The occurrence of MACE was recorded. The prognostic relevance between PCI-related MI (PMI) group and non-PCI-related MI group, as well as different postoperative cTnI levels, were compared. Low-density lipoprotein cholesterol (LDL-C), age, Gensini Score, total stent length, and intra-operative complication were found positively correlated with PCI-related MI occurrence, while hemoglobin and prior PCI history were negatively correlated. After 3-year follow-up, the Kaplan-Meier survival curve showed MACE occurrence was significantly increased in PCI-related MI group. Comparing to patients with normal postoperative cTnI, MACE occurrence was increased in patients with a 10×upper limit of normal (ULN)≤cTnI<70×ULN and cTnI≥70×ULN, while there was no difference in patients with 1×ULN≤cTnI<5×ULN and 5×ULN≤cTnI<10×ULN. Cox proportional hazard regression analysis revealed PMI, NT-proBNP, and left ventricular ejection function (LVEF)<50% were positively correlated with MACE occurrence, while maximum inflation pressure and apoA-I were negatively correlated. Prognosis of PCI-related MI was poor, as well as in patients with postoperative cTnI≥10×ULN. Among the risk factors of PMI, LDL-C, age, Gensini Score, total stent length, and intra-operative complication were positively correlated with PCI-related MI occurrence, while hemoglobin and prior PCI history were negatively correlated.

Analysis of myocardial injury in patients with COVID-19 and association between concomitant cardiovascular diseases and severity of COVID-19

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 P<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 P<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 P<0.05). Multivariate logistic regression analysis showed that elevated cTnI(OR=26.909，95%CI 4.086-177.226，P=0.001) and CHD (OR=16.609，95%CI 2.288-120.577，P=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.

Clinical Significance of Increased Serum Levels of Troponin I in Patients from the Emergency Department of a County Hospital

Elevated cardiac troponin I (cTnI) levels are diagnostic for myocardial injury. Moreover, they are essential for risk stratification in patients with acute cardiac ischemia and heart failure. However, their usefulness is not limited to the previous clinical conditions. The aim of this study was to evaluate the clinical significance of cTnI levels in the emergency department.In 324 patients, out of the 4147 referred to the emergency department, serum levels of cTnI were evaluated and represented the study population. Subjects were divided into 2 groups: Group 1 (66 patients) with cTnI ≥ 0.04 ng/mL and Group 2 (258 patients) with cTnI level [ 0.04 ng/mL. The clinical characteristics, laboratory data, ECG findings, echocardiographic abnormalities and discharge diagnosis were compared between the two groups. Patients with cTnI ≥0.04 ng/mL had more often a history of ischemic heart disease, lower levels of oxygen saturation, higher levels of blood glucose, increased white blood cells count, higher heart rate and deeper ST-segment depressions on ECG. The most common discharge diagnosis was heart failure. Although an elevated level of cTnI is highly suggestive for myocardial injury, it should always be interpretated in the clinical context. Heart failure is an important diagnosis in patients with elevated cTnI levels.

Highly Sensitive and Fast Detection of C-Reactive Protein and Troponin Biomarkers Using Liquidgated Single Silicon Nanowire Biosensors

ABSTRACTC-reactive protein (CRP) and cardiac troponin I (cTnI) biomolecules represent the earliest enzymes that appear in the blood when a cardiac injury occurs. Real-time and selective detection of these biomarkers is essential for the prediction and detection of cardiovascular diseases at an early stage. Here we report on the label-free specific detection of both proteins at picomolar concentrations using fabricated nanowire-based biosensors. We demonstrate a novel functionalization technique based on the attachment of dibenzocyclooctyne (DBCO)-linked troponin-specific aptamers to azide-functionalized silicon (Si) nanowire (NW) surface. Due to the fast and reliable immobilization of cTnI-specific aptamers and CRP-specific antibodies on the Si NWs, the fabricated devices can rapidly detect target biomolecules demonstrating high sensitivity. We confirm the attachment of proteins to the surface of Si NWs by atomic force microscopy (AFM). Moreover, we demonstrate that nanowire structures of different sizes enable the detection of biomarkers in a wide concentration range (from 1 pg/ml to 1 µg/ml), corresponding to CRP and cTnI elevation levels during the early stage of disease formation.

Abstract WP382: Cardiac Troponin Assessment in Acute Ischemic Stroke Patients Presenting Within 4.5 Hours From Last Known Well

Introduction: American Heart Association guidelines recommend obtaining baseline troponin in all acute ischemic stroke (AIS) patients to detect an acute coronary syndrome (ACS). Yet, data regarding the prevalence and diagnostic yield of troponin elevation in patients presenting within the time window for thrombolysis is limited. We sought to determine the diagnostic yield of cTnI in detecting ACS when assessed before or after 4.5h from last known well (LKW). Methods: We retrospectively analyzed 526 consecutive patients admitted for AIS or transient ischemic attack, who presented within 4.5h and had cardiac troponin I (cTnI) obtained within 48h from LKW. Results: The median time from LKW to cTnI measurement was 3.8h (IQR 1.5h-7.9h). 58% patients (n=306) had cTnI obtained ≤ 4.5h from LKW. After adjustment, factors independently relating to an elevated cTnI were the time to cTnI assessment (p&lt;0.001), patient age (p=0.012), history of congestive heart failure (p&lt;0.001), and a history of stroke/TIA (p=0.049). Patients who had a cTnI obtained within 4.5 hours from LKW, had significantly more often a normal (≤0.04 ng/mL) than elevated (&gt;0.04 ng/mL) cTnI levels (61.9% vs. 44.7%; p=0.001). The sensitivity, specificity, and overall accuracy of an elevated cTnI assessed within 48h from LKW for ACS was 63.6%, 80.2%, and 79.5%, respectively. After stratification by the time to cTnI assessment within 4.5 h versus beyond 4.5h, the sensitivity of an elevated cTnI for ACS was markedly reduced to 42.9% whereas the specificity remained high at 84%. The optimal threshold to assess cTnI for detecting an ACS was 320 min in all included patients (sensitivity = 0.54, specificity = 0.67, Youden’s J = 0.203) and 340 minutes in patients with ACS (sensitivity 0.79, specificity 0.88, Youden’s J 0.661). Conclusions: Among patients presenting within the time window for rtPA treatment, the sensitivity of cTnI obtained within 4.5 hours from LKW to detect ACS is low. Our data suggests that cTnI routine assessment of cTnI in AIS subjects without cardiac symptoms should not be done within the first 6 hours from LKW.

Cardiac troponin I is associated with non-sustained ventricular tachycardia in patients with hypertrophic obstructive cardiomyopathy.

As highly sensitive and specific markers of myocardial damage, cardiac troponins were demonstrated to correlate with clinical parameters of patients with hypertrophic cardiomyopathy. However, the relationship between cardiac troponins and presence of non-sustained ventricular tachycardia (NSVT) in hypertrophic cardiomyopathy remains unclear. The aim of our study was to explore the association between serum cardiac troponin I (cTNI) and presence of NSVT in patients with hypertrophic obstructive cardiomyopathy (HOCM). A total of 309 HOCM patients were enrolled in our study. All participants underwent clinical evaluations, including collections of medical history, blood tests, 24-h Holter monitoring, echocardiography, and cardiac magnetic resonance imaging. There were 53 (17.2%) patients with NSVT and 256 patients without it. Compared to patients without NSVT, serum cTNI (P < 0.001) and plasma NT-proBNP (P = 0.042) were significantly higher in patients with NSVT. Moreover, cTNI and NT-proBNP were positively correlated with left atrial diameter, maximum wall thickness (MWT), left ventricular volume index and left ventricular mass index. In multivariable logistic analysis, log cTNI [odds ratio (OR) = 2.408, 95% confidence interval (CI) 1.108-5.325, P = 0.027], left ventricular end-diastole diameter (OR = 0.922, 95%CI 0.856-0.994, P = 0.034), MWT (OR = 1.131, 95%CI 1.035-1.235, P = 0.006) and left ventricular end-systole volume index (OR = 1.060, 95%CI 1.025-1.096, P = 0.001) were independent determinants of NSVT occurrence after adjustment for potential cofounders. Serum cTNI level was elevated in patients with NSVT. And it was independently associated with NSVT in patients with HOCM. Our results suggest that it may be more reasonable for HOCM patients with elevated serum cTNI to extend the time of Holter monitoring.

P1564 Changes in coronary flow velocity measuring during coronary bypass grafting can predict elevation of cardiac troponin

Abstract Background Stenosis of a coronary artery results in an increase in flow velocity in the pathologic segment. Effective grafting should decrease the stenotic native coronary velocity according to a hemodynamic law. The range of decreased velocity can hypothetically reflect the effectiveness of a graft. Grafting effect insufficiencies often cause elevations in periprocedural cardiac troponin (cTn) elevation. The aim of the study is to determine, if measuring coronary flow velocity changes during coronary artery bypass grafting (CABG) can predict further cTn elevation. Methods and results Consecutive 68 patients (48 men, 64 ± 9 years old), who were referred for CABG, were included into the study. A standard basic perioperative transesophageal echocardiography (TEE) examination was performed with additional scans of the left main, left anterior descending (LAD), and circumflex (LCx) arteries’ proximal segments. Measurements of coronary flow velocities was performed before and after grafting in the same sites of the arteries. The maximal value of cTnI within 48 hours after CABG was accounted for in the analysis. All patients had arterial hypertension, 15 patients (22%) had diabetes mellitus, 12 patients (18%) was current smokers. Forty-one patients (60%) had prior myocardial infarctions, 18 persons (26%) had previous coronary stenting. The ejection fraction before the operation was 56 ± 13%. Before grafting the mean velocity in the left main artery was 79 cm/s (25th-75th quartile, 42-111), in LAD 98 cm/s (25th-75th quartile, 71-125), and in LCx 116 cm/s (25th-75th quartile, 68-156). There was a strong significant correlation between changes in coronary flow velocities and the value of cTnI (R = 0.56, p &amp;lt; 0.0004). The patients with and without significant elevations in cTnI had differences in coronary velocity changes before and after grafting (p &amp;lt; 0.009). Patients with elevated cTnI in more than 5 times, had, on average, an increase in the velocities for native arteries of 21 ± 19 cm/s. Conclusion Coronary flow velocity assessment during CABG could predict an elevation of cardiac troponins after cardiac surgery. Abstract P1564 Figure.

Exploring the association between extra-cardiac troponin elevations and risk of future mortality.

Although the measurement of cardiac troponin I (cTnI) and T (cTnT) has now become the cornerstone for diagnosing cardiac injury, both ischemic and non-ischemic, recent evidence has become available that many patients display extra-cardiac causes of cTn elevations and carry a considerably enhanced risk of future mortality. The current literature data suggests that cTn elevations may be equally common in patients with cardiac and extra-cardiac diseases. Among the latter cohort of patients, the leading extra-cardiac diseases which may be responsible for either cTnI or cTnT elevations include infectious diseases/sepsis, pulmonary disorders, renal failure, malignancy, as well as gastrointestinal, neurological and musculoskeletal diseases. What also emerges rather clearly from the current literature data, is that the risk of dying for extra-cardiac diseases is higher (i.e., between two to three-fold) in patients with extra-cardiac cTn elevations than in those with cardiac pathologies, and that the most frequent cause of death would then be infections/sepsis, followed by malignancy, respiratory disorders, myocardial infarction, gastrointestinal and neurological diseases, heart failure, stroke, cardiac arrhythmias, renal failure, psychiatric, metabolic, urogenital and musculoskeletal disorders. These figures would lead to conclude that there is a considerable risk that the underlying pathology causing cardiac injury and cTn elevation would then become the cause of death in these patients. This important evidence shall lead the way to defining appropriate and effective strategies for managing patients with extra-cardiac cTn elevations, so that their risk of future death could be prevented or limited.

The Clinical Characteristics of Myocardial Injury in Severe and Very Severe Patients with 2019 Novel Coronavirus Disease

Background: Despite previous studies discussing the clinical and epidemiological features of 2019 Novel coronavirus disease (COVID-19), few have investigated the alteration of cardiac lesion markers and how it is correlated to disease severity. This study aims to describe the clinical characteristics of myocardial injury in severe and very severe COVID-19 patients. Methods: We enrolled in-hospital patients with COVID-19 admitted to the West District of Union Hospital of Tongji Medical College in the 7th floor ward from February 5th to February 13rd, 2020. Demographic data were collected upon admission. Laboratory confirmation of COVID-19, blood count, creatine, liver enzymes, and cardiac lesion markers were together tested by the laboratory department. Findings: 34 patients with COVID-19 were included in this study, 8 patients met the criteria for very severe COVID-19, and 26 for severe COVID-19. The median age was 63yrd (inter quartile range {IQR}:58-69) among severe COVID-19 group and 67yrd (IQR: 66-75) among very severe group. We noted significantly increased cTnI (46.8ng/L [IQR: 34.2-299.8] vs. 4.8ng/L [IQR: 34.2-299.8]), CK (199U/L [IQR: 77-285] vs. 88U/L [IQR: 45-125]), HBDB (453U/L [IQR: 347-547] vs. 245U/L [IQR: 207-275]) and LDH (513U/L [IQR: 414-641] vs. 287U/L [IQR: 246-331]) in very severe group as compared to severe group. Importantly, the percentage of very severe patients with elevated cTnI levels was markedly higher, with 8/8 patients exhibiting increased cTnI in very severe group, and only 1/26 patient in severe group (P value<0.001). Interpretation: We have found high percentage of increased cTnI levels in very severe COVID-19. Protecting from myocardial injury could be of vital importance for reducing the mortality rate in very severe COVID-19. Funding Statement: This study was funded by the Clinical Research Award of the First Affiliated Hospital of Xi'an Jiaotong University, China (No.XJTU1AF-CRF-2018-025). Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The study was approved by the ethics committee of the local hospital and data were collected retrospectively.

P1885Cha2ds-2vasc score lacks of ability to predict mortality in patients attending the emergency department with atrial fibrillation in the presence of troponin i

Abstract Background CHA2DS2-VASc score has been used as a surrogate marker for predicting outcomes beyond thromboembolic risk in patients with atrial fibrillation (AF). Likewise, cardiac troponin I (cTnI) is a predictor of mortality in AF. Purpose This study aimed to investigate the association of cTnI and CHA2DS2-VASc score with long-term prognosis in patients admitted to the emergency department with AF. Methods A retrospective cohort study conducted between January 2012 and December 2013, enrolling patients admitted to the emergency department with AF and having documented cTnI measurements. CHA2DS2-VASc score was estimated. Primary endpoint was 5-year all-cause mortality, readmission for heart failure (HF), readmission for myocardial infarction (MI) and the composite end point of major adverse cardiac events defined as death, readmission for HF or readmission for MI (MACE). Results A total of 578 patients with AF were studied, of whom 252 patients had elevated levels of cTnI (43.6%) and 334 patients had CHA2DS2-VASc score &gt;3 (57.8%). Patients with elevated cTnI tended to be oldercompared with those who did not have cTnI elevation and were more frequently comorbid and of higher ischemic risk, including hypertension, prior MI, prior HF, chronic renal failure and peripheral artery disease. The overall median CHA2DS2-VASc score was higher in those with cTnI elevation compared to those patients elevated cTnI levels (4.2 vs 3.3 points, p&lt;0.001). Main diagnoses at hospital discharge were tachyarrhythmia 30.3%, followed by heart failure 17.7%, respiratory infections 9.5% and acute coronary syndrome 7.3%. At 5-year follow-up, all-cause death was significantly higher for patients with cTnI elevation compared with those who did not have cTnI elevation (56.4% vs. 27%; logrank test p&lt;0.001). Specifically, for readmissions for HF and readmissions for MI there were no differences in between patients with or without cTnI elevation. In addition, MACE was reached in 165 patients (65.5%) with cTnI elevation, compare to 126 patients (38.7%) without cTnI elevation (p&lt;0.001). On multivariable Cox regression analysis, cTnI elevation was an independent predictor of all-cause death (hazard ratio, 1.67, 95% confidence interval [CI]: 1.24–2.26, p=0.001) and of MACE (hazard ratio 1.47, 95% confidence interval 1.15–1.88; P=0.002), but it did not reach statistical significance for readmissions for MI and readmissions for HF. CHA2DS2-VASc score was a predictor on univariate Cox regression analysis for each endpoint, but it did not reach significance on multivariable Cox regression analysis for any endpoint. Conclusions cTnI is independently associated with long-term all-cause mortality in patients attending the emergency department with AF. cTnI compared to CHA2DS2-VASc score is thus a biomarker with predictive capacity for mortality in late follow-up, conferring utility in the risk stratification of patients with atrial fibrillation.

P4425The exercise-induced troponin I elevation is highly correlated with power output during exercise in recreational cyclists with coronary atherosclerosis

Abstract Background Following strenuous exercise there is an increase cardiac Troponins (cTn) elevation considered being a physiological response. During prolonged strenuous physical activity, high work-loads may induce demand myocardial ischemia due to an oxygen demand/supply mismatch in susceptible subjects, causing an excessive cTn elevation. Purpose This study aimed to assess the relationship between exercise-induced cTnI elevation and direct measurement of work performed during prolonged strenuous exercise in subjects with and without atherosclerotic CAD. Methods Work during a 91 km mountain bike race was quantified by Stages™ power meters. Power (Watt) and heart rate data were stored in Garmin™ Forerunner 935 monitors. Coronary computed tomography angiography was performed after the race. Blood pressure was measured 4 times during the race. Blood samples (hs-cTnI from Abbot Diagnostics) were obtained one day prior to the race and at 3 and 24 h after the race. Data are presented as mean±SD or median (25th and 75th percentile). Results 40 subjects (10 women) were included in the final analysis. 15 Participants (4 women) had atherosclerosis, none had obstructive CAD. These participants were significantly older (55±8 years vs. 46±8 years p=0.007) and had higher training volumes (METS: 69 (64–102) hrs/week) compared with normal subjects (METS: 51 (33–88) hrs/week) (p=0.03). Baseline cTnI was higher (p=0.04) in the atherosclerotic group (4.5 (3.4–8.8) ng/L) compared with normals (2.6 (1.6–4.8) ng/L). There were no differences in baseline blood pressure, peak VO2 max, heart rate or BMI. There was no significant difference in race duration between normals (3.9 (3.5–4.5) hrs) and subjects with atherosclerosis (4.1 (3.6–4.5) hrs). During the race there were no differences in peak power or peak Watt/kg. cTnI increased after the race in all participants, but there were no differences between groups: 3h: atherosclerosis: 89 (27–131) ng/L vs. normal 77 (36–104) ng/L, 24h: atherosclerosis: 13 (6.3–23.7) ng/L vs. normal: 17 (12–37) ng/L. There were no significant difference between the groups in average power during the race: atherosclerosis: 167±50 Watt vs. 174 (±50) Watt or ratio: 2.0±0.49 Watt/kg vs 2.2±0.58 Watt/kg during the race. Maximal systolic and diastolic blood pressures during the race were higher (p=0.002) in the atherosclerotic group: SBP: 241±14 mmHg vs. 219±26 mmHg, DBP: 107±8 vs 95±8 mmHg. In atherosclerotic subjects cTnI both at 3h and 24 h were highly correlated (p&lt;0.001) with Watt/kg ratio during the race in contrast to no correlations in the normal group (Figure). Conclusions Our findings suggest that the presence of coronary atherosclerosis, even in the absences of significant stenosis, alters the relationship between workload and the troponin response. This indicates different release kinetics in exercise-induced cTn in participants with and without CAD, with prolonged elevation in cTnI in CAD subjects exceeding the highest work-intensities. Acknowledgement/Funding Grant Western Norway Health service, Grant ConocoPhillips, Grant Simon Fougner Hartmanns Familyfund

P1513Exercise-induced cardiac troponin I release and incident cardiovascular morbidity and mortality

Abstract Background Blood concentrations of cardiac troponin I (cTnI) above the 99th percentile (upper reference limit, URL) are a key criterion for the diagnosis of acute myocardial injury and infarction. cTnI concentrations, even below the URL, also predict adverse outcomes in general and patient populations. cTnI increases after exercise, but the clinical significance of this exercise-induced cTnI increase is unknown. We examined the association between exercise-induced cTnI elevations and clinical outcomes in long-distance walkers. Methods cTnI was measured in 726 participants (median 61 [54–69] yrs) before and immediately after 30–55 km of walking. The primary endpoint was a composite of all-cause mortality and major adverse cardiovascular events (MACE, i.e. myocardial infarction, stroke, heart failure, revascularization or sudden cardiac arrest). Results Participants walked 498 [440–555] min at 68±10% of their maximum heart rate. Baseline cTnI concentrations were 2 [0–8] ng/L, with 9 participants (1%) demonstrating a baseline cTnI value above the URL (&gt;40 ng/L). cTnI increased after walking (8 [1–18] ng/L, p&lt;0.001) and 63 participants (9%) had a post-exercise cTnI value &gt;URL. During 43 [23–77] months of follow-up, 62 participants (9%) experienced a primary endpoint; 29 died and 33 had MACE. 27% of participants with post-exercise cTnI &gt;URL experienced a primary endpoint compared to only 7% with cTnI below the URL (log-rank p&lt;0.001). The hazard ratio was 2.35 (95% CI: 1.21–4.53) after adjusting for age, sex, cardiovascular risk factors (hypertension, hypercholesterolemia or diabetes mellitus), cardiovascular diseases (myocardial infarction, stroke or heart failure) and baseline cTnI. Kaplan-Meier of Mortality and MACE Conclusion Post-exercise cTnI concentrations &gt;URL were associated with higher all-cause mortality and MACE, independent of age, sex, presence of cardiovascular risk factors or cardiovascular diseases and baseline cTnI concentrations in a large cohort of older long-distance walkers. Exercise-induced increases in cTnI may not be a benign physiological response to exercise in all, but an early marker of future mortality and cardiovascular events. Acknowledgement/Funding V.L.A was supported by a grant from the Radboud Institute for Health Sciences, T.M.H.E by a Horizon 2020 grant from the European Commission

Early assessment of cardiac troponin I predicts the postoperative cardiac status and clinical course after congenital heart disease surgery.

Cardiac troponin I (cTnI) is a regulatory protein with a high sensitivity and specificity for cardiac injury. Preoperative and postoperative elevations of cTnI are usually considered predictors of the mortality and morbidity. However, little is known about the relationship between the cTnI and postoperative course after the congenital heart disease (CHD) operation. Sixty-five consecutive patients who underwent cardiac surgery for CHD at our institution between March 2016 and January 2017 were included. The cTnI was measured after the operation. Also, the association between the cTnI and duration of the catecholamine use, ICU stay, aortic cross clamp time, and other clinical parameters were assessed. The cTnI level on postoperative day 1 was positively correlated with the duration of the catecholamine use (p < 0.001) and ICU stay (p < 0.001). Also, a higher cTnI level was associated with a lower urine volume and higher lactate level 24h after the ICU admission. In the multivariable regression analysis, the cTnI was a significant independent predictor of the catecholamine use (p = 0.002) and ICU stay (p = 0.003). The cTnI level on postoperative day 1 was a predictor of the duration of the catecholamine use and ICU stay.

Postoperative Myocardial Injury Does Not Predict Early and 1-Year Mortality After Living Donor Liver Transplantation

BackgroundPreoperative cardiac troponin-I (cTnI) elevation has been shown to be a predictor of mortality after liver transplantation. Myocardial injury after non-cardiac surgery (MINS) has been defined as elevation of serum cardiac troponin levels in the perioperative period that does not fulfill the criteria for myocardial infarction. MINS has been shown to be a prognostic factor for in-hospital and long-term mortality, but there is limited data in patients undergoing living-donor liver transplantation (LDLT). In this study, we aimed to evaluate the relationship between MINS and postoperative mortality. Material and methodsPatients who had undergone adult LDLT at Florence Nightingale Hospital Liver Transplantation Unit between December 2012 and December 2015 were retrospectively analyzed for 30-day in-hospital and 1-year mortality. Myocardial injury was defined as cTnI level above 0.04 ng/mL. Patients (N = 214) were divided into 2 groups according to postoperative cTnI levels. The following were the exclusion criteria: 1. patients under 18 years old, 2. patients undergoing deceased-donor liver transplantation or dual liver-kidney transplantation, 3. cTnI elevation due to other causes (sepsis, renal failure, pulmonary embolism, myocardial infarction), and 4. patients without postoperative troponin levels. ResultsMINS occurred in 123 (57.4%) patients after LDLT. There was no difference between the groups according to age, sex, creatinine levels, presence of ischemic heart disease, hypertension, diabetes mellitus, and tobacco use. The presence of MINS did not predict 30-day and 1-year mortality in the study population. ConclusionMyocardial injury detected by serum cTnI elevation was frequent after LDLT; however, it was not associated with 30-day in-hospital and 1-year mortality.