Serial Measurements Of Cardiac Troponin Research Articles

Machine Learning for Myocardial Infarction Compared With Guideline-Recommended Diagnostic Pathways.

Collaboration for the Diagnosis and Evaluation of Acute Coronary Syndrome (CoDE-ACS) is a validated clinical decision support tool that uses machine learning with or without serial cardiac troponin measurements at a flexible time point to calculate the probability of myocardial infarction (MI). How CoDE-ACS performs at different time points for serial measurement and compares with guideline-recommended diagnostic pathways that rely on fixed thresholds and time points is uncertain. Patients with possible MI without ST-segment-elevation were enrolled at 12 sites in 5 countries and underwent serial high-sensitivity cardiac troponin I concentration measurement at 0, 1, and 2 hours. Diagnostic performance of the CoDE-ACS model at each time point was determined for index type 1 MI and the effectiveness of previously validated low- and high-probability scores compared with guideline-recommended European Society of Cardiology (ESC) 0/1-hour, ESC 0/2-hour, and High-STEACS (High-Sensitivity Troponin in the Evaluation of Patients With Suspected Acute Coronary Syndrome) pathways. In total, 4105 patients (mean age, 61 years [interquartile range, 50-74]; 32% women) were included, among whom 575 (14%) had type 1 MI. At presentation, CoDE-ACS identified 56% of patients as low probability, with a negative predictive value and sensitivity of 99.7% (95% CI, 99.5%-99.9%) and 99.0% (98.6%-99.2%), ruling out more patients than the ESC 0-hour and High-STEACS (25% and 35%) pathways. Incorporating a second cardiac troponin measurement, CoDE-ACS identified 65% or 68% of patients as low probability at 1 or 2 hours, for an identical negative predictive value of 99.7% (99.5%-99.9%); 19% or 18% as high probability, with a positive predictive value of 64.9% (63.5%-66.4%) and 68.8% (67.3%-70.1%); and 16% or 14% as intermediate probability. In comparison, after serial measurements, the ESC 0/1-hour, ESC 0/2-hour, and High-STEACS pathways identified 49%, 53%, and 71% of patients as low risk, with a negative predictive value of 100% (99.9%-100%), 100% (99.9%-100%), and 99.7% (99.5%-99.8%); and 20%, 19%, or 29% as high risk, with a positive predictive value of 61.5% (60.0%-63.0%), 65.8% (64.3%-67.2%), and 48.3% (46.8%-49.8%), resulting in 31%, 28%, or 0%, who require further observation in the emergency department, respectively. CoDE-ACS performs consistently irrespective of the timing of serial cardiac troponin measurement, identifying more patients as low probability with comparable performance to guideline-recommended pathways for MI. Whether care guided by probabilities can improve the early diagnosis of MI requires prospective evaluation. URL: https://www.clinicaltrials.gov; Unique identifier: NCT00470587.

Serial measurement of cardiac troponin I in hospitalised dogs with canine parvoviral enteritis: Association with outcome and canine pancreas-specific lipase concentration

The aim of this study was to serially evaluate serum cardiac troponin I (cTnI) concentrations in dogs with parvoviral enteritis (CPVE), and investigate the association with outcome and serum pancreas-specific lipase (Spec cPL) concentrations. Dogs with CPVE that were hospitalised for at least 5 days were included. cTnI and Spec cPL concentrations were measured on days 1, 3 and 5 of hospitalisation. Twenty-nine dogs (20 survivors, 9 non-survivors) were included. Spec cPL was indicative of pancreatitis (>400 μg/L) on at least one day in 10/29 (34.5%) dogs. Serum median (range) cTnI concentration was higher (P = 0.021) in non-survivors on day 5 [0.032 (0.001–0.395) ng/mL] compared to day 1 [0.012 (0.003–0.196) ng/mL]. Non-survivors had higher (P = 0.014) cTnI concentrations on day 5 [0.032 (0.001–0.395) ng/mL] compared to survivors [0.001 (0.001–0.042) ng/mL], but not at admission or on day 3 (P > 0.05). Serum cTnI concentrations were not significantly different (P = 0.465) between the three Spec cPL groups [group 1 (Spec cPL ≤ 200 μg/L): 0.007 (0.001–0.527) ng/mL; group 2 (Spec cPL: 201-399 μg/L): 0.0045 (0.001–0.196) ng/mL; group 3 (Spec cPL ≥ 400 μg/L): 0.011 (0.001–0.278) ng/mL]. cTnI and Spec cPL concentrations were not significantly correlated (rho = −0.043, P = 0.703). Serial measurement of cTnI had prognostic value in the examined cohort. However, cTnI was not correlated with spec cPL.

Development of a Biosensor for fast point-of-care Blood Analysis of Troponin.

We present the development of novel tetrapolar EIS biosensor for the detect of troponin. Troponin has considerable diagnostic power and provide invaluable prognostic information for risk stratification. of acute coronary syndromes. Clinical Relevance- A feasibility study was undertaken to assess the diagnostic performance of serial cardiac troponin measurements which is excellent as these structural proteins are unique to the heart and thus sensitive and specific of damage to the myocardium. clinical molecular diagnostics and home healthcare. Troponin's biosensors would provide point-of-care and rapid decision making for the early detection of CS. Clinically relevant window of cTnI testing, concentrations from 10pM to 0.1μM were achieved.

Trajectories of high-sensitivity cardiac troponin I in the two decades before cardiovascular death in Whitehall II

Abstract Background High-sensitivity cardiac troponin may be a promising biomarker that could be used for personalised cardiovascular risk prediction and monitoring in the general population. Temporal changes in high-sensitivity cardiac troponin before cardiovascular death are largely unexplored. Purpose Using the longitudinal Whitehall II cohort, we evaluated whether three serial high-sensitivity cardiac troponin I measurements over 15 years improved prediction of cardiovascular death when compared to a single time point at baseline. Methods Whitehall II is an ongoing longitudinal observation cohort study of 10,308 civil servants, and we included participants who had at least one cardiac troponin measurement and outcome data available. We constructed time trajectories to evaluate the temporal pattern of cardiac troponin I in those who died from cardiovascular disease as compared to those who did not. Cox regression and joint models were used to investigate the association of cardiac troponin I in relation to cardiovascular death using single time point (at baseline) and repeated measurements (at baseline, 10 and 15 years), respectively. The discriminative ability was assessed by the concordance index. Results In total, we included 7,293 individuals (mean age of 58 years [SD 7] at baseline, 29.4% women). Of these, 5,818 (79.8%) and 4,045 (55.5%) individuals had a second and third cardiac troponin I concentration measured, respectively. Cardiovascular death occurred in 281 (3.9%) individuals during a median follow-up of 21.4 [IQR, 15.8 to 21.8] years. In the 21-year trajectories of cardiac troponin I, we observed higher baseline concentrations in those who died due to cardiovascular disease as compared to those who did not (median 5 [IQR, 2 to 9] ng/L versus 3 [IQR, 2 to 5] ng/L respectively, Figure). Cardiac troponin I was an independent predictor of cardiovascular death, and the hazard ratio (HR) derived from the joint model that included serial cardiac troponin measurements was higher than the HR derived from the single time point model (single time point model: adjusted HR 1.53, 95% Confidence Interval [CI] 1.37 to 1.70 per naturally log transformed unit of cardiac troponin I, versus repeated measurements model: adjusted HR 1.79, 95% CI 1.58 to 2.02). The discriminative ability of the cardiac troponin model improved when using repeated measurements (concordance index of unadjusted cardiac troponin models, single time point: 0.668 versus repeated measurements: 0.724). Conclusions Our study shows that cardiac troponin I trajectories were persistently higher among individuals who died from cardiovascular disease. Cardiac troponin I is a strong independent predictor of cardiovascular death, and incorporating repeated measurements of cardiac troponin improves cardiovascular risk prediction in the general population. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Cardiac troponin I measurements and analysis were supported by were supported by Siemens Healthineers. The study was supported by Health Data Research UK which receives its funding from HDR UK Ltd (HDR-5012) funded by the UK Medical Research Council, Engineering and Physical Sciences Research Council, Economic and Social Research Council, Department of Health and Social Care (England), Chief Scientist Office of the Scottish Government Health and Social Care Directorates, Health and Social Care Research and Development Division (Welsh Government), Public Health Agency (Northern Ireland), British Heart Foundation and the Wellcome Trust. NLM is supported by the British Heart Foundation through a Senior Clinical Research Fellowship (FS/16/14/32023), Programme Grant (RG/20/10/34966) and a Research Excellence Award (RE/18/5/34216). The funders had no role in the study and the decision to submit this work to be considered for publication.

Diagnostic algorithms for non-ST-segment elevation myocardial infarction: open issues.

The use of serial measurement of cardiac troponin (cTn) is recommended by international guidelines for the diagnosis of myocardial infarction (MI) since 2000. This article focuses on factors influencing temporal changes in high-sensitive cTn (hs)-cTn and the impact of these factors on the diagnosis of non-ST-segment elevation MI (NSTEMI). The recommendations proposed by three different international guidelines published in 2020-2021 for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation (NSTE) show some discrepancies. In particular, there is no agreement among these guidelines about cut-off or absolute change values to be used for the rule-in, especially regarding the use of sex-specific cut-off values. Furthermore, there are no sufficient evidences on the diagnostic accuracy and cost effectiveness related to cut-off values suggested for algorithms to be used by some hs-cTnI methods.

Abstract 13670: Single versus Serial Measurements of Cardiac Troponin in the Evaluation of Emergency Department Patients With Suspected Acute Myocardial Infarction

Introduction: Chest pain is among the most common reasons for emergency department (ED) presentations. However, most patients are low risk for acute coronary syndrome (ACS) with low cardiac adverse outcomes. Biomarker testing with troponins is the mainstay of initial assessment for ACS. Although serial troponin testing can improve diagnosis of ACS, in clinical practice, some patients deemed to be low risk are discharged after a single negative troponin measurement. Our study evaluated the safety of single-troponin rule-out strategy using a conventional troponin assay. Hypothesis: We assessed the hypothesis that there is no significant difference in the clinical outcomes of patients deemed low-risk and discharged after a single negative troponin compared to patients discharged after serial troponin measurements. Methods: This is a retrospective study of ED encounters from January 2015 to December 2017 across 13 community emergency departments within an integrated healthcare system in Southern California. The study cohort includes adult ED encounters evaluated for suspected ACS with a HEART score and an initial conventional troponin-I below the level of detection (<0.02). Multivariate logistic regression model was performed to evaluate the association between testing strategies and clinical outcomes. Results: Among 27,918 patients with an initial troponin measurement below the level of detection, 14,459 (51.8%) were discharged after a single measurement, and 13,459 patients (48.2%) had serial troponin orders. After adjusting for cardiac risk factors and comorbidities, there was no statistically significant difference in the primary outcome of AMI or cardiac mortality within 30 days between the two groups (single troponin 0.4% vs. serial troponin 0.4%, OR 1.41, 95% CI (0.96-2.07)). Single troponin was associated with a lower rate of CABG (OR 0.24, 95% CI: 0.11-0.48) and invasive coronary angiogram (OR 0.46, 95% CI: 0.38-0.56). Conclusions: When compared to serial troponin testing, discharge after a single negative troponin is routinely done among ED patients, and appears safe based on current physician decision making with no difference in rates of 30-day cardiac mortality and AMI.

Incidence of major adverse cardiac events following non-cardiac surgery.

Major adverse cardiac events (MACE) triggered by non-cardiac surgery are prognostically important perioperative complications. However, due to often asymptomatic presentation, the incidence and timing of postoperative MACE are incompletely understood. We conducted a prospective observational study implementing a perioperative screening for postoperative MACE [cardiovascular death (CVD), acute heart failure (AHF), haemodynamically relevant arrhythmias, spontaneous myocardial infarction (MI), and perioperative myocardial infarction/injury (PMI)] in patients at increased cardiovascular risk (≥65 years OR ≥45 years with history of cardiovascular disease) undergoing non-cardiac surgery at a tertiary hospital. All patients received serial measurements of cardiac troponin to detect asymptomatic MACE. Among 2265 patients (mean age 73 years, 43.4% women), the incidence of MACE was 15.2% within 30 days, and 20.6% within 365 days. CVD occurred in 1.2% [95% confidence interval (CI) 0.9-1.8] and in 3.7% (95% CI 3.0-4.5), haemodynamically relevant arrhythmias in 1.2% (95% CI 0.9-1.8) and in 2.1% (95% CI 1.6-2.8), AHF in 1.6% (95% CI 1.2-2.2) and in 4.2% (95% CI 3.4-5.1), spontaneous MI in 0.5% (95% CI 0.3-0.9) and in 1.6% (95% CI 1.2-2.2), and PMI in 13.2% (95% CI 11.9-14.7) and in 14.8% (95% CI 13.4-16.4) within 30 days and within 365 days, respectively. The MACE-incidence was increased above presumed baseline rate until Day 135 (95% CI 104-163), indicating a vulnerable period of 3-5 months. One out of five high-risk patients undergoing non-cardiac surgery will develop one or more MACE within 365 days. The risk for MACE remains increased for about 5 months after non-cardiac surgery. https://www.clinicaltrials.gov. Unique identifier: NCT02573532.

Biological variation of cardiac troponins in chronic kidney disease.

Background Patients with chronic kidney disease often have increased plasma cardiac troponin concentration in the absence of myocardial infarction. Incidence of myocardial infarction is high in this population, and diagnosis, particularly of non ST-segment elevation myocardial infarction (NSTEMI), is challenging. Knowledge of biological variation aids understanding of serial cardiac troponin measurements and could improve interpretation in clinical practice. The National Academy of Clinical Biochemistry (NACB) recommended the use of a 20% reference change value in patients with kidney failure. The aim of this study was to calculate the biological variation of cardiac troponin I and cardiac troponin T in patients with moderate chronic kidney disease (glomerular filtration rate [GFR] 30–59 mL/min/1.73 m2). Methods and results Plasma samples were obtained from 20 patients (median GFR 43.0 mL/min/1.73 m2) once a week for four consecutive weeks. Cardiac troponin I (Abbott ARCHITECT® i2000SR, median 4.3 ng/L, upper 99th percentile of reference population 26.2 ng/L) and cardiac troponin T (Roche Cobas® e601, median 11.8 ng/L, upper 99th percentile of reference population 14 ng/L) were measured in duplicate using high-sensitivity assays. After outlier removal and log transformation, 18 patients’ data were subject to ANOVA, and within-subject (CVI), between-subject (CVG) and analytical (CVA) variation calculated. Variation for cardiac troponin I was 15.0%, 105.6%, 8.3%, respectively, and for cardiac troponin T 7.4%, 78.4%, 3.1%, respectively. Reference change values for increasing and decreasing troponin concentrations were +60%/–38% for cardiac troponin I and +25%/–20% for cardiac troponin T. Conclusions The observed reference change value for cardiac troponin T is broadly compatible with the NACB recommendation, but for cardiac troponin I, larger changes are required to define significant change. The incorporation of separate RCVs for cardiac troponin I and cardiac troponin T, and separate RCVs for rising and falling concentrations of cardiac troponin, should be considered when developing guidance for interpretation of sequential cardiac troponin measurements.

Serial measurements of cardiac troponin I in heart failure secondary to canine mitral valve disease

Serial measurements of cardiac troponin I (cTnI) levels are considered to be better predictors of cardiac death than single-time-point analyses in human medicine. We hypothesised that cTnI levels could reflect...

Abstract WMP63: New Onset Nonvalvular Paroxysmal Atrial Fibrillation After Acute Ischemic Stroke Without Atrial Cardiopathy- to or Not to Anticoagulant

Introduction: Cardiac outcome in acute ischemic stroke (AIS) remains less well understood as do the neuroanatomic correlates of AIS associated myocardial injury. For patients with new onset paroxysmal atrial fibrillation (Afib), anticoagulant therapy is determined based on the CHA 2 DS 2 -VASc score. However, newly diagnosed short-run Afib after AIS could be neurogenic, without an increase in the risk of AIS recurrence. The present study of 68 patients with acute insular infarcts describes cardiac outcomes including newly diagnosed Afib and clinical significance. Methods and Results: Serial measurements of cardiac troponin I (cTnI), EKG, echocardiography (Echo) (some had transesophageal Echo) were conducted in all patients with MRI-confirmed AIS involving insular cortex. The severity of insular damage was measured with diffusion-weighted imaging. Thirty-one patients (46%) had right MCA infarcts involving insular cortex, and 37 patients had left MCA (54%) stroke with insular involvement. Patients with left MCA infarcts had higher cTnI but did not reach statistical significance. By linear regression analysis in either right or left insular AIS, there was a significant correlation between elevated cTnI and the severity of insular injury. Six patients (3 right and 3 left MCA AISs) were found to have transient cardiac dysfunction. Nine out of 68 AIS patients detected new onset transient Afib in the absence of prior heart disease, cardiac arrhythmia, or evidence of atrial myopathy. Five of them are not on anticoagulant therapy due to varied reasons. None of them experienced recurrent major cardiac events, recurrent Afib, or ischemic stroke during the 12-month follow up. Conclusions: Our study shows that either left or right MCA AIS involving the insular cortex may cause cardiac injury including transient Afib. We further demonstrated a correlation between the severity of insular damage and cardiac sequelae. However, there is no increased risk of recurrent ischemic stroke at 1 year in 5 patients with newly diagnosed Afib not on anticoagulant therapy. A long-term study with large number of AIS patients with newly diagnosed Afib is needed to determine if lifelong anticoagulation is required in this particular group of patients with presumed neurogenic Afib.

Abstract 66: Practical Application of Serial Measurement of Cardiac Troponin I for Risk Stratification in Acute Ischemic Stroke

Background: Serum cardiac troponin can be increased in acute ischemic stroke and regarded as a prognostic marker after stroke as similar as coronary artery disease (CAD). However, interpretation of troponin elevation in ischemic stroke patients is complex. Therefore, the aim of this study was to elucidate the possible causes and long-term prognostic value of troponin elevation in ischemic stroke patients. Methods: In a prospective, single center cohort study, we performed serial measurement of serum troponin and 12-lead electrocardiogram (ECG) at 48 hours after stroke onset followed by admission. Based on troponin I level at 48 hours, patients were categorized into 3 groups; elevated (≥0.04 ng/mL), minimally elevated (0.040-0.010 ng/mL) and non-detectable (<0.010 ng/mL) level. Comorbidities with possible impact on troponin elevation were documented based on either historical information or abnormalities in disease-related biomarkers. The primary endpoint was death and major adverse cardiac and cerebrovascular event (MACCE). Results: Among 1092 consecutive patients during 2-year period, 145 patients (13.3%) and 335 patients (30.7%) had a positive and minor elevation troponin. Multivariable analysis identified six-comorbidities included atrial fibrillation (AF), hypertrophic myocardium (HM), heart failure (HF), chronic kidney disease (CKD), active cancer and possibly ischemic heart disease (IHD), and composite neurological factor (defined as moderate to severe deficits or insular lesions) associated with troponin elevation. In a multivariate Cox model, minimally and elevated troponin were independently associated with death (hazard ratio [HR]: 1.77, 95% confidence interval [CI]: 1.07-2.91 for minor elevation and HR: 3.63, 95% CI: 2.13-6.19 for positive troponin) and combined endpoints of MACCE. Conclusions: Troponin elevation even minor elevation are associated with mortality and MACCE in patients with acute stage of ischemic stroke.

“30-minute-delta” of high-sensitivity troponin I improves diagnostic performance in acute myocardial infarction

BackgroundRapid and accurate diagnosis of acute myocardial infarction (AMI) are critical for the initiation of effective medical treatment. Recently, a high-sensitivity cardiac troponin I (hs-cTnI) assay was developed as a biochemical marker for the early diagnosis of AMI. Current guidelines recommend that serial measurements of cardiac troponin should be performed in patients who present symptoms suggestive of acute coronary syndrome. The aim of this study was to evaluate the diagnostic performance of 30-minute serial measurements of hs-cTnI for the detection of AMI. MethodsWe prospectively enrolled patients presenting with suspected AMI within 12h from symptom onset. We measured hs-cTnI levels at presentation and 30min later to calculate the “30-minute-delta”. The diagnostic performance was determined by the area under the receiver operating characteristic curve (AUC). ResultsAmong the 71 patients enrolled in this study, 55 (77%) were diagnosed with AMI. The hs-cTnI level at presentation was significantly greater in the patients with AMI than in those without AMI [306.2 (77.3–1809.9)pg/mL versus 22.5 (7.2–115.5)pg/mL, p<0.01]. The “30-minute-delta” was also significantly greater in patients with AMI [54.6 (13.5–288.0)pg/mL versus 1.9 (0.6–6.3)pg/mL, p<0.01]. The AUC of the “30-minute-delta” was significantly greater than that of a single measurement at presentation (0.911 versus 0.829, p<0.05). ConclusionsThe “30-minute-delta” of hs-cTnI presents improved diagnostic performance for AMI compared with a single measurement.

Strong diurnal rhythm of troponin T, but not troponin I, in a patient with renal dysfunction

Cardiac troponin T (cTnT) and I (cTnI), measured with high-sensitive assays, are the preferred biomarkers for the diagnosis of acute myocardial infarction [ 1 Roffi M. Patrono C. Collet J.P. Mueller C. Valgimigli M. Andreotti F. et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur. Heart J. 2016; 37: 267-315 Crossref PubMed Scopus (4337) Google Scholar , 2 Mills N.L. Churchhouse A.M. Lee K.K. Anand A. Gamble D. Shah A.S. et al. Implementation of a sensitive troponin I assay and risk of recurrent myocardial infarction and death in patients with suspected acute coronary syndrome. JAMA. 2011; 305: 1210-1216 Crossref PubMed Scopus (271) Google Scholar ]. Serial cardiac troponin measurements, and the interpretation of a “troponin rise-or-fall” in patients with chest pain discriminate between acute and chronic troponin elevations [ [1] Roffi M. Patrono C. Collet J.P. Mueller C. Valgimigli M. Andreotti F. et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur. Heart J. 2016; 37: 267-315 Crossref PubMed Scopus (4337) Google Scholar ]. This diagnostic concept assumes that troponin levels in patients without acute cardiac injury fluctuate randomly around an individual's homeostatic setpoint. However, it has recently been demonstrated that cTnT exhibits a diurnal rhythm [ 3 Klinkenberg L.J. van Dijk J.W. Tan F.E. van Loon L.J. van Dieijen-Visser M.P. Meex S.J. Circulating cardiac troponin T exhibits a diurnal rhythm. J. Am. Coll. Cardiol. 2014; 63: 1788-1795 Abstract Full Text Full Text PDF PubMed Scopus (65) Google Scholar , 4 Aakre K.M. Roraas T. Petersen P.H. Svarstad E. Sellevoll H. Skadberg O. et al. Weekly and 90-minute biological variations in cardiac troponin T and cardiac troponin I in hemodialysis patients and healthy controls. Clin. Chem. 2014; 60: 838-847 Crossref PubMed Scopus (75) Google Scholar ]. The amplitude of the diurnal cTnT rhythm and its diagnostic implication in patients with chronically elevated cTnT levels are unexplored. Also, whether cTnT and cTnI are equally affected by rhythmic diurnal oscillation is unknown.

Fully automated ultrasensitive digital immunoassay for cardiac troponin I based on single molecule array technology.

The association between increases in cardiac troponin and adverse cardiac outcomes is well established. There is a growing interest in exploring routine cardiac troponin monitoring as a potential early indicator of adverse heart health trends. Prognostic use of cardiac troponin measurements requires an assay with very high sensitivity and outstanding analytical performance. We report development and preliminary validation of an investigational assay meeting these requirements and demonstrate its applicability to cohorts of healthy individuals and patients with heart failure. On the basis of single molecule array technology, we developed a 45-min immunoassay for cardiac troponin I (cTnI) for use on a novel, fully automated digital analyzer. We characterized its analytical performance and measured cTnI in healthy individuals and heart failure patients in a preliminary study of assay analytical efficacy. The assay exhibited a limit of detection of 0.01 ng/L, a limit of quantification of 0.08 ng/L, and a total CV of 10% at 2.0 ng/L. cTnI concentrations were well above the assay limit of detection for all samples tested, including samples from healthy individuals. cTnI was significantly higher in heart failure patients, and exhibited increasing median and interquartile concentrations with increasing New York Heart Association classification of heart failure severity. The robust 2-log increase in sensitivity relative to contemporary high-sensitivity cardiac troponin immunoassays, combined with full automation, make this assay suitable for exploring cTnI concentrations in cohorts of healthy individuals and for the potential prognostic application of serial cardiac troponin measurements in both apparently healthy and diseased individuals.

Cardiac involvement of lung cancer mimicking myocardial infarction

A 58-year-old man (a heavy smoker), without prior medical history, was admitted to the Department of Cardiology in the emergent diagnosis of acute coronary syndrome with ST segment elevation in the third hour of retrosternal pain. The initial ECG revealed sinus rhythm 85/min, left anterior fascicular block, QS pattern in V1–V3 with ST-segment elevation in the leads V2 through V6 (up to 2 mm in V2–V3), with symmetric negative T waves in the leads I, aVL, V2–V5 (Fig. 1). Laboratory tests, except for a small leukocytosis (11 × 109/L, N to 10 × 109/L), and elevations of troponin T (30 ng /L, N to 14 ng/L), were within normal limits. Urgent coronary angiography was performed, which showed critical changes in the distal circumflex branch narrow artery (< 2 mm), with no significant haemodynamic atherosclerosis in other arteries. Due to the location of the stenosis and artery calibre, coronary angioplasty was not performed. Despite typical pharmacological treatment, pain relief was not achieved. The subsequent ECG recorded persistent ST-segment elevation with negative T waves in precordial leads, without a change in troponin values (the II. troponin: 27 ng/L and the III: 28 ng/L). Based on radiological images of the chest, a tumour in the left lung with obliteration of the left heart border was suspected. Transthoracic echocardiography demonstrated the presence of a tumour sized 10 × 7 × 11 cm with involvement of the pericardium (without evidence of fluid), and probably the anterior wall of the left ventricle. To differentiate the cardiac mass, we performed cardiac magnetic resonance imaging and confirmed an anterior mediastinal tumour, causing extensive atelectatic changes in the left lung and infiltrating the anterior wall of the left ventricle (Figs. 2, 3). The patient was referred to the oncology centre where metastatic small cell carcinoma of the left lung was diagnosed. Three months after the start of chemotherapy, the patient died. The most common neoplasms associated with cardiac metastasis are lung cancer, oesophageal cancer, lymphoma, breast cancer, leukaemia, stomach cancer, and melanoma. Their symptomatology is largely dependent on the size of the tumour and its location. Myocardial infiltration by tumour cells may lead to the occurrence of arrhythmias and cardiac conduction, and less non-specific ST segment changes. In this case, the clinical and ECG changes initially showed a myocardial infarction with ST segment elevation anterior wall. However, subsequent ECGs, serial measurements of cardiac troponin and results of imaging studies did not confirm the initial diagnosis. In the era of invasive treatment of myocardial infarction, it is necessary to consider other causes of ST-T changes in the ECG and increased troponin values. Extended cardiac diagnosis and a multidisciplinary approach are often necessary to determine the correct diagnosis.

GW24-e2277 Cardiac Diastolic Dysfunction may Hold Promise as Markers of Cardiotoxicity during Daunorubicin Treatment in Acute Nonlymphocytic Leukemia Patients

ObjectivesDaunorubicin causes cardiac injury in acute nonlymphocytic leukemia. Early identifying caridotoxicity induced by daunorubicin might help individualise cardiac protect treatment. Dexrazoxane can reduce cardiac damage. In this study, we assess...

Serial measurements of cardiac troponin I in patients with myasthenia gravis-related cardiomyopathy

Myasthenia gravis (MG) primarily affects skeletal muscle through the production of autoantibodies against the nicotinic acetylcholine receptor in the motor endplates; in addition, heart muscle is an autoimmune target [1,2]. Although MG is believed to be relatively rare, 16% of patients with MG exhibit several types of cardiac involvement, ranging from asymptomatic electrocardiogram (ECG) changes to myocarditis, heart failure, and sudden death [2]. A persistent increase in cardiac troponins reportedly indicates ongoing myocardial damage during heart failure and a poor prognosis [3–6].

Abstract WP131: Correlation of Cardiac Derangement in Patients with Right-Sided Ischemic Stroke and the Severity of Insular Damage

Objective: Although it is known that neurogenic cardiac damage can occur after an ischemic stroke, the mapping of the neuroanatomic correlation of ischemic stroke-related myocardial injury remains to be defined. Our previous animal study found a higher incidence of myocardial damage from left-sided insular infarction comparing to the right side. However, the results from various clinical studies have been inconclusive. This clinical study aims to identify a quantitative correlation between adverse cardiac outcomes and insular infarction, left-sided versus right-sided, as well as potential prognostic factors that may be used to aid in assessing patient outcomes and making treatment decisions. Methods and Results: A serial measurements of cardiac troponin T (cTnT) and creatine phosphokinase-MB (CK-MB), 12-lead EKG, and two- dimensional echocardiography were performed in 42 patients with MRI-confirmed ischemic stroke involving the insular cortex. The severity of insular damage was measured with diffusion-weighted imaging studies (DWI). Patients with renal failure, recent cardiac ischemic events, or congestive heart failure were excluded. Twenty-two patients (52.4%) had left-sided middle cerebral artery (MCA) infarcts with insular involvement, whereas 20 (47.6%) had a right-sided MCA infarcts involving the insular cortex. When compared to patients with left MCA infarcts involving the insular cortex, patients with right MCA infarcts with insular involvement had significantly higher levels of cTnT elevation. By using the linear regression analysis we also identified a statistically significant correlation between cTnT elevation and severity of right insular damage, instead of the NIH stroke score (NIHSS) as commonly assumed. Moreover, two patients were found to have transient left ventricular wall hypokinesis which mimics Takotsubo cardiomyopathy. Conclusions: This study showed that patients with right MCA ischemic stroke involving the insular cortex, comparing to those with left-sided insular stroke, tend to have more severe cardiac insult leading to higher levels of cTnT. The study also identified severity of insular damage as a potential prognostic factor in assessing cardiac derangement as a complication of insular infarction.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Association of serial measurements of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults

Association of serial measurements of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults