UNASSIGNED: Elevated troponin T (cTnT) and/or troponin I (cTnI) can be ascribed to multiple causes, mostly resulting from cardiac tissue damage and in lesser numbers resulting from non-cardiac related causes. The presence of macrotroponins is easily overlooked, with potentially negative consequences.
UNASSIGNED: This case report presents a case study of a 12-year-old child known to have MYH7 gene-associated hypertrophic cardiomyopathy with acute chest pain combined with an unexpected high cTnT and cTnI. A cardiac cause was deemed unlikely after additional investigation, as these showed no abnormalities. After consulting a laboratory specialist, it could be concluded that the high cTnT and cTnI were a result of macrotroponin complexes, a protein complex consisting of circulating protein and endogenous autoantibodies against that protein, resulting in elevated values with misguiding and uncertain clinical significance.
UNASSIGNED: Awareness of the existence of macrotroponins could have prevented costly diagnostics and prolonged hospital admission with grave psychological impact, especially in children.

BACKGROUND: This study aimed to demonstrate potential measures to discern interference and establish an algorithm for identifying interference in an hs-cTnT assay with a clinical discrepancy.
METHODS: Laboratory error and disease factors were first excluded. Then, a serial dilution test, polyethylene glycol (PEG) precipitation, and heterophile antibody blocking reagents (HBRs) were performed to confirm the interference substance. In addition, high-speed centrifugation and western blot were tried.
RESULTS: The sample diluted linearly (R2 = 0.9966). However, there was a dramatic reduction in the concentration of hs-cTnT concentration to a normal level after both PEG precipitation and HBR1 treatment. The results were inconclusive in high-speed centrifugation and western blot assay.
CONCLUSIONS: This study elucidated a heterophile antibody interference in measurement of hs-cTnT alone on a Roche analyzer.

UNASSIGNED: To investigate the differences in biochemical characteristics between Coronavirus Disease 2019 (COVID-19) patients with and without delirium in non-intensive care (IC) COVID-19 units was aimed.
UNASSIGNED: This study was designed as an observational, single-centered, and case-control study consisting of 43 delirious patients and matched 45 non-delirious patients admitted to non-IC COVID-19 units. Delirium was diagnosed by a consultant psychiatrist according to the DSM-5 delirium diagnostic criteria. Independent variables such as laboratory tests at the time of admission, clinical features, and patient characteristics were obtained from electronic medical records by researchers. In the primary analyses, binomial logistic regression models were used to investigate the factors associated with delirium, which was identified as the outcome variable. Multivariate logistic models were then adjusted for potential confounding factors, including age, gender, history of neurocognitive disorders and Charlson Comorbidity Index (CCI).
UNASSIGNED: We observed higher levels of urea, d-dimer, troponin-T, proB-type natriuretic peptide, and CCI in patients with delirium compared to patients without delirium. We also observed lower levels of estimated glomerular filtration rate (eGFR), serum albumin, and O2 saturation and a decrease in the length of stay at the hospital. After adjusting for confounding factors such as gender, age, and comorbidity, we found that urea (adjusted estimate=0.015; 95% Confidence Interval [CI]=0.058-0.032, P=0.039), urea/creatinine ratio (adjusted estimate=0.008; 95% CI=0.002-0.013, P=0.011), and troponin-T (adjusted estimate=0.066; 95% CI=0.014-0.118, P=0.014) were independent biomarkers associated with delirium.
UNASSIGNED: Delirium is associated with higher urea levels and urea/creatinine ratios in COVID-19 patients. In addition, the relationship between troponin-T and delirium may help understand the potential link between the brain and the heart in COVID-19. Additional multi-centred studies with larger sample sizes are needed to generalise these results.

BACKGROUND: Duchenne muscular dystrophy (DMD) is an X-linked muscular disease which is caused by the absence of dystrophin. Troponin elevation with acute chest pain may indicate acute myocardial injury in these patients. We report a case of DMD that presented with ACP and troponin elevation, who was diagnosed with acute myocardial injury, and successfully treated with corticosteroids.
METHODS: A 9-year-old with DMD was admitted to the emergency department with the complaint of acute chest pain. His electrocardiogram (ECG) revealed inferior ST elevation and serum troponin T was elevated. The transthoracic echocardiography (TTE) demonstrated inferolateral and anterolateral hypokinesia with depressed left ventricular function. An ECG-gated coronary computed tomography angiography ruled out acute coronary syndrome. Cardiac magnetic resonance imaging revealed mid-wall to sub-epicardial late gadolinium enhancement at the basal to the mid inferior lateral wall of the left ventricle and corresponding hyperintensity on T2-weighted imaging, consistent with acute myocarditis. A diagnosis of acute myocardial injury associated with DMD was made. He was treated with anticongestive therapy and 2 mg/kg/day of oral methylprednisolone. Chest pain resolved the next day, and ST-segment elevation returned to normal on the third day. Troponin T decreased in the sixth hour of oral methylprednisolone treatment. TTE on the fifth day revealed improved left ventricular function.
CONCLUSIONS: Despite advances in contemporary cardiopulmonary therapies, cardiomyopathy remains the leading cause of death in patients with DMD. Acute chest pain attacks with elevated troponin in patients with DMD without coronary artery disease may indicate acute myocardial injury. Recognition and appropriate treatment of acute myocardial injury episodes in DMD patients may delay the development of cardiomyopathy.

Cardiac troponins T and I are the main (most sensitive and specific) laboratory indicators of myocardial cell damage. A combination of laboratory signs of myocardial cell damage (elevated levels of cardiac troponins T and I) with clinical (severe chest pain spreading to the left side of the human body) and functional (rise or depression of the ST segment, negative T wave or emergence of the Q wave according to electrocardiography and/or decrease in the contractility of myocardial areas exposed to ischemia according to echocardiography) signs of myocardial ischemia is indicative of the ischemic damage to cardiomyocytes, which is characteristic of the development of acute coronary syndrome (ACS). Today, with early diagnostic algorithms for ACS, doctors rely on the threshold levels of cardiac troponins (99th percentile) and on the dynamic changes in the serum levels over several hours (one, two, or three) from the moment of admission to the emergency department. That said, some recently approved highly sensitive methods for determining troponins T and I show variations in 99th percentile reference levels, depending on gender. To date, there are conflicting data on the role of gender specificities in the serum levels of cardiac troponins T and I in the diagnostics of ACS, and the specific mechanisms for the formation of gender differences in the serum levels of cardiac troponins T and I are unknown. The purpose of this article is to analyze the role of gender specificities in cardiac troponins T and I in the diagnostics of ACS, and to suggest the most likely mechanisms for the formation of differences in the serum levels of cardiac troponins in men and women.

Ventricular noncompaction (VNC) is a cardiomyopathy characterized by overdeveloped ventricular trabeculaes and deep recess, which has been rarely reported.
A 29-year-old Chinese pregnant woman with no obvious fetal abnormality in regular prenatal examination during first and second trimester. However, at 32 weeks of gestation, both obstetric growth scan and fetal echocardiogram revealed an enlarged heart with grid-like changes at the apical region. Eventually, the genetic and autopsy findings indicated the deceased infant with VNC.
Isolated VNC could be detected prenatally, even during the late pregnancy. Fetuses suspected of VNC should be offered genetic tests.

UNASSIGNED: Takotsubo syndrome is an acute cardiac condition involving sudden, transient apical ballooning of the left ventricle of the heart that may be triggered by emotional stress and some non-cardiac conditions. Its diagnosis is based on clinical presentation, electrocardiogram, cardiac imaging and biomarkers.
UNASSIGNED: Here, we present a novel and original case report of a patient presenting very soon in the post-partum period with an unusual form of Takotsubo syndrome without clinical symptoms of cardiac disease and accompanied by HELLP syndrome. The overall dynamics of the changes in troponin I, troponin T and NT-proBNP levels after delivery were generally similar, but the amount of troponin I was much greater than that of troponin T and troponin I was already elevated before delivery. NT-proBNP levels peaked around the same time as the troponins and the peak concentration was within the same range as that of troponin I.
UNASSIGNED: Our findings indicate that assaying circulating cardiac biomarkers, especially troponin I and NT-proBNP, may be a useful complement to non-invasive cardiac imaging including transthoracic echocardiography and cardiovascular magnetic resonance imaging, in the diagnosis of Takotsubo syndrome. They illustrate the importance of cardiac biomarkers in assisting diagnosis of this disease.

OBJECTIVE: Macrotroponin is due to cardiac troponin (cTn) binding to endogenous cTn autoantibodies. While previous studies showed a high incidence of macrotroponin affecting cTnI assays, reports of macrotroponin T, particularly without cTnI reactivity, have been rare. Although the clinical significance of macrotroponin is not fully understood, macroenzymes and complexes are recognised to cause confusion in interpretation of laboratory results. The potential for adverse clinical consequences due to misinterpretation of affected results is very high.
METHODS: We describe four cases of macrotroponin T with persistently low high sensitivity cTnT (hs-cTnT) by the 9 min compared to the 18 min variant of the assay. Three cases were serendipitously identified due to the use of a lot number of Roche hs-cTnT affected by non-reproducible results, necessitating measurement of cTnT in duplicate. We identified and characterised these macrotroponin specimens by immunoglobulin depletion (Protein A and PEG precipitation), mixing studies with EDTA and recombinant cTnT.
RESULTS: In cases of macro-cTnT, a lower result occurred on the hs-cTnT using the 9 min compared to 18 min variant assay (ratio of 9-18 min hs-cTnT <0.80). Mixing studies with recombinant cTnT or EDTA demonstrated a difference in recovery vs. controls. One of these patients demonstrated a high molecular weight complex for cTnI and cTnT demonstrating a macrocomplex involving both cTn. This patient demonstrated a rise and fall in cTn when measured by several commercial assays consistent with genuine acute cardiac injury.
CONCLUSIONS: We identified several cases of macro-cTnT and described associated clinical and biochemical features.

OBJECTIVE: To assess the association between computed tomography pulmonary angiography (CTPA) atrial measurements and both 30-day pulmonary embolism (PE)-related adverse events and mortality, and non-PE-related mortality, and to identify the best predictors of these outcomes by comparing atrial measurements and widely used clinical and imaging variables.
METHODS: Retrospective single-center pilot study. Acute PE patients diagnosed on CTPA who also had a transthoracic echocardiogram, electrocardiogram, and troponin T were included. CTPA left atrial (LA) and right atrial (RA) volume and short-axis diameter were measured and compared between outcome groups, along with right ventricular/left ventricular diameter ratio, interventricular septal bowing, tricuspid annular plane systolic excursion, electrocardiogram, and troponin T.
RESULTS: A total of 350 patients. LA volume and diameter were associated with PE-related adverse events (P≤0.01). LA volume was the only atrial measurement associated with PE-related mortality (P=0.03), with no atrial measurements associated with non-PE-related mortality. Troponin was most associated with PE-related adverse events and mortality (both area under the curve [AUC]=0.77). On multivariate analysis, combination models did not greatly improve PE-related adverse events prediction compared with troponin alone. For PE-related mortality, the best models were the combination of troponin, age, and either LA volume (AUC=0.86) or diameter (AUC=0.87).
CONCLUSIONS: Among patients with acute PE, CTPA LA volume is the only imaging parameter associated with PE-related mortality and is the best imaging predictor of this outcome. Reduced CTPA LA volume and diameter, along with increased RA/LA volume and diameter ratios, are significantly associated with 30-day PE-related adverse events, but not with non-PE-related mortality.

The electrocardiogram (ECG) is the key player in the diagnosis of an acute coronary syndrome. In the light of normal ECG findings, the diagnosis can be missed. The high-sensitive troponin is a necessary laboratory value for patients with uncommon symptoms.
A 53-year-old man without a history of coronary heart disease initially presented to his general practitioner with persistent hiccups for 3 weeks. In the emergency department, the patient complained of nausea and burping. The high-sensitive troponin T was 989 pg/mL and led to the diagnosis of an acute coronary syndrome.
The troponin algorithm helps to identify this patient group, especially in the setting of elevated creatine kinase and lactate dehydrogenase. Awareness of these symptoms can help lead to a timely reperfusion therapy and thus improved outcomes. The 2015 European Society of Cardiology algorithm for troponin may not only help for the initial diagnosis, but rather should be regarded as crucial.