Biomarkers Of Cardiac Damage Research Articles

Serial Troponin for Early Detection of Nivolumab Cardiotoxicity in Advanced Non-Small Cell Lung Cancer Patients.

Rare cases of severe myocarditis are reported during treatment with nivolumab. Troponin, a biomarker of cardiac damage, is a key component of the diagnostic workup of many cardiac disorders, including myocarditis. This study investigates the role of troponin to assess cardiac involvement during nivolumab therapy for non-small cell lung cancer (NSCLC). We evaluated 59 NSCLC patients, analyzing serum samples collected within a translational research study. Troponin above the upper normal limit (0.046 ng/mL) was defined as Tn+, whereas normal but detectable troponin (0.015-0.045) was defined as Tndet. Troponin alterations were interpreted on the grounds of the following elements: peak values and time curve, cardiac comorbidities, signs and symptoms coincident to troponin elevation, ECG, echocardiography, and disease progression. No patient had cardiovascular events. Among 362 available blood samples, Tn+ (max 0.317 ng/mL) was found in 13 determinations belonging to 6 patients. Seven other patients had isolated Tndet. In five patients, Tn+ was attributed to cardiac comorbidities, disease progression, or worsening clinical status. One patient without cardiac history and in good clinical condition had a sustained troponin increase-soon after the start of therapy-and after careful evaluation of all relevant elements, it was interpreted as a marker of nivolumab-related subclinical myocarditis. Tn+ may occur in NSCLC patients treated with nivolumab, but in most cases it does not indicate nivolumab cardiotoxicity. In some cases, however, a careful interpretation of troponin alteration, especially at the beginning of therapy, enables identification of subclinical myocarditis, thus allowing early cardiac treatment. Myocarditis is a rare but serious adverse event of immune checkpoint blockade with nivolumab, which needs to be recognized as soon as possible. This article suggests that troponin, a user-friendly biomarker of myocardial cytotoxicity, might be useful for early detection of immune-mediated myocarditis. However, because troponin abnormalities might also be related to a number of conditions capable of causing myocardial oxygen demand-supply mismatch, a careful cardiac assessment should be performed in non-small cell lung cancer patients in order to properly interpret any troponin increase. According to the available evidence, monitoring troponin during the first weeks of treatment can be considered reasonable.

Cardiovascular biomarkers in clinical studies of type 2 diabetes.

When planning cardiovascular (CV) studies in type 2 diabetes (T2D), selection of CV biomarkers is a complex issue. Because the pathophysiology of CV disease (CVD) in T2D is multifactorial, ideally, the selected CV biomarkers should cover all aspects of the known pathophysiology of the disease. This will allow the researcher to distinguish between effects on different aspects of the pathophysiology. To this end, we discuss a host of biomarkers grouped according to their role in the pathogenesis of CVD, namely: (1) cardiac damage biomarkers; (2) inflammatory biomarkers; and (3) novel biomarkers (oxidative stress and endothelial dysfunction biomarkers). Within each category we present the best currently validated biomarkers, with special focus on the population of interest (people with T2D). For each individual biomarker, we discuss the physiological role, validation in the general population and in people with T2D, analytical methodology, modifying factors, effects of glucose-lowering drugs, and interpretation. This approach will provide clinical researchers with the information necessary for planning, conducting and interpreting results from clinical trials. Furthermore, a systematic approach to selection of CV biomarkers in T2D research will improve the quality of future research.

Could inflammatory biomarkers be of greater interest than troponins for patients admitted for myocardial syndromes? A single-center real life retrospective study

Diagnosis of myocardial syndromes is a challenge in clinical practice because of overlapping forms. Biomarkers for cardiac damage are the cornerstone for the diagnosis and management of the patients admitted for chest pain. Primary objective is to assess which criteria are used by physicians to make the diagnosis of myocarditis before cardiac MRI and compare them with the results of MRI. We conducted a retrospective observational and monocentric study from the exhaustive French medico-administrative hospitalizations database records, collected from January 2015 to December 2016 in our center. A total of 91 patients were included (mean age 38 years, 75.8% male). Diagnosis of myocarditis was immediately suspected in 66% of cases based on the mean age (33 years), previous infectious disease (58%), pericarditis chest pain (87%), ST/T wave change on ECG (78%), and elevation of biomarkers levels: ultra-sensitive (us) Troponin T, creatine kinase (CK) and C-reactive protein (CRP). Eighty-one patients had cardiac MRI, myocarditis was confirmed for 66 patients. Compared with patients with negative MRI, patients were younger ( P = 0.037) and male ( P = 0.044). Mean us Troponin T and CK levels were significantly higher (respectively P = 0.007 and 0.04). In patients with positive MRI, at the admission, there were significant correlations between CRP and us Troponin T levels ( P = 0.003, r = 0.36), and with CRP levels and ST/T wave change ( P = 0.02). CRP levels at the admission and left ventricular ejection fraction (LVEF) were poorly correlated ( P = 0.08, r = −0.002). There was no correlation between us troponin T and LVEF ( P = 0.44). Age, male gender, us Troponin and CK levels at the admission are significantly associated with the diagnosis of myocarditis. Besides, it seems to be that CRP levels could provide additional information when compared to us Troponin levels in myocarditis, but these observations have to be confirmed by a larger study.

RVAD Support in the Setting of Submassive Pulmonary Embolism

Patients with submassive pulmonary embolism (PE), although normotensive, are characterized by right ventricular (RV) dysfunction and elevated levels of biomarkers of cardiac damage. The best treatment option in these cases is still a subject of debate and the use of thrombolysis in submassive PE remains controversial. A 57-year-old Caucasian male with unprovoked PE, normal blood pressure, and elevated troponin I values was referred to the cardiovascular department. In view of the presence of a right atrium thrombus, the patient underwent surgical embolectomy under extracorporeal circulation, with the extraction of a huge thrombus together with fragmented thrombi from both pulmonary arteries. The patient developed an acute right heart failure solved with a temporary RV assist device (RVAD) support. The RV recovery was observed after 72 hours following the implantation. RVAD placement should be considered in the management of PE in case of acute right heart failure after reperfusion therapy since it can bring the patient out of a death spiral.

Severe Pneumococcal Pneumonia Causes Acute Cardiac Toxicity and Subsequent Cardiac Remodeling.

Up to one-third of patients hospitalized with pneumococcal pneumonia experience major adverse cardiac events (MACE) during or after pneumonia. In mice, Streptococcus pneumoniae can invade the myocardium, induce cardiomyocyte death, and disrupt cardiac function following bacteremia, but it is unknown whether the same occurs in humans with severe pneumonia. We sought to determine whether S. pneumoniae can (1) translocate the heart, (2) induce cardiomyocyte death, (3) cause MACE, and (4) induce cardiac scar formation after antibiotic treatment during severe pneumonia using a nonhuman primate (NHP) model. We examined cardiac tissue from six adult NHPs with severe pneumococcal pneumonia and three uninfected control animals. Three animals were rescued with antibiotics (convalescent animals). Electrocardiographic, echocardiographic, and serum biomarkers of cardiac damage were measured (troponin T, N-terminal pro-brain natriuretic peptide, and heart-type fatty acid binding protein). Histological examination included hematoxylin and eosin staining, immunofluorescence, immunohistochemistry, picrosirius red staining, and transmission electron microscopy. Immunoblots were used to assess the underlying mechanisms. Nonspecific ischemic alterations were detected by electrocardiography and echocardiography. Serum levels of troponin T and heart-type fatty acid binding protein were increased (P < 0.05) after pneumococcal infection in both acutely ill and convalescent NHPs. S. pneumoniae was detected in the myocardium of all NHPs with acute severe pneumonia. Necroptosis and apoptosis were detected in the myocardium of both acutely ill and convalescent NHPs. Evidence of cardiac scar formation was observed only in convalescent animals by transmission electron microscopy and picrosirius red staining. S. pneumoniae invades the myocardium and induces cardiac injury with necroptosis and apoptosis, followed by cardiac scarring after antibiotic therapy, in an NHP model of severe pneumonia.

Nonmediated, Label-Free Based Detection of Cardiovascular Biomarker in a Biological Sample.

Direct electrochemical (EC) monitoring in a cell culture medium without electron transporter as called mediator is attractive topic in vitro organoid based on chip with frequently and long-time monitoring since it can avoid to its disadvantage as stability, toxicity. Here, direct monitoring with nonmediator is demonstrated based on impedance spectroscopy under the culture medium in order to overcome the limitation of mediator. The applicability of EC monitoring is shown by detecting alpha-1-anti trypsin (A1AT) which is known as biomarkers for cardiac damage and is widely chosen in organoid cardiac cell-based chip. The validity of presented EC monitoring is proved by observing signal processing and transduction in medium, mediator, medium-mediator complex. After the observation of electron behavior, A1AT as target analyte is immobilized on the electrode and detected using antibody-antigen interaction. As a result, the result indicates limit of detection is 10 ng mL-1 and linearity for the 10-1000 ng mL-1 range, with a sensitivity of 3980 nF (log [g mL])-1 retaining specificity. This EC monitoring is based on label-free and reagentless detection, will pave the way to use for continuous and simple monitoring of in vitro organoid platform.

Asymmetric dimethylarginine and heart-type fatty acid-binding protein 3 are risk markers of cardiotoxicity in carbon monoxide poisoning cases in Zagazig university hospitals.

Carbon monoxide (CO) poisoning is a leading cause of toxicity-related mortality and morbidity worldwide. Recent studies focused on CO-induced cardiovascular toxicity. Oxidative stress plays an important role in the pathophysiology of CO toxicity. The aim of this study was to elucidate the relationship between cardiac damage biomarkers and oxidative stress biomarkers in patients with CO-induced cardiotoxicity. This study was carried out on 36 CO-poisoned patients admitted to Zagazig University Hospitals. Forty healthy individuals (age- and sex-matched) were selected as a control group. Clinical examination and electrocardiography (ECG) were performed for CO-poisoned patients. These patients have been investigated for carboxyhaemoglobin percent (COHB%) and cardiac damage biomarkers; cardiac troponin I (cTn-I), heart-type fatty acid-binding protein 3 (H-FABP3). Oxidative stress biomarkers comprising malondialdehyde (MDA), asymmetric dimethylarginine (ADMA), and total antioxidant capacity (TAC) have been also assessed. All biomarkers have been assessed on admission (0 h) and 6 h after treatment of CO-poisoned patients with high-flow oxygen and compared with those of the control groups. ECG findings were abnormal in 31 patients (86.11%), where sinus tachycardia was the commonest finding (58.33%). There was a statistically significant increase of COHB%, MDA, ADMA, and H-FABP3 levels, and a significant decrease of TAC level in CO-poisoned patients compared to controls with no significant changes in cTn-I. Six hours following treatment, all measured parameters were significantly improved except for cTn-I, which was significantly increased when compared with admission status (0 h). Furthermore, H-FABP3 showed a significant positive correlation with COHB%, MDA, ADMA, and a negative correlation with TAC, while cTn-I was significantly correlated with COHB% only. ADMA and MDA seem to be the strongest determinants for the prediction of H-FABP3 changes and hence cardiovascular toxicity. Thus, cardiac damage in patients with CO poisoning could be partially mediated by CO-induced oxidative stress, where H-FABP3 level was directly and strongly associated with MDA and ADMA levels.

Late Effects of Total-Body Gamma Irradiation on Cardiac Structure and Function in Male Rhesus Macaques.

Heart disease is an increasingly recognized, serious late effect of radiation exposure, most notably among breast cancer and Hodgkin's disease survivors, as well as the Hiroshima and Nagasaki atomic bomb survivors. The purpose of this study was to evaluate the late effects of total-body irradiation (TBI) on cardiac morphology, function and selected circulating biomarkers in a well-established nonhuman primate model. For this study we used male rhesus macaques that were exposed to a single total-body dose of ionizing gamma radiation (6.5-8.4 Gy) 5.6-9.7 years earlier at ages ranging from ∼3-10 years old and a cohort of nonirradiated controls. Transthoracic echocardiography was performed annually for 3 years on 20 irradiated and 11 control animals. Myocardium was examined grossly and histologically, and myocardial fibrosis/collagen was assessed microscopically and by morphometric analysis of Masson's trichrome-stained sections. Serum/plasma from 27 irradiated and 13 control animals was evaluated for circulating biomarkers of cardiac damage [N-terminal pro B-type natriuretic protein (nt-proBNP) and troponin-I], inflammation (CRP, IL-6, MCP-1, sICAM) and microbial translocation [LPS-binding protein (LBP) and sCD14]. A higher prevalence of histological myocardial fibrosis was observed in the hearts obtained from the irradiated animals (9/14) relative to controls (0/3) (P = 0.04, χ(2)). Echocardiographically determined left ventricular end diastolic and systolic diameters were significantly smaller in irradiated animals (repeated measures ANOVA, P < 0.001 and P < 0.008, respectively). Histomorphometric analysis of trichrome-stained sections of heart tissue demonstrated ∼14.9 ± 1.4% (mean ± SEM) of myocardial area staining for collagen in irradiated animals compared to 9.1 ± 0.9 % in control animals. Circulating levels of MCP-1 and LBP were significantly higher in irradiated animals (P < 0.05). A high incidence of diabetes in the irradiated animals was associated with higher plasma triglyceride and lower HDLc but did not appear to be associated with cardiovascular phenotypes. These results demonstrate that single total-body doses of 6.5-8.4 Gy produced long-term effects including a high incidence of myocardial fibrosis, reduced left ventricular diameter and elevated systemic inflammation. Additional prospective studies are required to define the time course and mechanisms underlying radiation-induced heart disease in this model.

Pentraxin 3, ischemia-modified albumin, and myeloperoxidase in predicting a cardiac damage in acute carbon monoxide poisoning

BackgroundCarbon monoxide (CO) poisoning is associated with cardiac injuries or manifestations, frequently attributing to direct hypoxic damage at cellular level. For this, the aims were to evaluate the role of serum pentraxin 3 (PTX 3), ischemia-modified albumin (IMA), and myeloperoxidase (MPO) as an early biomarker for cardiac damage when compared to cardiac troponin I (cTnI) and creatine kinase-MB fraction (CK-MB) in adult patients with acute CO poisoning. MethodsForty patients with acute CO poisoning admitted to the emergency department. The patients were divided into 2 main groups as follows: cardiac injury (group I, n=19) and nonsuspected cardiac injury (group II, n=21). Pentraxin 3, IMA, MPO, cTnI, CK-MB, and the other assays in the circulation were measured on admission. ResultsUpon measuring the serum PTX 3, IMA, MPO, cTnI, and CK-MB levels as well as large electrocardiography and echocardiography abnormalities of patients with cardiac injury on admission, no statistical difference for PTX 3, IMA, and MPO was found between the groups (P>.05). However, cTnI, CK-MB, and leukocyte count (white blood cell) were higher determined in patients of group I compared to group II (P<.05). Receiver operating characteristic curve was also performed to evaluate the diagnostic performance of these tests in patients with cardiac injury. ConclusionsOur results suggest that PTX, IMA, and MPO assays are not superior to cTnI and CK-MB in predicting a cardiac damage in patients with acute CO intoxication.

AMELIORATIVE EFFECT OF GALLIC ACID ON DOXORUBICIN INDUCED CARDIOTOXICITY IN ADULT WISTAR RATS

Doxorubicin is a potent antineoplastic anthracycline drug however, its use is greatly limited by its toxic side effects which occurs by formation of reactive oxygen species that disruption of cell function. This present study was conducted to assess the possible cardioprotective effect of gallic acid against doxorubicin‐ induced cardiotoxicity in rats.In this study, sixty (60) male Wistar rats were divided into six groups. Group A was the control. Group B rats was intoxicated with Doxorubicin (Dox) at 15 mg/kg body weight i.p. Group C pre‐treated with 60 mg/kg Gallic Acid (GA) orally for 7 days prior to administration of Dox 15 mg/kg, Group D pre‐treated with 120 mg/kg Gallic Acid (GA) orally for 7 days prior to administration of Dox 15 mg/kg, Group E received 60 mg/kg Gallic Acid (GA) orally alone for 7 days and Group F received 120 mg/kg Gallic Acid (GA) orally alone for 7 days. The parameters of study were cardiac antioxidant status, serum biomarker of cardiac damage and electrocardiography measurements.Exposure of rats to doxorubicin led to a significant (p &lt; 0.05) decrease in cardiac glutathione peroxadise (GPx), glutathione‐S‐transferase (GST), reduced glutathione (GSH) content, superoxide dismutase (SOD) and catalase (CAT) activity. Similarly, a significant (p &lt; 0.05) increase in protein thiol was recorded in doxorubicin treated rats while it was reduced in those pre‐treated with GA. Dox also caused elevation of Creatinine kinase‐muscle brain (CK‐MB) and Lactate Dehydrogenase (LDH). Histopathology of rats exposed to Dox showed focal areas of infiltration by inflammatory cells and degeneration of myofibres. Electrocardiography results showed a significant decrease in heart rate; increase in P wave duration, R‐amplitude, PR interval, QRS and QT‐segment prolongation.Pre‐treatment with GA significantly alleviated Dox associated ECG abnormalities, restored the antioxidant enzyme and decreased serum Creatinine kinase‐muscle brain CK‐MB and LDH. However, administration of GA alone in a set of groups led to a significant prolongation of QT interval which could predispose to the potentially fatal ventricular tachycardia, torsades de pointes. All these findings confirm the efficacy of GA against Dox induced cardiotoxicity but caution must be taken in its use.Support or Funding InformationNone

Endurance sport and cardiovascular health

The cardiovascular benefits of exercise are established and individuals exercising regularly reduce their risk of adverse events from coronary artery disease by 50% and gain at least 3 additional years of life. When one considers the burgeoning epidemic of childhood obesity and its complications, exercise may be regarded as the most clinically and cost effective prescription dispensed by healthcare professionals. The intensity of exercise required to achieve these benefits is 6-8 METS which equates to walking briskly or jogging for 30 minutes daily. Competitive athlete, particularly those engaging in endurance events such as long distance running, cycling, rowing, canoeing, triathlon, marathon and iron man events partake in physical activity of a much higher intensity for as many as 20 hours per week. The requirement of a 5-6 fold increase in cardiac output is met by physiological structural and functional adaptations within the heart. Sinus bradycardia, large QRS complexes and a 15-20% increase in ventricular cavity size are the hall mark of the ‘athlete’s heart’ and are most pronounced in large male endurance athletes. Up to 50% of male endurance athletes show ventricular dimensions exceeding predicted upper limits for the general population. Such alterations are considered benign and reverse after a period of detraining. The potential hazards of intensive exercise are occasionally highlighted by the sudden cardiac death of an individual during or immediately after exercise, however, such catastrophes are extremely rare, largely striking young athletes harboring inherited or congenital arrhythmogenic substrates. Despite the emotive visibility afforded by these deaths in the media, the positive reputation of exercise remains unscathed by the fact that exercise is regarded as a mere trigger for arrhythmia in a small proportion of predisposed individuals but never directly incriminated in the pathogenesis of the fatal substrate. The past 2 decades has witnessed an extraordinarily engaging athletic milieu where humanly possible achievements seem infinite. In parallel there have been multiple reports of increased serum concentrations of biomarkers of cardiac damage and transient cardiac dysfunction after intensive endurance exercise. The mechanisms for these observations is uncertain but raise the possibility that repeated bouts of intensive endurance exercise may culminate in adverse cardiac remodeling and arrhythmogenic substrates in a small minority of endurance athletes. Perhaps the most persuasive evidence for this concern is the 5-fold increase in the prevalence of atrial fibrillation in middle aged endurance athletes compared with the relatively sedentary population of the same age.

One night of partial sleep deprivation affects biomarkers of cardiac damage, but not cardiovascular and lipid profiles, in young athletes

Sleep loss is among the most common yet frequently overlooked problems. This disruptive influence is associated with an adverse lipid profile (LP) and consequently results in an increased risk of cardiovascular disease. Furthermore, it has been well established that athletes are increasingly confronted with sleep problems. The aim of this study was to explore the effect of one night of partial sleep deprivation (PSD) on the cardiovascular profile and LP in young, trained athletes. Ten male Taekwondo athletes were randomized for three sleep conditions in a counterbalanced order: (i) following a baseline sleep night (BN), (ii) following PSD at the beginning of the night (PSDBN), and (iii) following PSD at the end of the night (PSDEN). Basal cardiovascular physiological measures were recorded, and blood samples were taken in the fasted state following each sleep session (i.e., in the morning at 07:00 h). The results showed that myoglobin and creatine phosphokinase increased significantly after PSDEN but not after PSDBN. By contrast, no alteration was observed in the LP and physiological parameters following the two types of PSD. In conclusion, these results show that PSDEN increases cardiac damage biomarkers significantly, even though they do not reach clinical significance. Thus, one night of PSD does not affect the physiological responses and biomarkers of LP in Taekwondo athletes.

Acute cardiotoxicity evaluation of the marine biotoxins OA, DTX-1 and YTX.

Phycotoxins are marine toxins produced by phytoplankton that can get accumulated in filter feeding shellfish. Human intoxication episodes occur due to contaminated seafood consumption. Okadaic acid (OA) and dynophysistoxins (DTXs) are phycotoxins responsible for a severe gastrointestinal syndrome called diarrheic shellfish poisoning (DSP). Yessotoxins (YTXs) are marine toxins initially included in the DSP class but currently classified as a separated group. Food safety authorities from several countries have regulated the content of DSPs and YTXs in shellfish to protect human health. In mice, OA and YTX have been associated with ultrastructural heart damage in vivo. Therefore, this study explored the potential of OA, DTX-1 and YTX to cause acute heart toxicity. Cardiotoxicity was evaluated in vitro by measuring hERG (human èter-a-go-go gene) channel activity and in vivo using electrocardiogram (ECG) recordings and cardiac damage biomarkers. The results demonstrated that these toxins do not exert acute effects on hERG channel activity. Additionally, in vivo experiments showed that these compounds do not alter cardiac biomarkers and ECG in rats acutely. Despite the ultrastructural damage to the heart reported for these toxins, no acute alterations of heart function have been detected in vivo, suggesting a functional compensation in the short term.

Cardiac and inflammatory biomarkers do not correlate with volume of heart or lung receiving radiation.

BackgroundThoracic and cardiac irradiation increases the risk of pulmonary and cardiovascular disease. In addition, radiation, often in combination with chemotherapy, can cause treatment-related pneumonitis. Previously, we showed that the common marker for cardiac damage, troponin T, was not elevated by chemoradiation [Lung Cancer 62:351–355, 2008]. In this study, we explore whether dose-volume metrics and biomarkers for cardiac damage, inflammation or angiogenesis could identify patients receiving thoracic radiation who would later have cardiac or pulmonary complications.FindingsTo this end, we quantified cardiac biomarkers including c-reactive protein (cRP) as well as a panel of angiogenic and inflammatory molecules in thirty patients who received radiation therapy to the thorax with or without concurrent chemotherapy between May 2006 and May 2007. Serum was collected at baseline, 2 weeks into radiation treatment and at the completion of radiation therapy. Heart and lung dosimetric parameters and clinical risk factors were also examined, along with the monitoring of adverse pulmonary and cardiac events during follow-up. Contrary to our hypothesis, there was no correlation between serum biomarker levels and cardiac radiation dose. Similarly there was little association between lung dose-volume metrics and inflammatory or angiogenic biomarkers. Furthermore, there was no correlation with serum biomarkers and adverse pulmonary or cardiovascular events.ConclusionBased on these data, acute elevations in serum biomarkers of cardiac damage, inflammation or angiogenesis should not be attributed to thoracic (chemo)radiation and elevations in such biomarkers of tissue damage should be further evaluated.

Synergistic protective role of mirazid (Commiphora molmol) and ascorbic acid against tilmicosin-induced cardiotoxicity in mice.

Tilmicosin (TIL) is a long-acting macrolide antibiotic approved for the treatment of cattle with Bovine Respiratory Disease. However, overdose of TIL has been reported to induce cardiotoxicity. The purpose of our experiment was to evaluate the protective effects of Commiphora molmol (mirazid (MRZ); myrrh) and (or) ascorbic acid (AA) against TIL-induced cardiotoxicity in mice. MRZ and AA were orally administered using stomach gavage, either alone or in combination for 5 consecutive days, followed with a single TIL overdose. TIL overdose induced a significant increase in serum levels of cardiac damage biomarkers (AST, LDH, CK, CK-MB, and cTnT), as well as cardiac lipid peroxidation, but cardiac levels of antioxidant biomarkers (GSH, SOD, CAT, and TAC) were decreased. Both MRZ and AA tended to normalize the elevated serum levels of cardiac injury biomarkers. Furthermore, MRZ and AA reduced TIL-induced lipid peroxidation and oxidative stress parameters. MRZ and AA combined produced a synergistic cardioprotective effect. We conclude that myrrh and (or) vitamin C administration minimizes the toxic effects of TIL through their free-radical-scavenging and potent antioxidant activities.

OP0251 Troponin T in Systemic Sclerosis: A Biomarker of Cardiac Involvement and Disease Severity

BackgroundHeart involvement is common in Systemic Sclerosis (SSc), even though it is often clinically silent, and represents one of the leading causes of death in these patients.ObjectivesThe aim of the...

The Diagnostic Value of Brain-Fatty Acid Binding Protein in Traumatic Brain Injury

Journal of NeurotraumaVol. 31, No. 4 Letter to the EditorThe Diagnostic Value of Brain-Fatty Acid Binding Protein in Traumatic Brain InjuryJan B. Hulscher, Broes H.D. Vervliet, Nadine Wilczak, and Joukje van der NaaltJan B. HulscherDepartment of Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.Search for more papers by this author, Broes H.D. VervlietDepartment of Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.Search for more papers by this author, Nadine WilczakDepartment of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.Search for more papers by this author, and Joukje van der NaaltNeurology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.Search for more papers by this authorPublished Online:10 Feb 2014https://doi.org/10.1089/neu.2013.3099AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"The Diagnostic Value of Brain-Fatty Acid Binding Protein in Traumatic Brain Injury." Journal of Neurotrauma, 31(4), p. 411FiguresReferencesRelatedDetails Volume 31Issue 4Feb 2014 InformationCopyright 2014, Mary Ann Liebert, Inc.To cite this article:Jan B. Hulscher, Broes H.D. Vervliet, Nadine Wilczak, and Joukje van der Naalt.The Diagnostic Value of Brain-Fatty Acid Binding Protein in Traumatic Brain Injury.Journal of Neurotrauma.Feb 2014.411-411.http://doi.org/10.1089/neu.2013.3099Published in Volume: 31 Issue 4: February 10, 2014Online Ahead of Print:December 10, 2013Online Ahead of Editing: September 17, 2013PDF download

Cardiac Damage Biomarkers Following a Triathlon in Elite and Non-elite Triathletes.

The purpose of the present study was to investigate cardiac damage biomarkers after a triathlon race in elite and non-elite athlete groups. Fifteen healthy men participated in the study. Based on performance, they were divided into elite athlete group (EG: n=7) and non-elite athlete group (NEG: n=8). Participants' blood samples were obtained during four periods: before, immediately, 2 hours and 7 days after finishing the race. creatine kinase (CK), creatine kinase-myoglobin (CK-MB), myoglobin, and lactate dehydrogenase (LDH) were significantly increased in both groups immediately after, and 2 hours after finishing the race (p<.05). CK, CK-MB, and myoglobin were completely recovered after 7 days (p<.05). Hematocrit (Hct) was significantly decreased in both groups (p<.05) 7 days after the race. LDH was significantly decreased in the EG (p<.05) only 7 days after the race. Homoglobin (Hb) was significantly decreased in the NEG (p<.05) only 2 hours after the race. Although cardiac troponin T (cTnT) was significantly increased in the EG but not in the NEG 2hours after the race (p<.05), there was no group-by-time interaction. cTnT was completely recovered in both groups 7 days after the race. In conclusion, cardiac damage occurs during a triathlon race and, is greater in elite than in non-elite. However, all cardiac damage markers return to normal range within 1 week.

N-terminal pro-brain natriuretic peptide, left ventricular diastolic function and prognosis in burn patients

Background: Elevation of serum pro-BNP and Troponin T are associated with cardiac diastolic dysfunction, an independent prognostic marker for the mortality of burn patients. The objective of this study was to test the above association and whether pro-BNP and/or TrI interact with LV diastolic dysfunction to affect prognosis in burn patients. Study design: We consecutively enrolled 56 critically burned patients who admitted the intensive care unit and performed transthoracic echocardiography to evaluate LV diastolic function. 30 healthy subjects served as controls. The participants were classified as having LV diastolic dysfunction by echocardiographic findings including mitral inflow E/A ratio 220 cm/s, or decreased peak annular early diastolic velocity in tissue Doppler imaging. Soluble plasma levels of pro-BNP and TrI were measured in all subjects. Results: The total body surfaced area of burned patients was proportional to serum level of NT-proBNP and hs-Troponin T (p < 0.001 for each). Significant correlations were found for NT-proBNP and decelerating time, E/A, and E/Em (r2 = 0.59, 0.45, and 0.52; p <0.001 for each), and for hs-Troponin T and decelerating time, E/A, and E/Em (r2 = 0.59, 0.62, and 0.65; p < 0.001 for each). Diastolic function improved significantly in association with decrease of cytokines after burned patients transferred to general ward (p < 0.001). There was a significant correlation between LV diastolic dysfunction and in-hospital mortality in critically burned patients (HR = 3.67, p = 0.032) after risk factors adjusted. Conclusions: Biomarkers of cardiac damage and mechanical stress may be associated with cardiac diastolic dysfucntion, which could be an independent prognostic factor in burn patients. NT-proBNP and hs-Troponin T may be a useful tool to predict clinical outcome in critically burned patients with LV diastolic dysfunction.

Cardiac indexes, cardiac damage biomarkers and energy expenditure in professional cyclists during the Giro d’Italia 3-weeks stage race

The study of cardiac response to strenuous and continuous exercise is crucial to understanding the physiology of endurance. N-terminal proB-type natriuretic peptide (NT-proBNP) is a potential marker for monitoring myocardial wall stress, and troponins (TnT and TnI) are widely used in the diagnosis of cardiac ischemia and infarction. Strenuous exercise may generate transitory ischemia, myocardial stress, and diastolic left ventricular dysfunction, inducing the increased production of both these biomarkers. We measured changes in NT-proBNP and TnT in elite cyclists during a 3-week stage race, a model of strenuous exercise. The study population was 9 professional cyclists participating in the 2011 Giro d'Italia. Pre-analytical and analytical phases scrupulously followed official recommendations. Anthropometric data, net energy expenditure and cardiac indexes (rate, diastolic and systolic blood pressure) were recorded. Blood samples were drawn pre-race (day - 1) and at days 12 and 22; NT-proBNP and highly sensitive-troponin (Hs-TnT) concentrations were assayed and corrected for plasma volume changes. Body-mass index decreased and energy expenditure increased by 52% during the race. NT-proBNP concentrations increased [day -1:23.52 ng/L (9.67-34.33); day 12:63.46 ng/L (22.15-93.31); P = 0.039; day 22:89.26 ng/L (34.66-129.78) vs.day -1; P < 0.001] and correlated with heart rate (r = -0.51; P = 0.006), systolic pressure (r = 0.39; P = 0.046) and energy expenditure (r = 0.70; P < 0.001). TnT concentrations did not vary, but a widened TnT amplitude distribution was observed. Increases in NT-proBNP correlated with higher energy expenditure over a 3-week cycling stage race, possibly indicating myocardial stress.