Serum Cardiac Troponin Research Articles

EVALUATION OF 5-FLUOROURACIL-INDUCED CARDIOTOXICITY: ROLE OF CARDIAC BIOMARKERS.

Side effects of chemotherapy in cancer patients need to be investigated in more detail. To determine the incidence of cardiotoxicity in patients treated with different chemotherapy regimens containing 5-fluorouracil (5-FU) in Zanjan, Iran. In a prospective cohort study, patients with different types of solid gastrointestinal tumors who were candidates for 5-FU based chemotherapy regimens were enrolled. The study population consisted of 100patients (48females and 52males) with a mean age of 63.99 ± 12.40years. We measured serum cardiac troponin I (cTnI) levels before and during each chemotherapy cycle and determined the occurrence of cardiotoxicity in patients based on the levels of cTnI, clinical signs and symptoms as well as electrocardiogram findings. In addition, we assessed a history of diabetes, hypertension, smoking, dyslipidemia and previous chest radiation as potential risk factors for cardiotoxicity. The incidence of cardiotoxicity was 8%, of which 5patients were diagnosed with acute coronary syndrome, 2patients with arrhythmias and one with hypotension. In addition, there was no significant association between studied risk factors and 5-FU induced cardiotoxicity. The incidence of cardiotoxicity in patients receiving 5-FU infusion regimens was notable. Thus, paying more attention to the 5-FU-induced cardiotoxicity is necessary in order to improve the prognosis of patients with cancer.

Recurrent myocardial injury is a strong predictor of ICU mortality in COVID-19

Abstract Funding Acknowledgements Type of funding sources: None. Background Myocardial injury is common in COVID-19, and has been linked to disease severity and mortality.1 Its pathophysiology is not fully elucidated and suggested mechanisms include cytokine damage, endotheliitis, myocarditis, ferroptosis, acute coronary syndrome, oxygen supply-demand mismatch and pulmonary embolism.2-3 Elevated serum cardiac troponin (cTn) – as surrogate marker of myocardial injury – at admission and during hospitalisation is associated with poor outcome.4-5 Comparison of available trial data, however, is unfeasible, because of variable definition and sampling timing/intervals/assays.6 Peculiarly, prognostic cut-off cTn values are often – retrospectively – set much lower than recommended by the guidelines.6-8 Furthermore, robust intensive care unit (ICU) outcome data regarding cTn evolution over time is lacking. Purpose The aim of this study is to critically explore the correlation between myocardial injury and mortality in a tertiary ICU population, using both standard and high cTn cut-off values, and to scrutinise the impact of timing and recurrence. Methods All adult COVID-19 patients admitted to our tertiary ICU between 06/03/2020 and 27/09/2021 were enrolled in this large, retrospective, single centre, cohort study. Patients requiring extracorporeal membrane oxygenation (n=29) were excluded. Myocardial injury was defined – as per ESC guidelines - as high-sensitive cardiac troponin I (hs-cTnI) peak >45ng/L (99th percentile upper reference limit) and ‘major’ myocardial injury was defined as hs-cTnI >135ng/L (3x upper limit of normal).6-7 Recurrent myocardial injury was considered if a new hs-cTnI peak above cut-off point occurred after normalisation. Patients were categorised according to peak (‘standard’ >45ng/L vs ‘high’ >135ng/L), onset (‘on admission’ vs ‘during hospitalisation’) and recurrence (‘single’ vs ‘multiple’) of hs-cTnI rise. Statistical analysis was done by logistic regression, using IBM SPSS version 28. Results A total of 193 COVID-19 ICU patients were included. Patient characteristics, disease severity indices and treatment details are summarised in Table 1. The mean age was 62 years and ICU mortality was 22%. Myocardial injury overall occurred in 51% (n=99) and major myocardial injury occurred in 39% (n=75) of patients. Obtained results were consistent across standard (>45ng/L) and high (>135ng/L) hs-cTnI cut-off groups. Myocardial injury only present at ICU admission was not correlated with mortality in our cohort, contradicting prior (mostly non-ICU) trials. Single hs-cTnI peak during ICU hospitalisation, however, and, especially recurrent hs-cTnI peaks were strong predictors of ICU mortality. The respective incidence, odds ratio, 95% confidence intervals and p-values are displayed in Table 2. Conclusion Myocardial injury occurring during ICU hospitalisation and, especially, recurrent myocardial injury is strongly correlated with ICU mortality in COVID-19 patients.

Validation of the myocardial-ischaemic-injury-index machine learning algorithm to guide the diagnosis of myocardial infarction in a heterogenous population: a prespecified exploratory analysis

SummaryBackgroundDiagnostic pathways for myocardial infarction rely on fixed troponin thresholds, which do not recognise that troponin varies by age, sex, and time within individuals. To overcome this limitation, we recently introduced a machine learning algorithm that predicts the likelihood of myocardial infarction. Our aim was to evaluate whether this algorithm performs well in routine clinical practice and predicts subsequent events.MethodsThe myocardial-ischaemic-injury-index (MI3) algorithm was validated in a prespecified exploratory analysis using data from a multi-centre randomised trial done in Scotland, UK that included consecutive patients with suspected acute coronary syndrome undergoing serial high-sensitivity cardiac troponin I measurement. Patients with ST-segment elevation myocardial infarction were excluded. MI3 incorporates age, sex, and two troponin measurements to compute a value (0–100) reflecting an individual's likelihood of myocardial infarction during the index visit and estimates diagnostic performance metrics (including area under the receiver-operating-characteristic curve, and the sensitivity, specificity, negative predictive value, and positive predictive value) at the computed score. Model performance for an index diagnosis of myocardial infarction (type 1 or type 4b), and for subsequent myocardial infarction or cardiovascular death at 1 year was determined using the previously defined low-probability threshold (1·6) and high-probability MI3 threshold (49·7). The trial is registered with ClinicalTrials.gov, NCT01852123.FindingsIn total, 20 761 patients (64 years [SD 16], 9597 [46%] women) enrolled between June 10, 2013, and March 3, 2016, were included from the High-STEACS trial cohort, of whom 3272 (15·8%) had myocardial infarction. MI3 had an area under the receiver-operating-characteristic curve of 0·949 (95% CI 0·946–0·952) identifying 12 983 (62·5%) patients as low-probability for myocardial infarction at the pre-specified threshold (MI3 score <1·6; sensitivity 99·3% [95% CI 99·0–99·6], negative predictive value 99·8% [99·8–99·9]), and 2961 (14·3%) as high-probability at the pre-specified threshold (MI3 score ≥49·7; specificity 95·0% [94·6–95·3], positive predictive value 70·4% [68·7–72·0]). At 1 year, subsequent myocardial infarction or cardiovascular death occurred more often in high-probability patients than low-probability patients (520 [17·6%] of 2961 vs 197 [1·5%] of 12 983], p<0·0001).InterpretationIn consecutive patients undergoing serial cardiac troponin measurement for suspected acute coronary syndrome, the MI3 algorithm accurately estimated the likelihood of myocardial infarction and predicted subsequent adverse cardiovascular events. By providing individual probabilities the MI3 algorithm could improve the diagnosis and assessment of risk in patients with suspected acute coronary syndrome.FundingMedical Research Council, British Heart Foundation, National Institute for Health Research, and NHSX.

Preventive effects of (−) epicatechin on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in isoproterenol-induced myocardial infarcted rats

Myocardial infarction (MI) is a life-threatening condition. No studies were conducted earlier on the effects of (−) epicatechin (EC) on tachycardia, cardiac hypertrophy, and inflammation in MI. Hence, the preventive effects of EC on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in experimental MI were appraised. This investigation included 4 groups of 24 male albino Wistar rats. Group:1. Normal control, Group: 2. EC (20 mg/kg body weight), Group: 3. Isoproterenol (100 mg/kg body weight), Group:4. EC (20 mg/kg body weight) + Isoproterenol (100 mg/kg body weight). MI was created in rats by isoproterenol (100 mg/kg body weight). The heart rate, heart weight, plasma myoglobin, serum cardiac troponin I, heart conjugated dienes, serum high-sensitivity C-reactive protein, and plasma total homocysteine were considerably (P < 0.05) raised in isoproterenol-induced myocardial infarcted rats. Further, reverse transcription-polymerase chain reaction study revealed a considerable (P < 0.05) increase in the expressions of heart pro-inflammatory cytokines such as nuclear factor- κB, tumor necrosis factor-α, interleukin-1β, interleukin-6, and a considerable (P < 0.05) decrease in anti-inflammatory cytokine gene, interleukin-10 in myocardial infarcted rats. Non-enzymatic antioxidants such as vitamin C, and vitamin E were considerably (P < 0.05) lessened in the heart. EC (20 mg/kg body weight) pre-treatment orally, daily, for 3 weeks prevented all changes in the above-mentioned functional, structural, biochemical, and molecular parameters investigated and improved cardiac function. The possible mechanisms are EC’s anti-tachycardial, anti-cardiac hypertrophic, antioxidant, and anti-inflammatory effects.

Estrogen inhibits endoplasmic reticulum stress and ameliorates myocardial ischemia/reperfusion injury in rats by upregulating SERCA2a

BackgroundThe incidence of coronary heart disease (CHD) in premenopausal women is significantly lower than that of men of the same age, suggesting protective roles of estrogen for the cardiovascular system against CHD. This study aimed to confirm the protective effect of estrogen on myocardium during myocardial ischemia/reperfusion (MI/R) injury and explore the underlying mechanisms.MethodsNeonatal rat cardiomyocytes and Sprague–Dawley rats were used in this study. Different groups were treated by bilateral ovariectomy, 17β-estradiol (E2), adenoviral infection, or siRNA transfection. The expression of sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2a) and endoplasmic reticulum (ER) stress-related proteins were measured in each group to examine the effect of different E2 levels and determine the relationship between SERCA2a and ER stress. The cell apoptosis, myocardial infarction size, levels of apoptosis and serum cardiac troponin I, ejection fraction, calcium transient, and morphology changes of the myocardium and ER were examined to verify the effects of E2 on the myocardium.ResultsBilateral ovariectomy resulted in reduced SERCA2a levels and more severe MI/R injury. E2 treatment increased SERCA2a expression. Both E2 treatment and exogenous SERCA2a overexpression decreased levels of ER stress-related proteins and alleviated myocardial damage. In contrast, SERCA2a knockdown exacerbated ER stress and myocardial damage. Addition of E2 after SERCA2a knockdown did not effectively inhibit ER stress or reduce myocardial injury.ConclusionsOur data demonstrate that estrogen inhibits ER stress and attenuates MI/R injury by upregulating SERCA2a. These results provide a new potential target for therapeutic intervention and drug discovery in CHD.BAgGUtqRXuc394yJDQeuxtVideo

Protection of Exogenous Phosphocreatine for Myocardium in Percutaneous Coronary Intervention Related to Inflammation.

Although injury of myocardium after percutaneous coronary intervention (PCI) has been reported, the mechanism and effect of exogenous phosphocreatine (PCr) supplementation on the injury are yet to be elucidated. Biomarkers, such as interleukin-6 (IL-6) and variations in white blood cells for inflammation, and serum cardiac troponin I (cTnI) for myocardial injury are examined. A total of 105 patients undergoing PCI were included and randomly divided into two groups: control (treated with routine hydration therapy) and PCr (treated with additional intravenous infusion of exogenous PCr). The serum levels of biomarkers were detected at administration and 4, 12, 24, and 48 h after PCI, with natural logarithmic (loge) transformation of data when modeling assumptions were not fulfilled. The level of loge-transformed IL-6 increased in both groups, especially at 12 and 24 h after the operation, and that of PCr group was less than the control group at 48 h. The content of loge-transformed cTnI was significantly increased in both groups, while that of the PCr group was markedly lower than the control group at all time points after PCI. Moreover, the ratio of neutrophils was elevated at all time points after PCI, while that of the PCr group was lower at 48 h, and the variations in the ratio of lymphocytes showed opposite results. Exogenous phosphocreatine reduces stent implantation, triggers inflammation manifested as decreased serum levels of IL-6 and the aggregation of neutrophils, and protects the myocardium of the patients undergoing PCI. These findings provided the potential mechanism and treatment for myocardial injury associated with PCI.

Serum cardiac troponin I is a candidate biomarker for cardiomyopathy in Duchenne and Becker muscular dystrophies.

Serum cardiac troponin I (cTnI), its relation to cardiomyopathy, and the contribution of the ACTN3 genotype to serum levels of cTnI in Duchenne and Becker muscular dystrophy (DMD and BMD, respectively) remain unknown. In this study we aimed to reveal the characteristics of cTnI, assess whether cTnI is a biomarker for cardiomyopathy in these dystrophinopathies, and evaluate the contribution of the ACTN3 genotype to the serum levels of cTnI in DMD patients. Serum cTnI values obtained from 127 DMD and 47 BMD patients were analyzed retrospectively. The relationship between cTnI and echocardiography data or the ACTN3 XX genotype was assessed. The cTnI levels and proportion of patients with abnormal cTnI levels were significantly higher among DMD patients than BMD, especially in the second decade of life. In DMD, the cTnI level reached a maximum at 13 years, and left ventricular ejection fraction (LVEF) became abnormal approximately 1year subsequently. In BMD, the cTnI level peaked at the age of 14 years, and LVEF became abnormal 3 years later. Decreased LVEF was observed after cTnI elevation in both populations. cTnI levels by age in DMD patients with the ACTN3 XX genotype tended to increase significantly and early. Myocardial injury indicated by cTnI elevation was more common and severe in DMD patients. cTnI elevation preceding cardiac dysfunction may represent an early phase of cardiomyopathy progression and may be a biomarker for early detection of cardiomyopathy in these dystrophinopathies. The ACTN3 XX genotype may be a risk factor for early myocardial injury.

Association of serum cardiac troponin I and severity of coronary stenosis in patients with varied renal functions: a retrospective cohort study

Background and objectiveRecent studies showed cardiac troponin I (cTnI) might be a non-invasive biomarker to estimate the severity of coronary stenosis. However, serum cTnI is also found associated with renal...

Prognostic implications of serial high-sensitivity cardiac troponin testing among patients with COVID-19: A Danish nationwide registry-based cohort study

BackgroundAlthough troponin elevation is associated with worse outcomes among patients with coronavirus disease 2019 (COVID-19), prognostic implications of serial troponin testing are lacking. We investigated the association between serial troponin measurements and adverse COVID-19 outcomes. MethodsUsing Danish registries, we identified COVID-19 patients with a high-sensitivity troponin measurement followed by a second measurement within 1–24 h. All measurements during follow-up were also utilized in subsequent time-varying analyses. We assessed all-cause mortality associated with the absence/presence of myocardial injury (≥1 troponin measurement >99th percentile upper reference limit) and absence/presence of dynamic troponin changes (>20% relative change if first measurement elevated, >50% relative change if first measurement normal). ResultsOf 346 included COVID-19 patients, 56% had myocardial injury. Overall, 20% had dynamic troponin changes. In multivariable Cox regression models, myocardial injury was associated with all-cause mortality (HR = 2.56, 95%CI = 1.46–4.51), as were dynamic troponin changes (HR = 1.66, 95%CI = 1.04–2.64). We observed a low incidence of myocardial infarction (4%) and invasive coronary procedures (4%) among patients with myocardial injury. ConclusionsMyocardial injury and dynamic troponin changes determined using serial high-sensitivity troponin testing were associated with poor prognosis among patients with COVID-19. The risk of developing myocardial infarction requiring invasive management during COVID-19 hospitalization was low.

Abstract TP223: Association Between Stroke Severity And Cardiac Troponins In Acute Stroke

Introduction: Cardiac troponins are often elevated in patients with acute stroke and have been associated poor outcomes. Whether the elevation in cardiac troponins, a marker of acute myocardial injury, is due to neurogenic mechanisms or the underlying cardiac risk factors is unknown. We evaluated the association between stroke severity and serum cardiac troponin levels in people with acute stroke. Methods: We conducted a retrospective study of adults (≥ 40 years) with a discharge diagnosis of imaging confirmed stroke admitted to a quaternary stroke centre in Toronto, Canada between January 1, 2018 and December 31, 2018. We collected demographic and clinical information, including stroke severity using the National Institutes of Health Stroke Scale [NIHSS], modelled as a continuous variable. We recorded serum cardiac troponin levels on admission. We modelled serum troponin level both as a continuous and a categorical variable (normal vs. high, ≥ 15 ng/L). We evaluated the association between admission NIHSS and serum troponin level using multivariable negative binomial models and logistic regression models, adjusting for demographics (age and sex) and comorbidities [history of congestive heart failure or stroke, stroke type (ischemic vs. hemorrhagic), ST elevation on ECG, and creatinine levels]. Results: We included 218 patients with acute stroke (median age 76 years, 48.6% women), of whom 190 (87.2%) had an ischemic stroke. Median NIHSS was 6 (Q1-Q3, 2-14), and median cardiac troponin level was 17 ng/L (Q1-Q3, 9-30), with 108 (53.2%) patients having higher than normal levels. A one-point increase in NIHSS (stroke severity) was associated with a higher serum troponin level in age- and sex- (RR 1.03; 1.00-1.05) and multivariable- (RR 1.03; 1.01-1.05) adjusted models. However, stroke severity was not associated with the odds of having high troponin levels in adjusted models (OR 1.03; 0.98-1.08). Conclusions: The modest, yet independent, association between greater stroke severity and higher cardiac troponins in patients with acute stroke could suggest a neurogenic basis for mild cardiac injury in patients with acute stroke. Future work on the association between elevated troponin and poor stroke outcomes should account for stroke severity on admission.

Golden Syrian hamster as a model to study cardiovascular complications associated with SARS-CoV-2 infection.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in the Golden Syrian hamster causes lung pathology that resembles human coronavirus disease (COVID-19). However, extrapulmonary pathologies associated with SARS-CoV-2 infection and post-COVID sequelae remain to be understood. Here, we show, using a hamster model, that the early phase of SARS-CoV-2 infection leads to an acute inflammatory response and lung pathologies, while the late phase of infection causes cardiovascular complications (CVCs) characterized by ventricular wall thickening associated with increased ventricular mass/body mass ratio and interstitial coronary fibrosis. Molecular profiling further substantiated our findings of CVC as SARS-CoV-2-infected hamsters showed elevated levels of serum cardiac troponin I, cholesterol, low-density lipoprotein, and long-chain fatty acid triglycerides. Serum metabolomics profiling of SARS-CoV-2-infected hamsters identified N-acetylneuraminate, a functional metabolite found to be associated with CVC, as a metabolic marker was found to be common between SARS-CoV-2-infected hamsters and COVID-19 patients. Together, we propose hamsters as a suitable animal model to study post-COVID sequelae associated with CVC, which could be extended to therapeutic interventions.

Assessment of Level of Serum Cardiac Troponin T in Neonates with Respiratory Distress Syndrome

Assessment of Level of Serum Cardiac Troponin T in Neonates with Respiratory Distress Syndrome

Rare survival of high-tension electrocution shock in a crossbred Jersey cattle: a complete profile on critical care monitoring.

Accidental electrocution was more common in animals and death was mostly due to shock and cardiac arrest. Survival of animals or humans could be possible if victims receive immediate medical support. A 3-year-old crossbred Jersey heifer was presented to the Emergency and Critical Care Medicine Referral Clinic of the Veterinary College and Research Institute, Orathanadu, with a history of accidental electrocution by broken high-tension overhead power transmission line during grazing in the paddy fields. The animal was dull and depressed, dark red, and some areas were charred in appearance on the dorsum and limbs. The animal showed difficulty walking due to the electrocution burn injury and was poorly responding to the surroundings. Clinical examination revealed subnormal temperature, polypnea, pale mucous membranes, ruminal atony, and arrhythmias on auscultation. On point of care (PoC) hematology testing, leukocytosis, neutrophilia, and microcytosis were observed. PoC electrolyte analysis revealed hypocalcemia (ionized calcium 0.89 mmol/L), mild hypochloremia, and severe hypokalemia (2.81 mmol/L). PoC biochemistry revealed hypoglycemia (41 mg/dl). PoC elevated levels of serum cardiac troponin (0.33 ng/dl) indicated cardiac damage. Aspartate aminotransferase (1794 U/L), CK-MB (699 U/L) and LDH (6.7 U/L) were also elevated. On PoC urinalysis, proteinuria, myoglobinuria, and glucosuria were observed. Evident clinical recovery, wound healing, and improvement in animal activities were observed. High-voltage electrocution injury is a serious type of accident with the potential risk of multi-organ damage and death. Early diagnosis of electrocution and immediate management enhances the expectancy of complete recovery.

Effect of Raised Cardiac Troponin Levels on Inpatient Mortality in Patients with Community Acquired Pneumonia

OBJECTIVE: To ascertain the frequency of raised cardiac troponin level and its association with in-hospital mortality among patients presenting with severe community-acquired pneumonia (CAP) at a public-sector tertiary care hospital in Karachi. METHODOLOGY: This prospective, observational study was performed at Jinnah Postgraduate Medical Center, Karachi throughout September 2020 till March 2021 with the approval of the hospital ethics committee. 146 patients who met the diagnostic measures were included. Serum cardiac troponin levels≥0.034 ng/mL were labeled as elevated. A detailed history of patients was taken upon their hospital admission to note down their demographic and clinical features. RESULT: A total of 146 patients were studied with the majority of age range 46-70 years (n=91, 62.3%). 95 (65.1%) had elevated troponin levels. Age was significantly different among patients with and without elevated troponin levels (p=0.038). 87 (59.6%) patients did not survive and 57 (65.5%) of them had elevated troponin levels. The risk of mortality was greater among patients having elevated troponin levels but it was not considered statistically (OR=1.05, 95% CI: 0.53 – 2.10). CONCLUSION: The study did not find evidence of a greater likelihood of mortality for patients having elevated troponin levels.

234 Echocardiographic visualization of retroaortic anomalous coronary artery

Abstract A 65-year-old female was admitted to our hospital for sudden onset of typical chest pain at rest lasting few minutes. Her medical background included systemic hypertension, type 2 diabetes, dyslipidaemia, and mild obesity. Upon arrival in the emergency room, the electrocardiogram didn’t reveal signs of acute myocardial ischaemia and serial cardiac troponin T measurements were persistently negative. A transthoracic echocardiogram (TTE) was performed, showing mild ventricular hypertrophy, no regional wall motion abnormalities, and a preserved left ventricular ejection fraction. A highly echogenic tubular structure, located slightly on the atrial side of the atrioventricular groove was noted in multiple apical views. Its tubular shape was suggestive of a vascular structure, but its location was atypical for a normal vessel; indeed its persistence in more than an echocardiographic plane excluded an artefact. According to patient’s clinical history and her high cardiovascular risk profile she was referred for coronary angiography, demonstrating no critical stenosis but an anomalous aortic origin of a coronary artery (AAOCA) from the inappropriate sinus of Valsalva: the left main coronary artery (LMCA) arose from the right coronary cusp and then took a caudal posterior loop running posterior to the aortic root. In light of these findings we could associate the tubular structure seen at TTE to the retroaortic course of LMCA, a finding recently described as retroaortic anomalous coronary (RAC) sign. Among AAOCA, the retroaortic course of the LMCA is an uncommon diagnosis in adults, and its association with a single coronary origin is extremely rare. Although it has been usually considered a benign clinical entity, it is associated with an increased risk in morbidity and mortality during valve surgery. The presence of RAC sign at TTE was demonstrated to be highly suggestive of an anomalous coronary artery (specificity 93.9%) and strongly associated with retroaortic LMCA course at computed tomography angiography. 234 Figure B

Exercise Training Increases Serum Cardiac Troponin T Independent of Left Ventricular Mass.

The purpose of this study was to determine whether exercise training mediated cardiac troponin T (cTnT) and whether this was associated with increases in left ventricular mass (LVM). Fifty-four sedentary obese women were randomised to high-intensity interval training (HIIT, repeated 4-min cycling at 90% V̇O2max interspersed with 3-min rest), work-equivalent continuous aerobic training (CAT, continuous cycling at 60% V̇O2max) or a control group (CON). Resting serum cTnT was assessed using a high-sensitivity assay before and after 12 weeks of training. LVM was determined from 2D echocardiography at the same timepoints. Both HIIT and CAT induced a similar elevation (median 3.07 to 3.76 ng.l-1, p<0.05) in resting cTnT compared with pre-training and the CON (3.49 to 3.45 ng.l-1, p>0.05). LVM index in HIIT increased (62.2±7.8 to 73.1±14.1 g.m-2, p<0.05), but not in CAT (66.1±9.7 to 67.6±9.6 g.m-2, p>0.05) and CON (67.9±9.5 to 70.2±9.1 g.m-2, p>0.05). Training-induced changes in resting cTnT did not correlate with changes in LVM index (r=-0.025, p=0.857). These findings suggest that twelve weeks of either HIIT or CAT increased resting cTnT, but the effects were independent of any changes in LVM in sedentary obese women.

Energy-sparing by 2-methyl-2-thiazoline protects heart from ischaemia/reperfusion injury.

AimsCardiac ischaemia/reperfusion (I/R) injury remains a critical issue in the therapeutic management of ischaemic heart failure. Although mild hypothermia has a protective effect on cardiac I/R injury, more rapid and safe methods that can obtain similar results to hypothermia therapy are required. 2‐Methyl‐2‐thiazoline (2MT), an innate fear inducer, causes mild hypothermia resulting in resistance to critical hypoxia in cutaneous or cerebral I/R injury. The aim of this study is to demonstrate the protective effect of systemically administered 2MT on cardiac I/R injury and to elucidate the mechanism underlying this effect.Methods and resultsA single subcutaneous injection of 2MT (50 mg/kg) was given prior to reperfusion of the I/R injured 10 week‐old male mouse heart and its efficacy was evaluated 24 h after the ligation of the left anterior descending coronary artery. 2MT preserved left ventricular systolic function following I/R injury (ejection fraction, %: control 37.9 ± 6.7, 2MT 54.1 ± 6.4, P < 0.01). 2MT also decreased infarct size (infarct size/ischaemic area at risk, %: control 48.3 ± 12.1, 2MT 25.6 ± 4.2, P < 0.05) and serum cardiac troponin levels (ng/mL: control 8.9 ± 1.1, 2MT 1.9 ± 0.1, P < 0.01) after I/R. Moreover, 2MT reduced the oxidative stress‐exposed area within the heart (%: control 25.3 ± 4.7, 2MT 10.8 ± 1.4, P < 0.01). These results were supported by microarray analysis of the mouse hearts. 2MT induced a transient, mild decrease in core body temperature (°C: −2.4 ± 1.4), which gradually recovered over several hours. Metabolome analysis of the mouse hearts suggested that 2MT minimized energy metabolism towards suppressing oxidative stress. Furthermore, 18F‐fluorodeoxyglucose‐positron emission tomography/computed tomography imaging revealed that 2MT reduced the activity of brown adipose tissue (standardized uptake value: control 24.3 ± 6.4, 2MT 18.4 ± 5.8, P < 0.05). 2MT also inhibited mitochondrial respiration and glycolysis in rat cardiomyoblasts.ConclusionsWe identified the cardioprotective effect of systemically administered 2MT on cardiac I/R injury by sparing energy metabolism with reversible hypothermia. Our results highlight the potential of drug‐induced hypothermia therapy as an adjunct to coronary intervention in severe ischaemic heart disease.

Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway

ABSTRACT We aimed to explore the effects of emodin on the energy metabolism of myocardial cells in rats with post-myocardial infarction (MI) heart failure (HF) and the extracellular signal-regulated kinase (ERK) pathway. The model of MI was established by ligation of the left anterior descending branch. After 4 weeks, the rats with left ventricular ejection fraction (LVEF) of ≤45% were used aspost-MI HF model animals and randomly divided into model, low-dose, middle-dose, high-dose and control groups (n=10). Low-, middle- and high-dose groups were gavaged with 20 mg/kg, 40 mg/kg and 60 mg/kg emodin daily, respectively. After administration for 14 d, the changes in LVEF, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD) and interventricular septum thickness (IVS) were analyzed. The apoptosis rate of myocardial cells was detected by TUNEL staining. The levels of serum cardiac troponin I (cTnI) and peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1) were determined using ELISA, and the expressions of mitochondrial respiratory chain complex I protein and phosphorylated-ERK (p-ERK) in myocardial tissues were determined by Western blotting. Compared with model group, LVEDD, LVESD, apoptosis rate of myocardial cells, levels of serum cTnI and PGC-1, and expressions of complex I and p-ERK in myocardial tissues significantly decreased, while LVEF and IVS increased in low-dose, middle-dose, high-dose and control groups (P<0.05). The changes in the above indices were significantly dependent on the dose of emodin (P<0.05).Emodin can significantly relieve post-MI HF, reduce the apoptosis rate of myocardial tissues, and ameliorate the cardiac function of rats.

Abstract 9185: Diagnostic Utility of R-R Interval Variations Under Deep Breathing Load in Patients With Cardiac Amyloidosis

Introduction: Autonomic disorder is one of important characteristics of cardiac amyloidosis. However, the prevalence of autonomic disorder in wild-type transthyretin amyloidosis (ATTR wt ) remains to be elucidated. Analysis of coefficient of variation of R-R interval (CVR-R) is a non-invasive method to measure the autonomic nervous system. In normal subjects, CVR-R values are higher during deep breathing load than those at rest. Diminished response of CVR-R to deep breathing reflects the parasympathetic nervous system disorder. We aimed to assess autonomic disorder of ATTRwt and investigate the utility of CVR-R for the detection of ATTRwt from other cardiac disease. Methods: Fifty patients with chronic heart failure (HF) patients aged &gt;70 were investigated. The etiology of HF was as follows: ATTR wt , n=10; previous myocardial infarction (MI), n=20; and left ventricular hypertrophy (LVH) due to other disease (e.g. aortic stenosis); n=20. Serum cardiac troponin I and plasma brain natriuretic peptide (BNP) were measured in all patients. Cardiac function was evaluated by echocardiography. We measured CVR-R at rest (CVR-R rest ), CVR-R with deep breaths (CVR-R beath ) and their change rate (CVR-R diff rate ). Relative change formula is CVR-R diff rate = (CVR-R beath - CVR-R rest )/ CVR-R rest . Results: There was no difference in age among the three groups. Plasma BNP levels, troponin I levels and left ventricular mass index were significantly higher in ATTR wt group. There was no difference in CVR-R rest levels among the three groups. CVR-R diff rate levels in ATTR wt group were significantly lower (ATTR wt : -8.77 [-43.8-10.9]; LVH: 67.4 [38.7-89.4]; MI: 83.7 [60.4-142.9], respectively). In the ROC analysis to identify ATTR wt in HF, the best cutoff value for CVR-R diff rate was 1.197 (AUC: 0.848). Conclusions: Autonomic nervous disorder is frequently observed in the patients with ATTR wt . Measurement of CVR-R is convenient support tool for detection of ATTRwt.

Pseudomyocardial Infarction: An Atypical Presentation of Chest Wall Necrotizing Fasciitis

A 75-year-old woman was admitted because of acute chest pain for one day. The electrocardiogram (ECG) showed progressive decreasing R wave amplitudes with new QS waves at precordial leads in three hours (Figure 1 A, B). Serial high-sensitivity cardiac troponin testing at baseline and three hours after admission were within normal range (8.8 pg/mL and 11.1 pg/mL respectively. Upper reference limit: 17.5 pg/mL). The white-cell count was 6800 /µL (reference range: 4800 to 10,800). The contrast-enhanced computer tomography of chest showed no aortic dissection or pulmonary embolism (Figure 3A).