Serum Cardiac Troponin Research Articles

Electrocardiographic Changes in a Man With Acute Pancreatitis: A Myocardial Infarction?

A 69-year-old man with a history of heavy alcohol use presented with abdominal pain and was diagnosed with alcohol-induced acute pancreatitis. On admission, he had not reported chest pain, palpitations, or dyspnea. Initial laboratory tests showed a lactic acid level of 8.3 mmol/L (normal, 0.5–2.2 mmol/L), normal renal function, and normal cardiac enzyme levels. An electrocardiogram (ECG) on admission showed sinus tachycardia. His symptoms and lactic acidosis resolved after aggressive fluid resuscitation and bowel rest. Two days later, sudden-onset dyspnea, tachycardia, and hypoxia necessitated the administration of 2 L of supplemental oxygen. A chest radiograph showed acute pulmonary edema. The patient's serum cardiac troponin level peaked at 0.35 ng/mL (normal, <0.03 ng/mL), and his brain natriuretic peptide level was 235 pg/mL (normal, <100 pg/mL). His ECG showed changes (Fig. 1).What is the most likely diagnosis? B) Stress-induced (takotsubo) cardiomyopathyFigure 1 shows sinus tachycardia with premature atrial contractions, new ST-segment elevations (STEs) in the inferior leads and in leads V2 through V6, and T-wave inversions throughout. Figure 2 shows the admission ECG.According to the Mayo Clinic criteria, the most common ECG changes associated with takotsubo cardiomyopathy (TTC) are STE and T-wave inversion. These changes are seen frequently in the precordial leads.1 Clinically, distinguishing TTC from acute coronary syndrome is challenging because of overlapping symptoms, elevated cardiac enzyme levels, and similar ECG changes. Certain ECG patterns indicate TTC rather than acute coronary syndrome, including the absence of ST-segment depression in the reciprocal leads; diffuse STEs extending beyond the territory of a single coronary artery; and STE in lead aVR with STE in the inferior, anterior, or anteroseptal leads.2Patients with suspected TTC may have known coronary artery disease (CAD) or associated risk factors; therefore, STEMI must be ruled out when STE is seen on an ECG.3 If angiograms reveal no fixed obstructive CAD, acetylcholine testing may be considered, because spasm-induced coronary obstruction has been proposed as the mechanism underlying TTC, with atherosclerotic CAD providing a protective “stenting” effect.4 Pulmonary embolism may trigger sinus tachycardia and T-wave inversions, but without STE or pulmonary edema. Wellens syndrome can cause isolated deep T-wave inversions in leads V1 through V3, but it cannot explain inferior-lead STE and T-wave changes.The pathophysiology of TTC involves transient stunning and reversible left ventricular (LV) systolic dysfunction after physiologic or emotional stress. Fewer than 20 cases of TTC have been reported as complications of acute pancreatitis. Of note, pancreatitis itself can cause STE, typically in the inferior leads.5 In our patient's case, an echocardiogram and left ventriculogram revealed severe apical hypokinesis and an LV ejection fraction of 40%; however, a coronary angiogram did not reveal obstructive CAD, so the diagnosis was TTC. Two months later, he had normal LV ejection function, consistent with expected recovery timelines.

Sodium-Glucose Co-Transporter 2 Inhibition With Empagliflozin Improves Cardiac Function After Cardiac Arrest in Rats by Enhancing Mitochondrial Energy Metabolism.

Empagliflozin is a newly developed antidiabetic drug to reduce hyperglycaemia by highly selective inhibition of sodium–glucose co-transporter 2. Hyperglycaemia is commonly seen in patients after cardiac arrest (CA) and is associated with worse outcomes. In this study, we examined the effects of empagliflozin on cardiac function in rats with myocardial dysfunction after CA. Non-diabetic male Sprague–Dawley rats underwent ventricular fibrillation to induce CA, or sham surgery. Rats received 10 mg/kg of empagliflozin or vehicle at 10 min after return of spontaneous circulation by intraperitoneal injection. Cardiac function was assessed by echocardiography, histological analysis, molecular markers of myocardial injury, oxidative stress, mitochondrial ultrastructural integrity and metabolism. We found that empagliflozin did not influence heart rate and blood pressure, but left ventricular function and survival time were significantly higher in the empagliflozin treated group compared to the group treated with vehicle. Empagliflozin also reduced myocardial fibrosis, serum cardiac troponin I levels and myocardial oxidative stress after CA. Moreover, empagliflozin maintained the structural integrity of myocardial mitochondria and increased mitochondrial activity after CA. In addition, empagliflozin increased circulating and myocardial ketone levels as well as heart β-hydroxy butyrate dehydrogenase 1 protein expression. Together, these metabolic changes were associated with an increase in cardiac energy metabolism. Therefore, empagliflozin favorably affected cardiac function in non-diabetic rats with acute myocardial dysfunction after CA, associated with reducing glucose levels and increasing ketone body oxidized metabolism. Our data suggest that empagliflozin might benefit patients with myocardial dysfunction after CA.

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.

Correlation of Cardiac Troponin I with Left Ventricular Systolic Function in Patients with Acute ST-segment Elevated Myocardial Infarction

Myocardial infarction is one of the leading cause of death globally and following acute myocardial infarction prognosis depends on extent of myocardial damage. This study was aimed to correlate cardiac troponin I level with the left ventricular systolic function in patients with acute ST-elevated myocardial infarction. A total of 104 patients of acute ST-segment elevated myocardial infarction receiving streptokinase therapy within 12 hours of onset of chest pain were studied. Cardiac troponin I concentration was measured by immunometric assay and echocardiographic left ventricular ejection fraction was calculated by modified biplane Simpson's method. Left ventricular ejection fraction (LVEF) was compared with serum cardiac troponin I concentration. Study subjects were divided into two groups on the basis of LVEF. In group I, there were 54 patients with LVEF < 50% and in group II, there were 50 patients with LVEF >_ 50%. The mean cTnI within 12 hours of onset was 129 ± 8.7 ng/ml in group I and11 ± 2.1 ng/ml group II and the difference was statistically significant (p<0.001). Serum cardiac troponin I concentration has a strong negative correlation with left ventricular ejection fraction after first acute myocardial infarction. A level of serum cardiac troponin I >_ 6.6 ng/ml provided a good indication for LVEF <50% and this can be used to detect patients with higher risk. Faridpur Med. Coll. J. 2021;16(1):34-38

Teaching an old dog new tricks: serum troponin T as a biomarker in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis is a devastating neurodegenerative disease characterized by progressive loss of upper and lower motor neurons. Diagnosis, management and therapeutic trials are hampered by a lack of informative biomarkers. Troponins are components of skeletal and cardiac muscles. Acute elevation of cardiac isoforms of troponin I and T in serum indicates myocardial injury. Case reports suggested that serum levels of cardiac troponin T, but not cardiac troponin I are chronically elevated in myotrophic lateral sclerosis and other neuromuscular disorders. Using standard clinical laboratory methodologies, we studied serum troponin levels in a multicentric cross-sectional cohort of 75 amyotrophic lateral sclerosis patients and 30 Alzheimer’s disease controls and 29 healthy controls (DESCRIBE-ALS cohort) and in a real-world cohort of 179 consecutive patients from our amyotrophic lateral sclerosis clinic at the University Hospital Bonn. We found that serum cardiac troponin T is elevated in >60% of amyotrophic lateral sclerosis patients, while cardiac troponin I is always normal. Serum cardiac troponin T levels increase over time and correlate with disease severity as measured with the revised Amyotrophic Lateral Sclerosis Functional Rating Scale score. There was no correlation with the phosphorylated neurofilament heavy chain levels in the cerebrospinal fluid. We propose that cardiac troponin T elevations in amyotrophic lateral sclerosis are of non-cardiac origin and may serve as a proxy of lower motor neuron or skeletal muscle involvement. They potentially help to stratify patients according to lower motoneuron involvement. Further research will determine the biological origin of the cardiac troponin T elevation and its validity as a diagnostic and/or prognostic marker. Our finding also serves as a reminder to interpret cardiac troponin T elevations in patients with neuromuscular diseases with caution.

68Ga-DOTATOC PET/CT to detect immune checkpoint inhibitor-related myocarditis

BackgroundImmune checkpoint inhibitor (ICI)-related myocarditis is a rare but potentially fatal adverse event that can occur following ICI exposure. Early diagnosis and treatment are key to improve patient outcomes. Somatostatin...

376 Dynamic Changes in High Sensitivity Troponin T Are Associated With Increased Sepsis Mortality

Elevated serum cardiac troponin is a marker of myocardial injury associated with increased mortality in sepsis. Increasing use of high sensitivity troponin T (hsTrop) in the emergency department (ED) has allowed earlier and more sensitive detection of myocardial injury in acute coronary syndromes but has yet to be studied in relation to sepsis. The objective of this study was to determine the association between hsTrop changes and mortality in sepsis. This was a retrospective cohort study performed at a single, tertiary academic center. A concurrent multicenter sepsis trial was being conducted during the study period (June 1st, 2018 and March 20th, 2020) and the cohort for this study was derived from the screening log of this unrelated study. Adult patients with a suspected infection and hypotension after 1 liter of crystalloid fluids were included. All data were collected via direct database query to the electronic health record. hsTrop was measured in the ED and again approximately 2 hours later. The difference (delta) between the second and first measurements was the primary exposure and treated as a 4- level categorical variable (delta >6 ng/L, - 6 > delta > 6, delta <- 6 and no delta obtained). The primary outcome was 28- day mortality and secondary outcomes included mechanical ventilation, use of vasopressors, and crystalloid fluid received. Inverse probability weighting (IPW) was used to weight covariates for the probability of obtaining a hsTrop delta measurement in the ED. Using IPW derived weights, a multivariable logistic regression model was used to determine the association between hsTrop delta and 28- day mortality. Descriptive statistics and univariate analyses were also performed. After exclusion of clinician suspected baseline hypotension or hypotension not due to sepsis cause, as well as non- sepsis causes of hsTrop delta, 763 patients met the inclusion and exclusion criteria. 48 had a delta > 6 ng/L, 54 had a delta < - 6 ng/L, 175 had a delta between - 6 and 6, and 486 had no hsTrop delta obtained in the ED. Patients who had a hsTrop testing skewed male, older and with history of renal, heart disease or with chief complaints of chest pain or shortness of breath. In the weighted multivariable analysis and after adjustment for sex, age, and Charlson comorbidity index, both an hsTrop delta > 6 (OR 3.4 [95% CI 1.7 - 7.2]) and delta < - 6 (OR 2.2 [95% CI 1.1 - 4.4]) were associated with increased mortality at 28 days. The hsTrop delta >6 group was also associated with an increased risk for early mechanical ventilation (HR 3.0 [95% CI 1.8 - 4.9]), use of vasopressors (OR 3.7 [95% CI 2.0 - 7.0]), and increased crystalloid fluids administered during the first 24 hours (mean 4060 mL vs. ∼ 3000 mL for all other groups, p = 0.01). Dynamic changes in hsTrop obtained at ED presentation are associated with increased mortality in sepsis. Both an increasing and decreasing hsTrop delta are associated with a higher risk for 28- day mortality. This study was limited by its retrospective and single site design. Future studies are required to determine how hsTrop can be used to modify treatment.

Glutathione Infusion Before and 3 Days After Primary Angioplasty Blunts Ongoing NOX2‐Mediated Inflammatory Response

BackgroundGlutathione is a water‐soluble tripeptide with a potent oxidant scavenging activity. We hypothesized that glutathione administration immediately before and after primary angioplasty (primary percutaneous coronary intervention) could be effective in modulating immune cell activation, thereby preventing infarct expansion.Methods and ResultsOne hundred consecutive patients with ST‐segment–elevation myocardial infarction, scheduled to undergo primary percutaneous coronary intervention were randomly assigned before the intervention to receive an infusion of glutathione (2500 mg/25 mL over 10 minutes), followed by drug administration at the same doses at 24, 48, and 72 hours elapsing time or placebo. Total leukocytes, NOX2 (nicotinamide adenine dinucleotide phosphate oxidase 2) activation, NO bioavailability, cTpT (serum cardiac troponin T), hsCRP (high‐sensitivity C‐reactive protein), and TNF‐α (tumor necrosis factor α) levels were measured. Left ventricular size and function were assessed within 120 minutes, 5 days, and 6 months from percutaneous coronary intervention. Following reperfusion, a significant reduction of neutrophil to lymphocyte ratio (P<0.0001), hsCRP generation (P<0.0001), NOX2 activation (P<0.0001), TNF‐α levels (P<0.001), and cTpT release (P<0.0001) were found in the glutathione group compared with placebo. In treated patients, blunted inflammatory response was linked to better left ventricular size and function at follow‐up (r=0.78, P<0.005).ConclusionsEarly and prolonged glutathione infusion seems able to protect vital myocardial components and endothelial cell function against harmful pro‐oxidant and inflammatory environments, thus preventing maladaptive cardiac repair and left ventricular adverse remodeling.RegistrationURL: https://www.clinicaltrialsregister.eu; Unique identifier: 2014‐004486‐25.

Type I Diabetes Mellitus Increases the Cardiovascular Complications of Influenza Virus Infection

People with diabetes mellitus are susceptible to both cardiovascular disease and severe influenza A virus infection. We hypothesized that diabetes also increases risks of influenza-associated cardiac complications. A murine type 1 (streptozotocin-induced) diabetes model was employed to investigate influenza-induced cardiac distress. Lung histopathology and viral titres revealed no difference in respiratory severity between infected control and diabetic mice. However, compared with infected control mice, infected diabetic mice had increased serum cardiac troponin I and creatine-kinase MB, left ventricular structural changes and right ventricular functional alterations, providing the first experimental evidence of type I diabetes increasing risks of influenza-induced cardiovascular complications.

COVID-19, Cardiovascular Diseases and Cardiac Troponins

There has been strong evidence of myocardial injury in coronavirus disease 2019 (COVID-19) patients with significantly elevated serum cardiac troponin (cTn). While the exact mechanism of injury is unclear, possible suggested pathological mechanisms of injury are discussed. These include increased susceptibility of the myocardium and endothelium to viral invasion, underlying hyperinflammatory state and subsequent cytokine storm, a hypercoagulable and prothrombotic state, and indirect myocardial injury due to hypoxemia. As a result of these pathological mechanisms in COVID-19 patients, cTn may be elevated largely due to myocarditis, microangiopathy or myocardial infarction. The utility of cTn as a biomarker for measuring myocardial injury in these patients and assessing its ability as a prognostic factor for clinical outcome is also discussed.

Nano-Curcumin Prevents Cardiac Injury, Oxidative Stress and Inflammation, and Modulates TLR4/NF-κB and MAPK Signaling in Copper Sulfate-Intoxicated Rats.

Copper (Cu) is essential for a plethora of biological processes; however, its high redox reactivity renders it potentially toxic. This study investigated the protective effect of curcumin (CUR) and nano-CUR (N-CUR) against Cu cardiotoxicity, emphasizing the role of oxidative stress, TLR4/NF-κB and mitogen-activated protein kinase (MAPK) signaling and cell death in rats. Rats received 100 mg/kg copper sulfate (CuSO4), a pesticide used for repelling pests, and were concurrently treated with CUR or N-CUR for 7 days. Cu caused cardiac injury manifested by elevated serum cardiac troponin I (cTnI), creatine kinase (CK)-MB, and lactate dehydrogenase (LDH), as well as histopathological alterations. Cardiac malondialdehyde (MDA), NF-κB p65, TNF-α, and IL-6 were increased, and reduced glutathione (GSH), superoxide dismutase (SOD) and catalase were decreased in Cu-treated rats. CUR and N-CUR prevented cardiac tissue injury, decreased serum cTnI, CK-MB, and LDH, and cardiac MDA, NF-κB p65, TNF-α, and IL-6, and enhanced cellular antioxidants. CUR and N-CUR downregulated TLR4 and AP-1, and decreased the phosphorylation levels of p38 MAPK, JNK, and ERK1/2. In addition, CUR and N-CUR increased cardiac Bcl-2 and BAG-1, decreased Bax and caspase-3, and prevented DNA fragmentation. In conclusion, N-CUR prevents Cu cardiotoxicity by attenuating oxidative injury, inflammatory response, and apoptosis, and modulating TLR4/NF-κB and MAPK signaling. The cardioprotective effect of N-CUR was more potent than the native form.

Diagnostic Performance of Serial High-Sensitivity Cardiac Troponin Measurements in the Emergency Setting.

Serial high-sensitivity cardiac troponin (hsTn) testing in the emergency department (ED) and the intensive cardiac care unit may assist physicians in ruling out or ruling in acute myocardial infarction (MI). There are three major algorithms proposed for high-sensitivity cardiac troponin I (hsTnI) using serial measurements while incorporating absolute concentration changes for MI or death following ED presentation. We sought to determine the diagnostic estimates of these three algorithms and if one was superior in two different Canadian ED patient cohorts with serial hsTnI measurements. An undifferentiated ED population (Cohort-1) and an ED population with symptoms suggestive of acute coronary syndrome (ACS; Cohort-2) were clinically managed with non-hsTn testing with the hsTnI testing performed in real-time with physicians blinded to these results (i.e., hsTnI not reported). The three algorithms evaluated were the European Society of Cardiology (ESC), the High-STEACS pathway, and the COMPASS-MI algorithm. The diagnostic estimates were derived for each algorithm for the 30-day MI/death outcome for the rule-out and rule-in arm in each cohort and compared to proposed diagnostic benchmarks (i.e., sensitivity ≥ 99.0% and specificity ≥ 90.0%) with 95% confidence intervals (CI). In Cohort-1 (n = 2966 patients, 15.3% had outcome) and Cohort-2 (n = 935 patients, 15.6% had outcome), the algorithm that obtained the highest sensitivity (97.8%; 95% CI: 96.0–98.9 and 98.6%; 95% CI: 95.1–99.8, respectively) in both cohorts was COMPASS-MI. Only Cohort-2 with both the ESC and COMPASS-MI algorithms exceeded the specificity benchmark (97.0%; 95% CI: 95.5–98.0 and 96.7%; 95% CI: 95.2–97.8, respectively). Patient selection for serial hsTnI testing will affect specificity estimates, with no algorithm achieving a sensitivity ≥ 99% for 30-day MI or death.

Clinical value and role of microRNA-29c-3p in sepsis-induced inflammation and cardiac dysfunction

BackgroundThe goal of this study was to investigate the diagnostic value of miR-29c-3p in sepsis and its role in sepsis-induced inflammatory response and cardiac dysfunction.MethodsSerum level of miR-29c-3p was detected by qRT-PCR. The ROC curve was used to evaluate the diagnostic value of miR-29c-3p for Sepsis. The cecal ligation and puncture method (CLP) was used to establish a rat sepsis model. To assess cardiac function, left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and maximum rate of rise/fall of left ventricle pressure (± dp/dtmax) in different experimental groups were detected, and the serum cardiac troponin I (cTnI), creative kinase isoenzyme MB (CK-MB) were measured by ELISA. Meanwhile, TNF-α, IL-1β, and IL-6 were detected by ELISA to assess the level of inflammatory response in animals.ResultsmiR-29c-3p level was upregulated in sepsis patients. ROC curve revealed that miR-29c-3p had the ability to distinguish sepsis patients from healthy controls. Cardiac dysfunction and inflammation were observed in sepsis rat, which were characterized by the decrease of LVSP and + dp/dtmax, the increase of LVEDP, − dp/dtmax, cTnI, CK-MB, TNF-α, IL-1β, IL-6. All effects were reversed by the injection of miR-29c-3p antagomir. Logistics regression analysis manifested miR-29c-3p is an independent factor in the occurrence of cardiac dysfunction in sepsis patients.ConclusionsmiR-29c-3p has potential as a biomarker for the diagnosis of sepsis, and inhibition of miR-29c-3p expression in animal models reduced sepsis-induced cardiac dysfunction and inflammatory response.

Prevalence of raised cardiac markers in SVT and variables associated with raised troponin I

Cardiac troponins are the major sensitive and specific markers of myocardial injury. Joint European Society of Cardiology/American College of Cardiology committee has given the redefinition of myocardial infarction (MI) stating that troponins are the preferred cardiac markers for detecting myocardial injury. Besides MI, elevated troponins are also seen in tachyarrhythmias, acute cerebrovascular accident, acute pulmonary thromboembolism, chronic kidney disease, septic shock, myocardial injury. Though Troponin I frequently increases during myocardial injury, the etiology may vary from coronary to non- coronary causes. Paroxysmal supraventricular tachycardia (PSVT) is the commonest form of arrhythmia seen in the Emergency Department. In contrast to ventricular tachyarrhythmias these patients are haemodynamically stable and they have good prognosis on treatment. Serum cardiac troponin I (cTnI) testing provides momentous risk stratification in these group of arrhythmias. This study will provide comprehensive data on prevalence, clinical profile, risk factors and prognosis of patients with elevated Troponin I in SVT in non CAD patients.

Exploration of serum cardiac troponin I as a biomarker of cardiomyopathy in southern sea otters (Enhydra lutris nereis).

To compare serum cardiac troponin I (cTnI) concentrations between sea otters with and without cardiomyopathy and describe 2 cases of cardiomyopathy with different etiologies. 25 free-ranging southern sea otters (Enhydra lutris nereis) with (n = 14; cases) and without (11; controls) cardiomyopathy and 17 healthy managed southern sea otters from aquariums or rehabilitation centers (controls). Serum cTnI concentration was measured in live sea otters. Histopathologic and gross necropsy findings were used to classify cardiomyopathy status in free-ranging otters; physical examination and echocardiography were used to assess health status of managed otters. Two otters received extensive medical evaluations under managed care, including diagnostic imaging, serial cTnI concentration measurement, and necropsy. A significant difference in cTnI concentrations was observed between cases and both control groups, with median values of 0.279 ng/mL for cases and < 0.006 ng/mL for free-ranging and managed controls. A cutoff value of ≥ 0.037 ng/mL yielded respective sensitivity and specificity estimates for detection of cardiomyopathy of 64.3% and 90.9% for free-ranging cases versus free-ranging controls and 64.3% and 94.1% for free-ranging cases versus managed controls. Cardiomyopathy is a common cause of sea otter death that has been associated with domoic acid exposure and protozoal infection. Antemortem diagnostic tests are needed to identify cardiac damage. Results suggested that serum cTnI concentration has promise as a biomarker for detection of cardiomyopathy in sea otters. Serial cTnI concentration measurements and diagnostic imaging are recommended to improve heart disease diagnosis in managed care settings.

Perioperative management of post-COVID-19 surgical patients: Indian Society of Anaesthesiologists (ISA National) Advisory and Position Statement.

Perioperative management of post-COVID-19 surgical patients: Indian Society of Anaesthesiologists (ISA National) Advisory and Position Statement.

Significantly High Serum Cardiac Troponin Level with Supraventricular Tachyarrhythmia in the Absence of Coronary Artery Disease

Although elevated cardiac troponin is considered to be the gold standard biomarker for the identification of acute coronary syndrome, it may also occur in other clinical situations as supraventricular tachyarrhythmia (SVT) and acute coronary syndrome. We reported the case of a 77-year-old patient with a highly elevated cTn after the onset of SVT. Normal coronary arteries were detected through coronary angiography and intravenous ultrasound. It seems that the association of the cardiac troponin elevation in SVT patients with future cardiovascular events is very low. Meanwhile, more attention should be paid to those patients with high cardiovascular risk factors.

Photoacoustic imaging study on spatial structure of microvessels around acupoints in mice with acute myocardial ischemia

To observe the changes of microvascular structure of acupoints caused by myocardial ischemia, so as to explore the application of photoacoustic imaging technology in the research of acupoint sensitization. Twelve BALB/c mice were randomly divided into normal, sham operation and acute myocardial ischemia (AMI) model groups, with 4 mice in each group. AMI model was established by ligating the left anterior descending coronary artery. Electrocardiogram (ECG) was recorded by physiological signal acquisition system at 12 h and on the 14th day after modeling, and serum cardiac troponin T (cTnT) and creatine kinase isoenzyme MB (CK-MB) levels were detected by enzyme-linked immunosorbent assay. The microvascular structure changes of acupoints "Feishu"(BL13), "Jueyinshu"(BL14), "Quze"(PC3) and "Chize"(LU5) were observed by photoacoustic imaging technology, and distance (DM), inflection count metric (ICM), sum of angle metric(SOAM)and microvessel density (MVD) were calculated by microvascular quantification algorithm. Compared with the normal and sham operation groups, the ST segment of ECG was obviously elevated, serum cTnT and CK-MB were significantly increased in AMI model group at 12 h and on the 14th day after AMI (P<0.01). The ICM of BL14 in AMI model group was significantly decreased on the 14th day than that on the 7th day after AMI. Compared with the normal group, the ICM of BL14 was significantly increased in AMI model group on the 7th day after AMI(P<0.05). There were no significant changes in DM, ICM, SOAM and MVD at other acupoints on the 7th and 14th day (P>0.05) among the three groups. The change of ICM may be one of the characteristics of acupoint sensitization and photoacoustic imaging technology can be used to study the structure of acupoint microvessels.

Levels of GP-Iib/Iiia Positive Platelet Microparticles (PMP) but Not CD31+/CD42+ PMP Predict Adverse Outcomes in Troponin-Negative Patients with Chest Pain.

Background: Cell derived microparticles (MP) are useful biomarkers in various thrombotic and inflammatory disorders. However, MP are heterogeneous in their phenotypes, functional properties, and origin. Platelet-derived microparticles (PMP) have been shown to be elevated in acute coronary syndromes but different species of PMP have not been compared. We performed a study to compare two subspecies of PMP, those identified by anti-GP-IIb/IIIa vs. those by CD31+/CD42+, for predicting adverse outcomes in patients with chest pain of possible ischemic cause.Methods: The study population consisted of 105 patients who presented to the emergency department with chest pain, non-diagnostic electrocardiograms and negative serial cardiac troponin I levels. Blood was obtained after the third negative troponin result for determination of levels of GP-IIb/IIIa positive PMP (PMPIIb/IIIa) and CD31+/CD42+ PMP (PMP31). All treatment decisions were left at the caregiver's discretion. Telephone follow-up was done at 6 months for the development of a combined endpoint of death, myocardial infarction or need for cardiac catheterization or revascularization. The mean age of our patients was 57.5 years. The age, diabetes, hypertension, smoking and history of coronary artery disease was not significantly different between patients who reached an endpoint at 6 months versus those who did not. Overall 19% reached an endpoint at 6 months. The endpoint was largely driven by the need for cardiac catheterization due to positive stress test results.Results: On univariate analysis, patients who reached an endpoint at 6 months had higher levels of PMPIIb/IIIa than those who did not (geometric means 2059.6 vs. 924.4 counts/μL; p=0.04; medians 2157.5 vs 1764.0 counts/μL; p=0.009). When adjusted for age, diabetes, hypertension, dyslipidemia, aspirin use and current smoking by analysis of covariance, the difference persisted (adjusted geometric means: 2484.9 vs. 829.5 counts/μL; p=0.01). In contrast, PMP31 levels were not significantly different between patients who reached an endpoint at 6 months versus those who did not (5908 ±7990 vs. 3812 ±3109 counts/μL; p=0.26).Conclusions: Our findings suggest that different subspecies of PMPs may reflect different pathophysiological phenomena. PMP31 levels did not correlate with the risk of adverse outcomes in this population. In contrast, GpIIb/IIIa-positive PMP appear to be promising prognostic indicators in chest pain patients with negative troponins and nondiagnostic EKGs. Our results are consistent with prior studies showing association between PMP and thrombosis, but suggest that not all PMP are equal. Further research is needed to investigate a possible role of PMP in the pathogenesis of ACS, and as prognostic markers in current stratification strategies. Assay of different species of MP is likely to provide more discriminating diagnostic and prognostic information.

RETRACTED: Two Dy(III) complexes: Crystal structures and treatment activity on cardiovascular disease

Two new lanthanide coordination polymers (CPs) of {[Dy(L) (H 2 O)]·3CH 3 CN} n ( 1 ) and {(Me 2 NH 2 ) 0.5 [Dy(L) (HCOO − ) 0.5 H 2 O]·DMF·4EtOH·H 2 O} n ( 2 ) have been prepared via utilizing the tris(4-carboxyphenyl)phosphane oxide (H 3 L) as the organic linker under solvothermal conditions. The treatment activity of the compounds on cardiovascular disease in children was evaluated. Several experiments were performed to develop new candidates for the cardiovascular disease treatment. For biological activity evaluation, the release of Creatine kinase isoenzyme (CK) and serum cardiac troponin (CT) was evaluated with enzyme linked immunosorbent assay (ELISA) detection kit. The cardiomyocytes apoptosis was determined by the apoptosis detection kit and Western blot. The accumulation of the ROS in the cardiomyocytes was also detected by flow cytometry. • Two lanthanide coordination polymers have been prepared. • The treatment activity of the compounds on cardiovascular disease in children was evaluated. • The treatment activity of the compounds on cardiovascular disease in children was evaluated.