Increase In Cardiac Biomarkers Research Articles

Modeling creatine-kinase MB concentrations following coronary artery bypass grafting

BackgroundAn increase in cardiac biomarkers is a prerequisite for diagnosing periprocedural myocardial infarction (PMI) after coronary artery bypass grafting (CABG). Early-phase risk detection may be aided by modeling time-dependent serum creatine kinase-MB (CK-MB) concentrations. This study aimed to model the kinetics of CK-MB while identifying its influencing factors. MethodsPatients who underwent elective CABG and had CK-MB measurements within 72 hours postoperatively were included. The primary outcome was the modeled post hoc kinetics of CK-MB in patients without potential PMI. These patients were defined as having no potential PMI based on the absence of ischemic electrocardiographic abnormalities, imaging abnormalities, in-hospital cardiac arrest, mortality, or postoperative unplanned catheterization. A web-based application was created using mixed-effect modeling to provide an interactive and individualized result. ResultsA total of 1589 CK-MB measurements from 635 patients who underwent elective isolated CABG were available for analysis. Of these, 609 patients (96%) had no potential PMI and 26 (4%) had potential PMI. Male sex, aortic cross-clamp time, and cardioplegia type significantly impacted CK-MB concentrations. The diagnostic accuracy of the model had an area under the receiver operating characteristic curve of 82.8% (95% confidence interval, 72.6%-90.2%). A threshold of 7 μg/L yielded a sensitivity of 94% and a specificity of 80% (positive predictive value, 17%; negative predictive value, 99%) for excluding potential PMI in our study population. ConclusionsCK-MB release after CABG depends on the timing of measurement, patient sex, aortic cross-clamp time, and cardioplegia type. The model (available at https://www.cardiomarker.com/ckmb) can be validated, reproduced, refined, and applied to other biomarkers.

Effect of Ultramarathon Trail Running at Sea Level and Altitude on Alveolar-Capillary Function and Lung Diffusion.

Endurance exercise at altitude can increase cardiac output and pulmonary vascular pressure to levels that may exceed the stress tolerability of the alveolar-capillary unit. This study examined the effect of ultramarathon trail racing at different altitudes (ranging from <1000 m to between 1500 and 2700 m) on alveolar-capillary recruitment and lung diffusion. Cardiac and lung function were examined before and after an ultramarathon in 67 runners (age: 41 ± 9 yr, body mass index: 23 ± 2 kg·m -2 , 10 females), and following 12-24 h of recovery in a subset ( n = 27). Cardiac biomarkers (cTnI and BNP) were assessed from whole blood, whereas lung fluid accumulation (comet tails), stroke volume (SV), and cardiac output ( Q ) were quantified via echocardiography. Lung diffusing capacity for carbon monoxide (DLco) and its components, alveolar membrane conductance (Dm) and capillary blood volume (Vc), were determined via a single-breath method at rest and during three stages of submaximal semirecumbent cycling (20, 30, and 40 W). Average race time was 25 ± 12 h. From pre- to post-race, there was an increase in cardiac biomarkers (cTnI: 0.04 ± 0.02 vs 0.13 ± 0.03 ng·mL -1 , BNP: 20 ± 2 vs 112 ± 21 pg·mL -1 ; P < 0.01) and lung comet tails (2 ± 1 vs 7 ± 6, P < 0.01), a decrease in resting and exercise SV (76 ± 2 vs 69 ± 2 mL, 40 W: 93 ± 2 vs 88 ± 2 mL; P < 0.01), and an elevation in Q at rest (4.1 ± 0.1 vs 4.6 ± 0.2 L·min -1 , P < 0.01; 40 W: 7.3 ± 0.2 vs 7.4 ± 0.3 L·min -1 , P = 0.899). Resting DLco and Vc decreased after the race ( P < 0.01), whereas Dm was unchanged ( P = 0.465); however, during the three stages of exercise, DLco, Vc, and Dm were all reduced from pre- to post-race (40 W: 36.3 ± 0.9 vs 33.0 ± 0.8 mL·min -1 ·mm Hg -1 , 83 ± 3 vs 73 ± 2 mL, 186 ± 6 vs 170 ± 7 mL·min -1 ·mm Hg -1 , respectively; P < 0.01). When corrected for alveolar volume and Q , DLco decreased from pre- to post-race ( P < 0.01), and changes in DLco were similar for all ultramarathon events ( P > 0.05). Competing in an ultramarathon leads to a transient increase in cardiac injury biomarkers, mild lung-fluid accumulation, and impairments in lung diffusion. Reductions in DLco are predominantly caused by a reduced Vc and possible pulmonary capillary de-recruitment at rest. However, impairments in alveolar-capillary recruitment and Dm both contribute to a fall in exertional DLco following an ultramarathon. Perturbations in lung diffusion were evident across a range of event distances and varying environmental exposures.

Frequency and Prognostic Value of Acute Periprocedural Myocardial Injury in Elective Percutaneous Coronary Interventions

Background. Periprocedural myocardial injury (PMI) is an acute complication of percutaneous coronary interventions (PCI) in patients with stable coronary artery disease. Its frequency and relationship with the prognosis of the disease are especially important in elective interventions due to the low risk of ischemic events in this cohort of patients. However, according to the literature, there are significant differences in the criteria for PMI and type 4a myocardial infarction (MI), and, accordingly, their frequency and their prognostic value. Aim. To study the frequency and magnitude of PMI during elective PCI in terms of the level of periprocedural increase in cardiospecific biomarkers, as well as to determine the relationship of PMI with long-term adverse events in patients with chronic coronary artery disease. Materials and methods. A single-center open retrospective cohort study was conducted, which included 435 patients (367/84.4 % men, mean age 58.3±8.6 years) from the elective PCI registry. PMI was diagnosed with an increase in the level of creatine phosphokinase MB fraction (CK-MB) or or cardiac troponin I (cTn I) &gt;1×99 percentile URL (Upper Reference Limit), while the level of increase in biomarkers &gt;1, 2, 3, 4 or &gt;5×99 percentile URL was recorded. An increase in biomarkers &gt;5x99 URL percentile was assessed as a large PMI, and in the presence of clinical and imaging evidence of new loss of viable myocardium, as periprocedural MI type 4a. Depending on the level of periprocedural increase in biomarkers, the relative risk (RR) of developing long-term (within 5 years after index PCI) adverse cardiovascular events, death, as well as clinically significant bleeding and newly diagnosed malignant oncological diseases was calculated. In addition, the correlation between PMI and the above endpoints was summarized using Kaplan-Meier analysis. Results. The frequency of periprocedural PMI diagnosed by increased biomarkers &gt;1×99 percentile URL was 40.2 %, &gt;2×99 percentile URL — 9.7 %, &gt;3×99 percentile URL — 6.7 %, &gt;4×99 percentile URL — 4.8 %, &gt;5×99 percentile URL — 3.5 %, type 4a MI — in 2 patients (0.46 %). An association of “major” PMI (&gt;5x99 percentile URL) with cardiovascular complications within 3 years after elective PCI, including fatal ones, was revealed: for acute myocardial infarction (AMI), RR — 6.516, confidence interval (CI) [2.375-17.881]; for death from cardiovascular causes RR — 6.538, CI [1.695-25.227]. An association of “moderate” PMI (&gt;3, but &lt;5 ×99 URL percentile) with acute ischemic events within 3 years after elective PCI was shown: for AMI, RR was 4.073, CI [1.598 — 10.378]. An association of “minor” AKI (&gt;1, but &lt;5 ×99 URL percentile) with acute ischemic events within 3 years after elective PCI was shown: for AMI, RR was 4.073, CI [1.598 — 10.378]. An association of “minor” AKI (&gt;1, but &lt;3 ×99 URL percentile) with newly diagnosed malignant oncological diseases within 5 years after index PCI was revealed: RR 2.319; CI [1.248- 4.310]. An association of late thrombotic events, such as stent thrombosis (index and re-interventions), stent occlusion (index and non-index) as a reason for re-intervention within 5 years after index PCI, was found with most PMI subgroups. Kaplan-Meier analysis of the dependence of clinically significant bleeding within 5 years after index PCI on the development of “moderate” PMI (p=0.003), as well as the association of non-cardiovascular death within 5 years after index PCI with “minor” PMI (p= 0.007). Conclusion. Registration of periprocedural increase in cardiac biomarkers should be carried out during planned PCI not only for the purpose of diagnosing and predicting acute and late ischemic events, but also for assessing the risk of developing stent occlusion, clinically significant bleeding and prognostically important comorbidities in the long-term (5-year) period in order to identification of groups of patients requiring active monitoring, additional examination and selection of an optimal treatment regimen at the outpatient stage of rehabilitation.

European Association of Cardio-Thoracic Surgery (EACTS) expert consensus statement on perioperative myocardial infarction after cardiac surgery.

Cardiac surgery may lead to myocardial damage and release of cardiac biomarkers through various mechanisms such as cardiac manipulation, systemic inflammation, myocardial hypoxia, cardioplegic arrest and ischaemia caused by coronary or graft occlusion. Defining perioperative myocardial infarction (PMI) after cardiac surgery presents challenges, and the association between the current PMI definitions and postoperative outcomes remains uncertain. To address these challenges, the European Association of Cardio-Thoracic Surgery (EACTS) facilitated collaboration among a multidisciplinary group to evaluate the existing evidence on the mechanisms, diagnosis and prognostic implications of PMI after cardiac surgery. The review found that the postoperative troponin value thresholds associated with an increased risk of mortality are markedly higher than those proposed by all the current definitions of PMI. Additionally, it was found that large postoperative increases in cardiac biomarkers are prognostically relevant even in absence of additional supportive signs of ischaemia. A new algorithm for PMI detection after cardiac surgery was also proposed, and a consensus was reached within the group that establishing a prognostically relevant definition of PMI is critically needed in the cardiovascular field and that PMI should be included in the primary composite outcome of coronary intervention trials.

Acute effects of resistance-type and cycling-type high-intensity interval training on arterial stiffness, cardiac autonomic modulation and cardiac biomarkers

BackgroundHigh-intensity interval training (HIIT) has been shown to enhance cardiovascular health. However, there is a lack of research investigating the specific cardiovascular effects of different HIIT training modes. Therefore, this study aimed to compare the acute effects of cycling-type high intensity interval training (C-HIIT) and resistance-type high intensity interval training (R-HIIT) on arterial stiffness, cardiac autonomic modulation, and cardiac biomarkers in healthy young men.MethodsThis is a cross-over randomized trial. Eleven healthy active young men took part in both C-HIIT and R-HIIT. Cardio-ankle vascular index (CAVI), heart rate variability (HRV), and systolic blood pressure (SBP) were measured before, immediately and 30 min after the exercise in C-HIIT and R-HIIT. Meanwhile, blood samples for cardiac troponin-T (cTnT) and amino-terminal pro-B-type natriuretic peptide (NT-proBNP) were assessed using ELISA before, 5min and 35min after exercise.ResultsThere was a significant time × group interaction effect (P = 0.019, ηp2 = 0.182) and time main effect for ⊿CAVI (P < 0.001, ηp2 = 0.729), and R-HIIT resulted in a more significant reduction in ⊿CAVI compared to C-HIIT (− 0.60 ± 0.30, P = 0.043, d = 0.924) immediately after exercise. There was a significant time main effect was observed for SBP (P = 0.001, ηp2 = 0.304). A significant time main effect for lnHF (P < 0.001, ηp2 = 0.782), lnRMSSD (P < 0.001, ηp2 = 0.693), and LF/HF (P = 0.001, ηp2 = 0.302) of HRV was observed. A significant time main effect was observed for cTnT (P = 0.023, ηp2 = 0.193) and NT-proBNP (P = 0.001, ηp2 = 0.334) of cardiac biomarkers.ConclusionR-HIIT and C-HIIT elicited similar acute responses in cardiac autonomic modulation and cardiac biomarkers. However, R-HIIT was more effective in reducing arterial stiffness in healthy young men. Furthermore, the increase in cardiac biomarkers induced by both C-HIIT and R-HIIT was reversible.Trial registrationThe study was prospectively registered on 22 February 2022 at www.chictr.org.cn with identification number ChiCTR2200056897.

Myocardial Injury After Transcatheter Mitral Valve Replacement Versus Surgical Reoperation

This study aimed to evaluate the incidence and clinical implications of myocardial injury, as determined by cardiac biomarker increase, in patients who underwent mitral bioprosthesis dysfunction treatment with transcatheter mitral valve replacement (TMVR) versus surgical mitral valve replacement reoperation (SMVR-REDO). Between 2014 and 2023, 310 patients with mitral bioprosthesis failure were included (90 and 220 patients for TMVR and SMVR-REDO, respectively). Multivariable analysis and propensity score matching were performed to adjust for the intergroup differences in baseline characteristics. Creatinine kinase-MB (CK-MB) and cardiac troponin I (cTn) were collected at baseline and 6 to 12, 24, 48, and 72 hours after intervention. The cardiac biomarkers values were evaluated in relation to their reference values. The outcomes were determined according to the Mitral Valve Academic Research Consortium criteria. CK-MB and cTn increased above the reference level in almost all patients after SMVR-REDO and TMVR (100% vs 94%, respectively), with the peak occurring within 6 to 12 hours. SMVR-REDO was associated with a two- to threefold higher increase in cardiac biomarkers. After 30 days, the mortality rates were 13.3% in the TMVR and 16.8% in the SMVR-REDO groups. At a median follow-up of 19 months, the mortality rates were 21.1% in the TMVR and 17.7% in the SMVR-REDO groups. Left ventricular ejection fraction, estimated glomerular filtration rate, CK-MB, and cTn were predictors of mortality. In conclusion, some degree of myocardial injury occurred systematically after the treatment of mitral bioprosthetic degeneration, especially after SMVR, and higher CK-MB and cTn levels were associated with increased cumulative late mortality, regardless of the approach.

Tenecteplase: A Review of Its Pharmacology and Uses.

Tenecteplase: A Review of Its Pharmacology and Uses.

P64 PERSISTENT ST–ELEVATION WITH HIGH MYOCARDIONECROSIS MARKERS: A CASE OF MYOCARDIAL CONTUSION

Abstract Myocardial contusion (MC) is a note rare and potentially fatal complication of blunt chest trauma (BCT). The spectrum of manifestations of post–traumatic cardiac injury varies widely: from clinically silent injuries to severe reductions in cardiac function, myocardial hematomas, heart ruptures, and life–threatening arrhythmias1. There is no unique definition for this entity, and the diagnostic criteria proposed by different authors vary widely. Some authors define MC as a mild increase in cardiac biomarkers in the context of chest trauma, while for others the diagnosis requires evidence on imaging of pathologic findings2. Consequently, the true incidence of MC remains unknown, varying in reports between 8% and 71%3. We describe a case of cardiac contusion secondary to a low–energy trauma manifested as persistent ST elevation and pathologic elevation of myocardiocytosis markers, with consequent myocardial stunning of the right ventricular free wall. As there is no consensus regarding the correct diagnostic pathway, it is essential to integrate first–level pathologic examinations (ECG and laboratory diagnostics) with cardiac magnetic Resonance Imaging (MRI) to define the presence of cardiac contusion and its extent, especially if the echocardiographic data are unconclusive.

The effect of tilmicosin and diclofenac sodium combination on cardiac biomarkers in sheep.

The aim of this study was to investigate the cardiotoxic effect of the combination of tilmicosin and diclofenac sodium in sheep. Thirty-two sheep were used and were randomly divided into four equal groups as tilmicosin (T), diclofenac sodium (D), tilmicosin+diclofenac sodium (TD) and control (C) group. Group T received a single dose of tilmicosin, Group D was administered diclofenac sodium once a day for 3 days, and group TD was administered diclofenac and tilmicosin at the same doses as group T and D. Group C received NaCl in a similar way. The blood samples were taken before dosing and at 4th, 8th, 24th and 72nd hour post-dosing for measurement of cardiac markers such as H-FABP, cTn-I, CK-MB. H-FABP level of group TD was found to be significantly (p⟨0.05) higher than of group C at the 8th, 24th and 72nd hour and group D and T at the 72nd hour. cTn-I and CK-MB levels of group TD were found significantly (p⟨0.05) higher compared with other groups. In conclusion, the combined use of tilmicosin and diclofenac in sheep causes an increase in cardiac biomarkers and it can be stated that this combination of drugs may cause cardiac damage.

Immune Checkpoint Inhibitor-Associated Myocarditis: From Pathophysiology to Rechallenge of Therapy – a Narrative Review

Even if immunecheckpoint inhibitors have revolutionized the landscape of cancer therapy, their use may be complicated by immune-related adverse events. Among these, myocarditis is the most severe complication. The clinical suspicion often arises after clinical symptoms onset and increase in cardiac biomarkers or electrocardiographic manifestations. Echocardiography and cardiac magnetic resonance imaging are recommended for each patient. However, since they may be misleadingly normal, endomyocardial biopsy remains the gold standard for establishing the diagnosis. Until now, treatment has been based on glucocorticoids even if increasing interest has risen in other immunosuppressive agents. Although myocarditis currently imposes immunotherapy discontinuation, case reports have suggested a safety rechallenge in low-grade myocarditis paving the way for further studies to respond to this unmet clinical need.

HFA-ICOS cardiovascular toxicity risk score validation in CARDIOTOX registry

Abstract Background Cancer therapy-related cardiovascular toxicity (CTox) is a growing medical problem and baseline cardiovascular (CV) risk assessment is recommended in all patients scheduled to receive potentially cardiotoxic cancer therapy. Based on literature review, the Heart Failure Association (HFA) Cardio-Oncology working group and the International Cardio-Oncology Society (ICOS) proposed a risk score to predict CTox but, it has not been validated. Purpose To validate the HFA-ICOS anthracycline risk assessment score in the CARDIOTOX registry cohort (NCT02039622). Methods The CARDIOTOX registry is a prospective multicenter study aiming at identifying factors related with CTox and assessing the utility of clinical, biochemical, and echo parameters for the early detection of CV disease during and after cancer therapy. A total of 1324 adult patients were prospectively included from April 2012 to October 2017. Data was collected at baseline, 3 weeks and 3, 6, 12, 18 and 24 months after initiation of treatment. Clinical follow-up was extended until January 2020. All patients receiving anthracycline chemotherapy were stratified according to HFA-ICOS risk score and Kaplan-Meier survival curves were analyzed to estimate the risk of all-cause mortality and anthracycline chemotherapy-related CV complications defined by HFA-ICOS risk score (left ventricular dysfunction (LVD), heart failure (HF) and arrhythmias). Results A total of 1066 patients were included in the analysis. Baseline characteristics are summarized in table 1. 571 patients (53.6%) meet low, 333 (31.2%) medium, 152 (14.3%) high and 10 (0.9%) very-high HFA-ICOS CTox risk criteria. 197 patients (18.4%) died of any cause during follow-up. CV death occurred in 4 patients (2%), all caused by HF. Any degree of CTox was identified in 519 (48.7%) patients during the 110 months follow-up (73 (6.8%) developed clinical HF/HF hospitalization, 29 (2.7%) asymptomatic LVEF &amp;lt;50%; 27 (2.5%) clinically relevant arrhythmias and 390 (36.6%) an asymptomatic increase in cardiac biomarkers or a relative decrease in GLS&amp;gt;15%). Figures 1A and 1B showed the cumulative mortality rate and CTox rate during follow-up. CTox and all-cause mortality rates increased significantly according to the estimated baseline HFA-ICOS score. Conclusions HFA-ICOS risk score categorizes patients according to their risk of developing anthracycline chemotherapy-related CTox, showing a good ability to predict both all-cause mortality and CTox. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Instituto de Salud Carlos III (PI13/00559).

Cardiac biomarkers and mortality in COVID-19 infection: A review.

Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), creatine kinase-myocardial band (CK-MB) and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. The purpose of this review is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes.

The COVID-19 viral 3a protein forms a potassium channel that can be inhibited by antiarrhythmic drugs

Funding AcknowledgementsType of funding sources: Public Institution(s). Main funding source(s): Deutsche Gesellschaft für Kardiologie /German Cardiac Society Joachim Herz Stiftung /Joachim Herz FoundationBackground/IntroductionSupraventricular and ventricular arrhythmias can often be observed in patients with COVID-19 infection. Both, the clinically observed increase in cardiac biomarkers as well as histological studies indicate virus replication within cardiomyocytes. The 3a open reading frame of the viral genome encodes for a transmembrane protein that is transported to the cell membrane where it can serve as a potassium channel.PurposeThe aim of this study was to investigate whether COVID-19 infected induced pluripotent stem cell (iPSC)-derived cardiomyocytes also express the 3a protein and whether the potassium currents that are conducted through the 3a protein can be inhibited by clinically used antiarrhythmic drugs.Methods and ResultsiPSC-derived cardiomyocytes were infected with COVID-19 and subsequently subjected to immunoblotting, where expression of the 3a protein could be observed. Plasmid DNA, encoding the COVID-19 3a protein, was generated by gene synthesis and used for in vitro transcription of cRNA. 3–5 days after intracytoplasmic injection of the 3a protein cRNA into Xenopus laevis oocytes, potassium currents could be measured by two-electrode voltage clamp recordings. While class I and class IV antiarrhythmic drugs showed only minor effects on the potassium currents of the 3a protein, a robust inhibition by several beta-blockers and by class III antiarrhythmic drugs could be observed. The strongest effects were found with dofetilide (58.1 % inhibition at 100 µM) and amiodarone (50.1 % inhibition at 100 µM, IC50 level 4.7 µM). An in silico docking analysis, based on the recently revealed crystal structure of the 3a protein, identified the amino acid residues K61 and D142 as part of the binding site of amiodarone. After deactivation of these amino acid residues by site-directed mutagenesis, the inhibition by amiodarone was significantly attenuated.ConclusionThe COVID-19 viral 3a protein is expressed in COVID-19-infected iPS-derived cardiomyocytes and forms a potassium channel that can be inhibited by antiarrhythmic drugs.

Gut Leakage and Cardiac Biomarkers after Prolonged Strenuous Exercise.

Transient increase in the cardiac biomarkers troponin T (cTnT) and NT-proBNP are observed during strenuous exercise, even in healthy athletes. Gut leakage, the translocation of bacterial lipopolysaccharide (LPS) into the circulation, is associated with atherosclerosis and cardiovascular disease but has also been reported after prolonged endurance exercise. We aimed to explore the link between exercise-induced gut leakage and cardiac biomarker release. Participants in Norseman Xtreme Triathlon (Norseman) were included ( n = 44, age 43 ± 9 yr, 9 [21%] women). Blood samples were taken before and immediately after the race for the determination of biomarkers. cTnT and NT-proBNP were measured by conventional methods. Gut leakage marker LPS was measured by the kinetic, chromogenic limulus amebocyte lysate assay method, whereas LPS-binding protein (LBP), soluble cluster of differentiation 14 (sCD14), and intestinal injury marker intestinal fatty acid-binding protein (I-FABP) were measured by enzyme-linked immunosorbent assay. Median (25, 75 percentiles) finish time was 14 h 33 min (13 h 42 min, 15 h 29 min). TnT and NT-proBNP increased significantly to 38 ng·L -1 (27, 56) and 495 ng·L -1 (310, 828) after the race ( P < 0.001, both). LBP and sCD14 also increased significantly ( P < 0.001, both), as did I-FABP ( P = 0.003), whereas LPS remained unchanged ( P = 0.13). No significant correlations between changes in gut leakage markers and changes in cardiac biomarkers were observed after adjusting for multiple testing. Cardiac and gut leakage biomarkers increased after Norseman Xtreme triathlon. However, changes in these biomarkers were not intercorrelated, suggesting that the exercise-induced increase in cardiac and gut leakage biomarkers occurs independently of each other.

Nauclea orientalis (L.) Bark Extract Protects Rat Cardiomyocytes from Doxorubicin-Induced Oxidative Stress, Inflammation, Apoptosis, and DNA Fragmentation.

The therapeutic efficacy of anthracycline antibiotic, doxorubicin (Dox), is hampered due to the dose-dependent cardiotoxicity. The objective of the study was to explore the counteraction of aqueous bark extract of Nauclea orientalis in Dox-induced cardiotoxicity in Wistar rats. The acute and subchronic toxicity study performed with 2.0 g/kg of the plant extract revealed biochemical and haematological parameters to be within the physiological range, and no histological alterations were observed in any organs isolated. Screening of plant extract for the protection of the myocardium from Dox-induced oxidative stress, inflammation, and apoptosis was performed on five groups of rats: control, plant extract control, Dox control (distilled water (D.H2O) 2 weeks + on the 11th day single injection of Dox, 18 mg/kg), plant + Dox (2.0 g/kg plant extract 2 weeks + on the 11th day Dox, 18 mg/kg), and positive control, dexrazoxane. A significant increase in cardiac biomarkers and lipid peroxidation (p < 0.001) and a significant decrease in antioxidant parameters (p < 0.001) were observed in the Dox control group. All these parameters were reversed significantly (p < 0.05) in the plant-pretreated group. The histopathological assessment of myocardial damage provided supportive evidence for the biochemical results obtained. Inflammatory markers, myeloperoxidase, expression of TNFα and caspase-3, and DNA fragmentation (TUNEL positive nuclei) were significantly elevated (p < 0.05), and expression of Bcl-2 was significantly decreased (p < 0.05) in the Dox control; however, all these parameters were significantly reversed in the plant extract-treated group. In conclusion, the aqueous bark extract of Nauclea orientalis (2.0 g/kg) has the ability to attenuate the Dox-induced oxidative stress, inflammation, apoptosis, and DNA fragmentation in Wistar rats.

Is left ventricular function reduced after ultra-endurance exercise?

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Norwegian Health Association Introduction Ultra-endurance exercise can be harmful according to previous studies, indicated by reduction in functional parameters and increase in cardiac biomarkers. Changes in load and heart rate with exercise influence left ventricle systolic function, making assessment of standard echocardiographic examination difficult. Purpose We investigated the effect of ultra-endurance exercise on myocardial function acutely and at restitution. Methods We investigated 10 participants aged 46 ±7 years, before (baseline), within 142 ± 78 minutes after finish (post run) and 5-10 days after (restitution) an ultra-endurance race (3.8 km swimming, 180 km bicycling and 42 km running with a total elevation of 5200 m). Echocardiography was performed at the three time points, including cardiac morphology and -function. Ejection fraction (EF) and stroke volume (SV) were measured by Simpson biplane. Cardiac output was calculated from SV and heart rate (HR). Cardiac power was calculated as the product of CO, mean arterial blood pressure and the conversion factor to Watt (W) 0.00222. Global longitudinal strain (GLS) was calculated using speckle-tracking echocardiography, and myocardial work was calculated by non-invasive pressure-strain analysis. Results Acutely after exercise, myocardial function by GLS (p = 0.002), myocardial work (p &amp;lt; 0.001), mitral annular plane systolic excursion (MAPSE, p = 0.003) and EF (p = 0.004) were substantially reduced compared to baseline, whereas cardiac power and cardiac output (CO) were maintained (see table and figure). Heart rate was moderately increased (p &amp;lt; 0.001). End-diastolic volume (EDV) as an index of preload was numerically, but not significantly reduced. End systolic volume (ESV) was numerically increased (p = NS) even though systolic blood pressure (sBP) was reduced (p = 0.01) post race. After restitution all parameters returned to baseline levels. Conclusions The temporary reduced strain and EF may be a physiologic response due to the higher heart rate. However, despite reduced systolic pressure the heart did not contract to a lower end systolic volume. This suggests loss of contractile function compensated by increase in heart rate. The findings should be explored in further studies. Abstract Figure Abstract Table

267 Cardiac biomarkers and mortality in COVID-19 infection

Abstract Aims The SARS-CoV-2 infection is mostly characterized by acute lung injury. Yet, some COVID-19 patients showed also neurological signs, acute myocardial injury, heart failure, myocarditis, and hypercoagulability, such as pulmonary embolism. Cardiac biomarkers can play an essential role in the diagnosis, management, and prognosis of COVID-19. In fact, during hospitalization, these patients develop biochemical abnormalities, with increasing of all Troponins (TnT), B-type natriuretic peptide (NT-pro-BNP) and creatine kinase-myocardial band (CK-MB) levels. This situation helps us to predict adverse outcomes, especially in patients with cardiovascular comorbidities or risk factors. Data emerged demonstrated a myocardial involvement which determines a high risk of adverse events and increasing of mortality. Methods and results Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such NT-pro-BNP, CK-MB, and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. Our purpose is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes. Results of aforementioned studies underline how cardiac biomarkers are associated with severe form of COVID-19 infection. Above all, higher levels of these biomarkers are significantly associated with an increased risk of the mortality in COVID-19 infected patients. Therefore, has been demonstrated COVID-19 infection is more severe in those patients with a previous history of arterial hypertension, cardiovascular diseases. In addition to classical laboratory parameters evaluated in COVID-19 infection, such as C Reactive Protein (CRP), d-dimer, and lactate dehydrogenase (LDH), which are currently used in clinical practice, others biomarkers could potentially be useful for screening, clinical management, and prevention of serious complications. Therefore, it is clinically significant that fluctuating levels of myocardial biomarkers are closely monitored and patients with high levels of myocardial biomarkers are treated promptly to improve prognosis. At the end, on basis of symptoms and cardiac biomarkers patients could be divided in mild, severe and critical. Conclusions Biomarkers of acute myocardial injury play an important role in predicting worsening prognosis for COVID-19 patients with and without myocardial injury. They are not only predictive of disease severity, but are also helpful for therapeutic management, based on drugs preventing the activation of coagulation processes. It’s important, above all, to identify a laboratory score, made by haematological, inflammatory, biochemical, and immunological parameters, may help to stratify COVID-19 positive patients into risk categories for deciding therapeutic management, thus avoiding cardiac compromise which, as we have previously analysed, is an indication of a poor prognosis.

​Histopathological Grading of Induced Cardiotoxicity Due to Arsenic and its Alleviation by Allium sativum in Ducks

Background: Arsenic present in underground water affects the overall health. The therapeutic effects of Allium sativum was investigated for ameliorating the toxic effects of arsenic exposed ducks. Even though, heavy metals especially arsenic toxicity and ameliorative effects of Allium sativum has been largely studied, yet the histopathological cardiac lesion grading and its correlation with oxidative stress and biochemical parameters is scarce. This study is aimed at evaluating cardiotoxic lesions due to arsenic and ameliorative effects of Allium sativum in accordance with histopathological grading with respect to oxidative and biochemical parameters. Methods: In the present study, 105 birds were randomly distributed in 5 groups. GRP II was given arsenic @ 30 ppm whereas GRP III, IV, V were given Allium sativum @ 0.5 gm/ kg feed, 1 gm/kg feed and 2 gm/kg feed respectively along with arsenic to study the ameliorative effects. At the end of 42 days, 6 birds from each group were slaughtered after blood collection and the extend of arsenic toxicity with Allium sativum effects were studied as biochemical and oxidative parameters with histopathological grading of lesions. The extent of lesions was graded as mild (+), moderate (++) and severe (+++). Result: Grossly, heart revealed dilatation and thickening of ventricular wall in GRP II along with congestion in coronary vessels. In GRP V, grossly heart revealed no congestion and comparatively reduced enlargement. Whereas microscopically, myocardial and epicardial oedema, disruption of muscle fiber and hemorrhage was observed. Along with this, there was increase in cardiac biomarkers - Total serum creatinine kinase (CK), creatine kinase-MB (CK-MB) levels and tissue oxidative parameters (LPO), with decrease in GSH, CAT, total antioxidant and SOD levels in GRP II which was comparably restored in GRP V.

Relationship of the cardiac biomarkers with COVID-19: A review

This review was designed to find out the effect of biomarkers used as predictive signs for the diagnosis of cardiac injury on COVID-19 patients and the probability of death. The current literature has been reviewed and some results considered. A systematic literary research has been conducted in Google Scholar, Web of Science and Pubmed for research starting from the date the disease appeared In December 2019 until the beginning of April 2020, the references used research phrases containing COVID-19 and its relationship to predictive indicators of cardiac injury. The results of the citations showed 8 researches related to this topic that used cardiac biomarkers that are high sensitive Cardiac troponin (Hs-cTn) and Natriuretic peptides (NP), creatine kinase type MB (CK-MB) and high sensitive C-reactive protein(Hs-CRP) and lactate dehydrogenase(LDH) with COVID-19 patients. This review concluded that there was a significant increase in cardiac biomarkers in those with COVID-19 who had a medical history of cardiac injury who were more likely to die.

Suppression of tumorigenicity 2 after exercise: a systematic review.

Exercise is a pivotal physiological activity, associated with benefits. Whilst the importance of physical activity is consensual along different steps of the cardiovascular (CV) continuum, there has been interest in assessing the CV adaptations to vigorous exercise. Indeed, exercise can be associated with increases in cardiac biomarkers, though the scope of this observation remains elusive. Interleukin 1 receptor related protein, Suppression of tumorigenicity 2 (ST2) is a biomarker related to the pathophysiology of fibrosis, having shown promise in the study of heart failure. Knowledge of ST2 kinetics could improve understanding of the mechanistic pathways related to CV adaptations to exercise. To assess the current state-of-the-art concerning ST2 levels after exercise in healthy individuals. A systematic review was carried out on three databases (Pubmed, ISI Web of Science and Scopus), up to October 2020, using the queries "ST2" or "ST-2" + "exercise" or "running". A total of six studies were included in the review, encompassing 349 subjects (73% male gender) in which ST2 was assessed. Most studies reported increases in ST2 levels after exercise. Three studies, encompassing a total of 219 individuals, described a cut-off level of 35 ng/dL for ST2. In these, 92.7% of subjects had ST2 levels above this cut-off after exercise (running in all studies). Most studies report increased levels of ST2 after exercise, with an important number of individuals exceeding the 35 ng/dL threshold. Given the small number of individuals represented and the lack of imaging data and long-term follow-up, further prospective larger studies should target this.