Creatinine Kinase Isoenzyme MB Research Articles

Simultaneous ST-elevation in lead augmented vector right (aVR) and III in non-ST-elevation acute coronary syndromes.

The value of ST-elevation in lead augmented vector right (aVR) remains controversial in clinical practice. This study aimed to investigate the association of simultaneous ST-elevation in lead aVR and III with angiographic findings and clinical outcomes in patients with non-ST-elevation acute coronary syndromes (NSTEACS). In this observational study, patients who had been diagnosed with NSTEACS and presented with ST-elevation in lead aVR and without ST-elevation in any other two contiguous leads were enrolled from January 2018 to June 2019. Demographic, baseline clinical, angiographic and interventional characteristics as well as clinical outcomes were collected and recorded on standardized case report forms. A total of 157 patients meeting the criteria were finally enrolled in this study and classified into two groups according to the presence of ST-elevation in lead III. Patients in the two groups were similar in average age and previous history of hypertension, diabetes mellitus, hyperlipidemia, chronic kidney disease, stroke, and peripheral vascular diseases (all P>0.05). Patients with ST-elevation in lead III tended to present with myocardial hypertrophy in the echocardiography (P=0.02). The cases with ST-elevation in lead III showed higher high sensitivity troponin T (hs-TnT; P=0.08) and creatinine kinase MB isoenzyme (CK-MB; P<0.01) whereas those without ST-elevation in lead III showed higher N-terminal pro brain natriuretic peptide (NT-proBNP; P=0.02). Of note, patients with ST-elevation in lead III presented with more ST-depression in multiple leads [especially in lead I, augmented vector left (aVL), V3-V6] as well as higher degree of ST-depression (all P<0.05) and were more likely to develop multi-vessel and left main trunk (LM) lesions (P=0.04), with 20% of the cases having a LM lesion and 60% having triple vessel lesions. Patients with ST-elevation in lead III were at increased risk of 3-year major adverse cardiovascular events (MACEs), despite no significant statistical difference between the two groups (hazard ratio =1.29; P=0.26). The NSTEACS cases with simultaneous ST-elevation in lead III and aVR tended to present with more multiple leads with ST-depression, higher degree of ST-depression, and more LM or multi-vessel lesions, suggesting a broader range of severe myocardial ischemia. The concurrent presentation of ST-elevation in lead III and aVR may play a vital role in the diagnosis, risk-stratification, and prediction of poor prognosis during the management of NSTEACS patients.

PO-649-01 CARDIAC ENZYME KINETICS AS MARKER FOR MYOCARDIAL DAMAGE AFTER PULSED FIELD ABLATION FOR PAROXYSMAL ATRIAL FIBRILLATION

Cardiac troponin T (cTnT), creatinine kinase (CK) and CK isoenzyme MB (CK-MB) concentrations after catheter ablation reflect the extent of myocardial lesion created. Pulsed field ablation (PFA) is a novel, non-thermal ablation modality that preferentially ablates myocardial tissue, with minimal collateral tissue effect. Therefore, there is no need to reduce ablation power. In preclinical studies, PFA can create deeper and larger myocardial lesions. The amount of myocardial damage due to PVI using PFA is unknown.

MiR-24-3p Attenuates Doxorubicin-induced Cardiotoxicity via the Nrf2 Pathway in Mice.

The nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) is associated with doxorubicin (DOX)-induced cardiac injury. It has been reported that microRNA-24-3p (miR-24-3p) may regulate the Keapl by mRNA degradation, whereas Keapl can suppress the activation of Nrf2. However, the role of miR-24-3p in DOX-related cardiotoxicity remains unclear. The mice receiving DOX were used as cardiac injury model. In this study, an adenoassociated virus 9 system was used to deliver miR-24-3p or miR-scramble to mice hearts. The echocardiographic and hemodynamic analyses were used to evaluate the effects of miR-24-3p on cardiac function under DOX stimulation. ELISA and RT-PCR were used to detect protein or mRNA expressions associated with cardiac injury, inflammation response, apoptosis and oxidative stress. Western Blot were used for quantitative analysis of the roles of miR-24-3p in regulating Nrf2 expression. H9C2 cells used to verify the role of miR-24-3p in vitro. We found that miR-24-3p mRNA was significantly decreased in DOX-treated mice and cardiomyocytes. Overexpression of miR-24-3p blocked cardiac injury caused by DOX injection, as reflected by the reduction in the levels of cardiac troponin I, creatinine kinase isoenzyme MB and the N-terminal pro brain natriuretic peptide. Furthermore, miR-24-3p reduced oxidative stress and cell loss without affecting the inflammation response. As expected, we found that Nrf2 was upregulated by miR-24-3p supplementation, and that the protective efforts of miR-24-3p supplementation were abolished when Nrf2 was silenced. The results from this study suggest that miR-24-3p protects cardiomyocytes against DOX-induced heart injury via activation of the Nrf2 pathway. miR-24-3p supplementation may be a novel strategy to counteract the cardiac side effects of DOX treatment.

Comprehensive Laboratory Data Analysis to Predict the Clinical Severity of Coronavirus Disease 2019 in 1,952 Patients in Daegu, Korea.

BackgroundLaboratory parameter abnormalities are commonly observed in COVID-19 patients; however, their clinical significance remains controversial. We assessed the prevalence, characteristics, and clinical impact of laboratory parameters in COVID-19 patients hospitalized in Daegu, Korea.MethodsWe investigated the clinical and laboratory parameters of 1,952 COVID-19 patients on admission in nine hospitals in Daegu, Korea. The average patient age was 58.1 years, and 700 (35.9%) patients were men. The patients were classified into mild (N=1,612), moderate (N=294), and severe (N=46) disease groups based on clinical severity scores. We used chi-square test, multiple comparison analysis, and multinomial logistic regression to evaluate the correlation between laboratory parameters and disease severity.ResultsLaboratory parameters on admission in the three disease groups were significantly different in terms of hematologic (Hb, Hct, white blood cell count, lymphocyte%, and platelet count), coagulation (prothrombin time and activated partial thromboplastin time), biochemical (albumin, aspartate aminotransferase, alanine aminotransferase, lactate, blood urea nitrogen, creatinine, and electrolytes), inflammatory (C-reactive protein and procalcitonin), cardiac (creatinine kinase MB isoenzyme and troponin I), and molecular virologic (Ct value of SARS-CoV-2 RdRP gene) parameters. Relative lymphopenia, prothrombin time prolongation, and hypoalbuminemia were significant indicators of COVID-19 severity. Patients with both hypoalbuminemia and lymphopenia had a higher risk of severe COVID-19.ConclusionsLaboratory parameter abnormalities on admission are common, are significantly associated with clinical severity, and can serve as independent predictors of COVID-19 severity. Monitoring the laboratory parameters, including albumin and lymphocyte count, is crucial for timely treatment of COVID-19.

Trimetazedine with hyperinsulinimea-euoglycemia, N-acetyl cysteine, and vitamin C: A new approach concept for management of aluminum phosphide poisoning.

Aluminum phosphide (AlP) is commonly used as a powerful suicidal tool. The exact mechanism of acute toxicity has not been well defined despite high mortality rates as well as its supportive treatment including rapid decontamination and institution of resuscitative measures. The current study aimed to investigate a new combination therapy using trimetazidine, N-acetyl cysteine, vitamin C, and hyperinsulinemia-euglycemia to manage acute AlP poisoning. Acute AlP-induced cardiotoxicity, hemodynamic changes, and hepatotoxicity were evaluated using electrocardiogram, creatinine kinase MB iso-enzyme, troponin-1, blood pressure, random blood glucose level, liver function tests, and histopathological changes in both the heart and liver in a rabbit model of AlP poisoning. The results showed that the new regimen therapy ameliorates the toxic effect of AlP with significant improvement in survival, cardiovascular and hemodynamic parameters in addition to histopathological changes. These results highlight the strong cardioprotective, antioxidant, hepatoprotective effects of the new combined therapy along with correction of hemodynamic changes and hyperglycemia as a potential target in the management of acute AlP poisoning.

Assessment of the Effects of SARS-Cov-2 Infection on Multiple Organs Using Laboratory Indices

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is still a severe threaft for human health currently, and the researches about it is a focus topic worldwide.&#x0D; Aim of the study: In this study, we will collect some laboratory results of the patients with coronavirus disease (COVID-19) to assess the function of liver, heart, kidney and even pancreas. &#x0D; Subjects and Methods: Laboratory results of the patients with COVID-19 are collected. The biochemical indices are classified and used to assess the according function of liver, heart, kidney; meantime, and blood glucose is also observed and taken as an index to roughly evaluate pancreas.&#x0D; Results: There were some indices exhibited abnormal. For patient 1, the ratio of albumin and globulin slightly was lower than the down-limit of reference range. For patient 2, alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), creatine kinase (CK), creatinine kinase-MB isoenzyme (CK-MB), lactate dehydrogenase (LDH), alpha-hydroxybutyric dehydrogenase (HBDH), and beta-2 microglobulin (β2-MG) were respectively higher than the according upper limit of the reference range, while prealbumin (PA) was lower than the down limit. For patient 3, GGT, CK, PA were high than normal range. For patient 4, CK, LDH, HBDH were higher than the upper range.&#x0D; Conclusion: Infection of SARS-Cov-2 could cause liver and heart injury, and it is suggested that clinicians and researchers should pay more attention on the prevention, treatment and causative mechanism of such an injury.

Abstract 17007: Cardiac Magnetic Resonance Assessment of Right Ventricular Remodeling After Anthracycline Therapy

Introduction: There are limited data characterizing the effect of anthracyclines on right ventricular (RV) structure and function. Hypothesis: The goal of this study was to test the effect of anthracyclines on RV myocardial remodeling using cardiac magnetic resonance (CMR). Methods: This was a prospective CMR and serum biomarker study of 27 women with breast cancer (BC) (51.8±8.9 years) who underwent a CMR prior, and up to 3-times after anthracycline therapy (240 mg/m 2 ). The primary measure of interest was the RV extracellular volume (ECV) and cardiomyocyte mass index (1-ECV). Additional measures of interest were the left ventricular (LV) ECV, and the LV and RV mass. Biomarkers included high-sensitive troponin T, and creatinine-kinase MB isoenzyme (CKMB). Results: Before anthracyclines, all subjects had normal LV ejection fraction (EF) (69.4±3.6%) and RVEF (55.6±9%). At 351-700 days after anthracyclines, the LVEF and LV mass index declined to 58±6% (P&lt;0.001) and 36±6g/m 2 (P&lt;0.001). Similarly, the RVEF and RV mass index also decreased, reaching 46.3±6.8% at (222-350] days (P&lt;0.001) and 8.13±2g/m 2 at (350-700] days (P&lt;0.001) after anthracycline, respectively (Figure 1). At (350-700] days after anthracycline, both LV and RV ECV increased by 0.037 to 0.36±0.04 (P=0.004) and by 0.12 to 0.40±0.07 (P&lt;0.001), respectively (Figure 2). In parallel, both the LV and RV cardiomyocyte mass also decreased after anthracyclines (Figure 2). Conclusions: In a prospective observational study among women with breast cancer, anthracyclines were associated with a decrease in the RV EF, an increase in the RV ECV and a decrease in the RV cardiomyocyte mass.

P2596Right ventricular function after anthracycline therapy: specificities of myocardial necrosis markers

Abstract Background Anthracycline therapy may induce left ventricle (LV) dysfunction. However, few studies investigated how it may affect the right ventricle (RV). Purpose The goal of this study was to assess RV systolic function and biomarkers that may predict early dysfunction in breast cancer patients treated with anthracyclines. Methods Twenty-seven women with breast cancer (51.8±8.9 years), underwent CMR prior, and up to 3-times after doxorubicin with matching measurements of biomarkers: high-sensitive troponin T (TnT), creatinine-kinase MB isoenzyme (CK-MB) and C reactive protein (CRP). Results Before anthracyclines, all subjects had normal LVEF (69.4±3.6%) and RVEF (55.1±9%) and LV and RV EF correlated significantly (ρ=0.42; p=0.031). At 351–700 days after anthracycline, LVEF and LV mass index declined to 58±6% (P&lt;0.001) and 36±6 g/m2 (P&lt;0.001) (table). RVEF also decreased, reaching 46±8% at 231,4 days after (P&lt;0.001), but lost the correlation with LVEF seen at baseline (r=0.22; P=0.068). RVEF showed strong negative association with serum CK-MB (r=−0.4, p=0.004) and no significant correlation with TnT (r=−0.18, p=0.28) or CRP (r=0.03, p=0.932) (figure). In patients with a peak TnT of &gt;10 pg/ml the change of RVEF overtime was significant (Regression Splines coefficients for RVEF: 1.0, p=0.731–peak TnT ≤10pg/ml; 2.51, p&lt;0.001–peak TnT &gt;10 pg/ml). LVEF was not associated with CK-MB (p=ns). Baseline and Follow-Up CMR Findings Median days after anthracycline Pre-DOX (79,146] (146,231] (231,350] (350,700] N 27 16 19 14 16 LVEF, % 69.4±3.6 61.1±7.6† 55.99±5.0† 53.8±8.4† 57.5±6.1† LVEDV index, ml/m2 60.2±9.9 64.3±9.6 66.7±17.7 * 56.9±18.5 59.2±12.6 LVESV index, ml/m2 18.3±4.0 24.7±7.3# 29.0±7.3† 26.2±9.7† 25.3±8.2† LV mass index, g/m2 51.4±8.0 45.3±3.8† 43.2±4.9† 39.9±5.4† 36.0±6.1† RVEF, % 55.1±9.4 51±8.1 48±8.5 46±8.5 50±7.4 RVEDV index, ml/m2 45.07±6.6 46.5±11.31 47.35±9.16 41.14±9.7 46.16±7.3 RVESV index, ml/m2 20.45±5.4 22.31±5.8 24.77±6.6 21.96±6.4 22.24±4.7 Data are presented as mean ± SD. LV: left ventricle; RV: right ventricle; EF: ejection fraction; EDV: end diastolic volume; ESV: end systolic volume (average±SD). *Significantly different from Pre-DOX level (p&lt;0.05 from linear mixed effects model). #Significantly different from Pre-DOX level (p&lt;0.01 from linear mixed effects model). †Significantly different from Pre-DOX level (p&lt;0.001 from linear mixed effects model). RVEF and correlate variables Conclusions RVEF reduction does not follow LVEF changes after anthracyclines and CK-MB may be a more specific biomarker to assess RV dysfunction. A higher peak cTnT could predict a greater change in RVEF during follow-up.

Transient depression of myocardial function after influenza virus infection: A study of echocardiographic tissue imaging.

BackgroundInfluenza virus infection (IVI) was reported to be associated with minor cardiac changes, mostly those detected on electrocardiogram with and without elevated blood markers of myocardial injury; however, the characteristics of myocardial involvement in association with IVI are poorly understood. This study used echocardiographic tissue imaging (tissue Doppler, strain, and strain rate) to evaluate changes in left atrial (LA) and left ventricular (LV) myocardial function after IVI.Methods and resultsWe examined 20 adult individuals (mean age, 43 years) at 2 and 4 weeks after diagnosis of IVI. For myocardial functional variables, we obtained LV global longitudinal strain (GLS), LV early diastolic strain rate (e'sr), LA strain, and LA stiffness (E/e’/LA strain), in addition to data on tissue Doppler (s’, e’, and a’) and myocardial performance index. Blood markers of myocardial injury were also examined. During follow-up, there were no significant changes in global chamber function such as LV ejection fraction, E/e’, and LA volume. However, significant changes in myocardial function were observed, namely, in s’ (8.0 ± 1.6 cm/s to 9.3 ± 1.5 cm/s; p = 0.01), e’ (10.2 ± 2.8 cm/s to 11.4 ± 3.0 cm/s; p < 0.001), e’sr (1.43 ± 0.44 1/s to 1.59 ± 0.43 1/s; p = 0.005), and LA strain (35 ± 8% to 40 ± 12%; p = 0.025), and the myocardial performance index (0.52 ± 0.20 to 0.38 ± 0.09; p = 0.009), but not in a’, LA stiffness, or GLS. Cardiac troponin T and creatinine kinase isoenzyme MB were not elevated significantly at any examination.ConclusionsMyocardial dysfunction during IVI recovery appeared to be transient particularly in the absence of myocardial injury. Echocardiographic tissue imaging may be useful to detect subclinical cardiac changes in association with IVI.

Comparative effectiveness and safety of xiyanping with ribavirin for rotavirus enteritis therapy in childhood: A systematic review and meta-analysis

Purpose : To employ meta-analysis to assess the effectiveness and adverse events of Xiyanping and ribavirin in children with rotavirus enteritis. Methods : Searches included PubMed, Embase, Medline, Cochrane Library, China National Knowledge Infrastructure (CNKI), China Biology Medicine Database (CBM), China Science and Technology Journal Database (VIP database), and Wanfang database from inception to March 2017. Clinical indicators, with respect to the total effectiveness rate, fever time, duration of diarrhea, creatinine kinase MB isoenzyme (CK-MB), rotavirus (RV) negative conversion rate, and adverse reaction, were compared between Xiyanping and ribavirin groups. Results : Five-hundred and twenty-six records were obtained after searching the databases, and 18 studies (3557 participants) that met the inclusion criteria were included. All of them assessed total effectiveness rate, and two records evaluated RV negative conversion rate. There were significantly higher rates in the Xiyanping group than in the ribavirin group {OR = 3.76, 95 %CI (3.03 - 4.66), p < 0.00001; OR = 2.68, 95 %CI (1.56 - 4.60), p = 0.0004}. Compared with ribavirin group, fever time, duration of diarrhea, and creatine kinase isoenzyme MB (CK-MB) were significantly lower in xiyanping group [MD = -1.23, 95 %CI (-1.64 to -0.81), p < 0.00001; MD= -2.15, 95 %CI (-2.68 to -1.62), p < 0.00001; MD = -16.90, 95 %CI (-17.23 to -16.57), p < 0.00001}. Six studies reported adverse reactions, but there was no significant difference between xiyanping and ribavirin groups {OR = 1.44, 95 %CI (0.40 - 5.17), p = 0.58}. Conclusion : This review suggests that xiyanping is more effective than ribavirin in children suffering from rotavirus enteritis. Keywords : Ribavirin, Rotavirus enteritis, Systematic review, Virazole®, Xiyanping

CARDIOPROTECTIVE EFFECT OF PHYLLANTHUS FRATERNUS LEAVES EXTRACT AGAINST CYCLOPHOSPHAMIDE - INDUCED MYOCARDIAL INJURY IN RATS

Objectives: This study was undertaken to investigate the possible protective effect of aqueous extract of Phyllanthus fraternus (AEPF) leaves against cyclophosphamide (CP) induced myocardial toxicity in rats.Methods: Wistar rats were given CP single intraperitoneally injection (200 mg/kg) on day 1 of the experiment and two doses of AEPF (200 mg/kg and 400 mg/kg) p.o. daily for 10 days. Cardiac biomarker enzymes such as creatinine kinase (CK), CK isoenzyme MB, lactate dehydrogenase, alkaline phosphatase, alanine transaminase, and aspartate transaminase were determined. Histopathological examinations of the hearts were done.Results: CP treated groups exhibited significantly increased in cardiac biomarker enzymes. Treatment with AEPF prevented the elevation of these enzymes. Potential protective effect was also seen in histopathological examination of the heart characterized by decreased myocardium cell damages in AEPF treatment group.Conclusion: The study showed the protective role of AEPF against CP-induced myocardial injury. The possible role of antioxidant activity is anticipated.

Highly sensitive cardiac troponin assays: a comprehensive review of their clinical utility.

Cardiovascular disease is a major source of morbidity and remains the leading cause of death in the United States. To evaluate patients with suspected cardiovascular disease, several laboratory markers of cardiac injury are available including creatinine kinase, creatinine kinase isoenzyme MB, myoglobin, and cardiac troponins (cTn) I and T. cTns have become the preferred marker of cardiac damage because they are highly sensitive and are almost completely cardiac specific. Recently, highly sensitive cTn (hs-cTn) assays were developed and have been used across the world to more quickly and accurately diagnose myocardial infarction. In the United States, these assays have not been U.S. Food and Drug Association approved for clinical practice and therefore are only being used for research purposes. Advancements have taken place over the years in diagnosing and treating cardiovascular disease, but predicting who will suffer future cardiovascular events still remains elusive. A comprehensive review of the literature was conducted to discover how new hs-cTn are being utilized throughout other parts of the world and what potential future use they may serve here in the United States. Major subject points discussed in this article include the prevalence of detectable troponins in the general population, the use of hs-cTn assays in diagnosing a myocardial infarction, determining prognosis in patients who have experienced an acute coronary syndrome and in patients with congestive heart failure, predicting future risk of cardiovascular events in patients with coronary heart disease, and its potential role as a screening tool in primary prevention. The implementation of hs-cTn testing in the United States may be very beneficial to patients; however, more research will need to be done to fully elucidate the potential use of hs-cTn in clinical practice.

Acute cardiac injury events ≤30days after laboratory-confirmed influenza virus infection among U.S. veterans, 2010-2012.

BackgroundCardiac injury is a known potential complication of influenza infection. Because U.S. veterans cared for at the U.S. Department of Veterans Affairs are older and have more cardiovascular disease (CVD) risk factors than the general U.S. population, veterans are at risk for cardiac complications of influenza infection. We investigated biomarkers of cardiac injury characteristics and associated cardiac events among veterans who received cardiac biomarker testing ≤30 days after laboratory-confirmed influenza virus infection.MethodsLaboratory-confirmed influenza cases among veterans cared for at U.S. Department of Veterans Affairs’ facilities for October 2010–December 2012 were identified using electronic medical records (EMRs). Influenza confirmation was based on respiratory specimen viral culture or antigen or nucleic acid detection. Acute cardiac injury (ACI) was defined as an elevated cardiac biomarker (troponin I or creatinine kinase isoenzyme MB) >99 % of the upper reference limit occurring ≤30 days after influenza specimen collection. EMRs were reviewed for demographics, CVD history and risk factors, and ACI-associated cardiac events.ResultsAmong 38,197 patients with influenza testing results, 4,469 (12 %) had a positive result; 600 of those patients had cardiac biomarker testing performed ≤30 days after influenza testing, and 143 (24 %) had one or more elevated cardiac biomarkers. Among these 143, median age was 73 years (range 44–98 years), and 98 (69 %) were non-Hispanic white. All patients had one or more CVD risk factors, and 98 (69 %) had a history of CVD. Eighty-six percent of ACI-associated events occurred within 3 days of influenza specimen collection date. Seventy patients (49 %) had documented or probable acute myocardial infarction, 8 (6 %) acute congestive heart failure, 6 (4 %) myocarditis, and 4 (3 %) atrial fibrillation. Eleven (8 %) had non-cardiac explanations for elevated cardiac biomarkers, and 44 (31 %) had no documented explanation. Sixty-eight (48 %) patients had received influenza vaccination during the related influenza season.ConclusionAmong veterans with laboratory-confirmed influenza infection and cardiac biomarker testing ≤30 days after influenza testing, approximately 25 % had evidence of ACI, the majority within 3 days. Approximately half were myocardial infarctions. Our findings emphasize the importance of considering ACI associated with influenza infection among patients at high risk, including this older population with prevalent CVD risk factors.

Creatinine kinase isoenzyme–MB: A simple prognostic biomarker in patients with pulmonary embolism treated with thrombolytic therapy

BackgroundCreatinine kinase isoenzyme–MB (CK-MB) is a biomarker for detecting myocardial injury. The aim of this study was to evaluate the association between admission CK-MB levels and in-hospital and long-term clinical outcomes in pulmonary embolism (PE) patients treated with thrombolytic tissue-plasminogen activator. MethodsA total of 148 acute PE patients treated with tissue-plasminogen activator enrolled in the study. The study population was divided into 2 tertiles, based on admission CK-MB levels. The high CK-MB group (n = 35) was defined as having a CK-MB level in the third tertile (>31.5 U/L), and the low group (n = 113) was defined as having a level in the lower 2 tertiles (≤31.5 U/L). ResultsHigh CK-MB group had a higher incidence of in-hospital mortality (37.1% vs 1.7%, P < .001). Admission systolic blood pressure and tricuspid annular plane systolic excursion were lower in the high CK-MB group. In the receiver-operating characteristic curve analysis, a CK-MB value of more than 31.5 U/L yielded a sensitivity of 86.7% and specificity of 83.5% for predicting in-hospital mortality. During long-term follow-up, recurrent PE, major and minor bleeding, and mortality rates were similar in both groups. ConclusionCreatinine kinase isoenzyme–MB is a simple, widely available, and useful biomarker for predicting adverse in-hospital clinical outcomes in PE.

Myocardial injury following aortic valve replacement for severe aortic stenosis: risk factor of postoperative myocardial injury and its impact on long-term outcomes.

BackgroundAs hypertrophied myocardium predisposes the patient to decreased tolerance to ischemia and increased reperfusion injury, myocardial protection is of utmost importance in patients undergoing aortic valve replacement (AVR) for severe aortic valve stenosis (AS).MethodsConsecutive 314 patients (mean age, 62.5±10.8 years; 143 females) with severe AS undergoing isolated AVR were included. Postoperative myocardial injury (PMI) was defined as 1) maximum postoperative creatinine kinase isoenzyme MB or troponin-I levels ≥10 times of reference, 2) postoperative low cardiac output syndrome or episodes of ventricular arrhythmia, or 3) left ventricular ejection fraction of less than 55% and decrease in left ventricle (LV) ejection fraction of more than 20% of the baseline value.ResultsThere were 90 patients (28.7%) who developed PMI. There were five cases of early death (1.6%), all of whom had PMI. On multivariable analysis, the use of histidine-tryptophan-ketoglutarate (HTK) solution instead of blood cardioplegia (odds ratio [OR], 3.06; 95% confidence interval [CI], 1.63 to 5.77; p=0.001), greater LV mass (OR, 1.04; 95% CI, 1.01 to 1.07; p=0.007), and increased cardiac ischemic time (OR, 1.13; 95% CI, 1.05 to 1.22; p<0.001) were independent predictors for PMI. Patients who had PMI showed significantly inferior long-term survival than those without PMI (p=0.049).ConclusionPMI occurred in a considerable proportion of patients undergoing AVR for severe AS and was associated with poor long-term survival. HTK cardioplegia, higher LV mass, and longer cardiac ischemic duration were suggested as predictors of myocardial injury.

Rapid Identification of Falsely Elevated Serum Cardiac Troponin I Values in a Stat Laboratory

To establish a rapid method for the stat laboratory to identify falsely elevated serum cardiac troponin I (cTnl) values caused by endogenous interferences. Serum specimens with elevated cTnI were recentrifuged and cTnI was measured again. If the difference between first and second cTnI value was less than +/- 30%, the specimen was diluted 1:2, 1:5, and 1:10, and the cTnI was measured in the diluted specimens. If the cTnI concentrations did not change linearly with dilution, the specimen was referred to an outside lab for re-analysis of cTnI by a different immunochemical method. Troponin I was elevated in 132 serum specimens. In 18 specimens, we attributed the elevation to the presence of fibrin or microparticles in the serum. Serial dilutions of 3 of the 114 remaining specimens produced nonlinear results. Overall, falsely elevated cTnI results were identified in 1.01% of all measurements. Our method, which uses combined measurement of cTnI, creatinine kinase MB isoenzyme (CK-MB), and myoglobin, together with incubation, re-centrifugation, and serial dilution, is a practical method to identify falsely elevated serum cTnI values.

Influence of Repeated Bouts of Table Tennis Training on Cardiac Biomarkers in Children

It is documented that exercise can increase serum cardiac troponins in adults and adolescents; however, there is a lack of related studies concerning the release of cardiac troponins in children. This study investigated the influence of table tennis training on cardiac biomarkers in children. Twenty-eight male children performed six 10-min forehand exercise sessions with 5-min recovery intervals. Serum cardiac troponin T (cTnT) and I (cTnI), and creatinine kinase isoenzyme MB (CK-MB) were assessed before exercise, immediately after the last 10 min of exercise (PEI), 4 h post-exercise (PE4), 24 h post-exercise (PE24), and 48 h post-exercise (PE48). Cardiac function was measured using an ultrasound system (GE Vivid7 Dimension) at rest state. Serum cTnT, cTnI, and CK-MB were significantly elevated from the PEI sample point, and returned to baseline at the PE48 sample point in children. Serum cTnT in four (14.29%), nine (32.14%), and two (7.14%) subjects at the PEI, PE4, and PE24 sample points, respectively, exceeded the cutoff for myocardial injury. At the PE4 sample point, cTnT in five subjects (17.86%) exceeded the cutoff for acute myocardial infarction. Serum cTnI in two (14.29%), seven (25%), and two (7.14 %) subjects at the PEI, PE4, and PE24 timepoints, respectively, exceeded the cutoff for myocardial injury. cTnI in two subjects (7.14%) exceeded the cutoff for acute myocardial infarction at the PE4 timepoint in children. Repeated bouts of table tennis forehand training can significantly increase the release of serum cardiac troponins in some children.

Ventricular septal rupture after blunt chest trauma

Ventricular septal rupture (VSR) is a rare complication of blunt chest trauma. The commonest effect of this non-penetrating injury of the thorax is pulmonary and myocardial contusion. We present the case of a 30-year-old man with post-traumatic ventricular septal rupture. Two days earlier he fell from a roof (about 4 m high) and was admitted to the emergency department of the regional hospital. On admission, he was fully conscious and by virtue of his left forearm being broken he was referred to the surgical department, where his left radius bone was attended to. Several hours later, the patient’s general clinical condition started gradually worsening. Symptoms of progressive pulmonary failure were observed, and eventually he was intubated and mechanically ventilated. Moreover, due to cardiac status deterioration, an echocardiographic examination was performed urgently and muscular VSR with left-to-right flow was visualised (Fig. 1). After this diagnosis was established, the patient was referred emergently to our Cardiosurgical Department. On admission he was mechanically ventilated and deeply unconscious with no reaction to pain. At that time no sedation was employed. Moreover, he required marked doses of positive inotropic agents (dobutamine and dopamine). By virtue of serious neurological status, he was disqualified from salvage cardiac surgical procedure. In transthoracic echocardiographic examination, a rupture in the middle, muscular part of the ventricular septum, about 10–12 mm in diameter, 40 mm from the mitral annulus and 30 mm from the apex, with accompanying left-right flow velocity of approximately 2.0 m/s was visualised. In the meantime, computed tomo graphy (CT) angiography was performed, which revealed normal thoracic aorta. Abdomen ultrasonography did not reveal serious abnormalities. Hypotonia (RR 70/40 mm Hg) was observed from the beginning and it was accompanied by high fever (up to 40°C). Several laboratory cardiac necrosis marker tests, such as cardiac troponin I, and creatinine kinase MB isoenzyme confirmed cardiac injury. Soon after admission, an intra-aortic balloon pump (IABP) was inserted through the puncture of the right femoral artery and continuous veno-venous haemofiltration (CVVH) was initiated due to renal failure with oliguria. In spite of the aggressive treatment with IABP and CVVH, the patient developed multi-organ failure including liver (alanine aminotransferase activity increased up to 8,328 IU/L and asparagine aminotransferase to 2,406 IU/L). A head CT (Fig. 2) revealed diffuse axonal injury, extensive post-traumatic changes in the form of significant swelling of the brain, overall tightening of the subarachnoid space in the third and fourth ventricles and also in the lateral ventricles. Disseminated air zones were found in the subcortical white matter. Small haemorrhagic changes were revealed in the right cerebellar hemisphere and single small (4 mm) changes were present in the frontal lobes. On the basis of the patient’s general status, and the results of imaging studies, the patient was disqualified from invasive treatment of VSR. On the seventh day of hospitalisation in the Department, the patient’s general condition rapidly worsened, hypotension non-responsive to increased doses of catecholamines appeared, and the patient developed coagulopathy. One day later, the patient developed progressive bradycardia and hypotension. Eventually, in spite of pharmacological resuscitation, he did not respond and he died.

Does leukocyte-depleted blood cardioplegia reduce myocardial reperfusion injury in cardiac surgery? A systematic review and meta-analysis

Blood cardioplegia in cardiac surgery contains leukocytes, which causes the inflammatory reaction and promotes myocardial reperfusion injury. The removal of leukocytes from the cardioplegia line, using specialized filters, has been proposed as one of the effective methods in attenuating the inflammatory response. We performed a two-level search to identify randomized, controlled trials concerning the effects of leukocyte-depleted blood cardioplegia on myocardial reperfusion injury. Sixteen studies, comprising 738 patients, met the selection criteria. There are significant reductions in creatinine kinase isoenzyme MB (CK-MB) during 4-8h postoperatively (SMD - 0.577; 95% CI -0.795 to -0.358; p=0.000), CK-MB peak (SMD - 0.713; 95% CI -1.027 to -0.400; p=0.000), troponin in the period of 4-8h postoperatively (SMD - 0.502; 95% CI -0.935 to -0.069; p=0.023), troponin peak (SMD - 0.826; 95% CI -1.373 to -0.279; p=0.003) and inotropic support (RR, 0.500; 95% CI 0.269 to 0.931; p=0.029). Leukocyte-depleted blood cardioplegia may reduce myocardial reperfusion injury in the early postoperative period, but there has been no evidence to support the clinically significant difference. Larger and more precise randomized control trials are needed to further elucidate the cardioprotective effects of cardioplegia leukofiltration.

Extrinsic Compression of the Left Anterior Descending Coronary Artery by Rib in a Patient With Progressive Left Ventricular Remodeling

A 78-year-old man with a history of dilated cardiomyopathy diagnosed 5 years previously was admitted to our clinic with accelerating chest pain and dyspnea. The initial ECG showed sinus tachycardia and left bundle-branch block. Laboratory tests revealed elevated levels of troponin T (0.409 ng/mL), creatinine kinase (218 U/L), and creatinine kinase-MB isoenzyme (9.8 μg/L). The peak level of creatinine kinase-MB isoenzyme was 41.9 μg/L. Transthoracic echocardiography revealed a more progressed left ventricular remodeling in comparison with an echocardiography conducted 2 years previously. Compared with the previous study, the end-diastolic dimension of the left ventricle (LV) was increased from 68 mm to 76 mm and the LV end-diastolic volume was increased from 199 mL to 331 mL. Previously, the LV showed global hypokinesia with decreased global LV systolic function (ejection fraction=30%). The present study showed worsened regional wall motion abnormality at the territories of the left anterior descending coronary artery (LAD) with aggravated LV dysfunction (ejection fraction=23%; online-only Data Supplement Movies I and II). Coronary angiography revealed an unusual obstruction of the distal LAD (Figure 1). In the course of distal LAD, a filling defect, evident as …