Improved assay of cardiac troponin I is more sensitive than other assays of necrosis markers

OBJECTIVE: Highly sensitive and specific assays of cardiac troponins I and T are the preferred biomarkers in diagnosing myocardial infarction (MI). Assays of cardiac troponin I (cTnI) have been improved with the addition of antibodies against the cTnI molecule and may have increased sensitivity. We hypothesized that a cTnI assay with modern antibody configuration will exhibit equal or better sensitivity in the setting of acute MI compared to cTnT and other markers of myocardial necrosis. MATERIAL AND METHODS: We investigated release kinetics of cTnI (Abbott ADV, Abbott Diagnostics), cTnT (Roche Diagnostics), CKMBmass, myoglobin and heart fatty acid binding protein (H-FABP) in 23 patients admitted with acute ST-segment elevation MI undergoing primary percutaneous coronary intervention. Calibrators for the Abbott ADV cTnI assay are traceable to the United States National Institute of Standards and Technology (NIST) reference material for cTnI. Eleven blood samples were drawn from each patient in the period from admission to 24 h. Biomarkers of necrosis showed marked increases in relative concentrations, especially within the first 2 h after admission. RESULTS: From 30 min after admission onwards, cTnI exhibited significantly higher relative concentrations compared to cTnT, CKMBmass, Myoglobin and H-FABP (p<0.05). CONCLUSIONS: The NIST standardized Abbott TnI ADV assay appears to be more sensitive than cTnT and other biomarkers in the early phase of MI.     

Clinical performance of a new point-of-care cardiac troponin I assay compared to three laboratory troponin assays

BackgroundStudies of cardiac markers in diagnosing acute myocardial infarction (AMI) have mostly been performed using central laboratory platforms. The AQT90 FLEX TnI (troponin I) assay is designed for quantitative point of care testing (POCT). This study evaluated clinical performance in diagnosing AMI of the AQT90 FLEX TnI POCT assay compared with central laboratory troponin assays.MethodsThe study included 458 chest pain patients. Blood samples were obtained on admission and after 6–9 h. Blood was analyzed using the following assays: AQT90 FLEX TnI, Access AccuTnI, Abbott AxSYM ADV, Roche cTnT, Roche CKMBmass. Patients were diagnosed with AMI according to the new universal definition of AMI.ResultsThe performance of the AQT90 FLEX TnI assay on admission was equivalent to the Abbott AxSYM ADV cTnI but inferior to the AccuTnI. After 6–9 h both laboratory based assays were superior. The AQT90 FLEX TnI had a negative predictive value (NPV) of 90 and 96% (admission; 6–9 h). No statistical differences were seen in receiver operating characteristics analysis.ConclusionsThe AQT90 FLEX TnI POCT assay was marginally inferior to the two laboratory based assays of cTnI in diagnosing AMI. A high (NPV) may make this assay suitable as a rule out marker.     

The antibody configurations of cardiac troponin I assays may determine their clinical performance

BACKGROUND: Previous studies have shown superior clinical performance of the cardiac troponin I (cTnI) assay from Beckman-Coulter Diagnostics. This assay had a unique combination of monoclonal antibodies with 2 monoclonal antibodies directed against epitopes near the NH(2) terminus of the heart-specific region of troponin I. The approach has been adopted by the new cTnI assay from Abbott Diagnostics. The aim of our study was to investigate whether this approach affects the clinical performance of cTnI assays. METHODS: Cardiac troponin concentrations were measured in a random sample of patients with unstable coronary artery disease included in the GUSTO IV trial (n = 696) by the AccuTnI (Beckman-Coulter Diagnostics), Architect cTnI (Abbott Diagnostics), Immulite 2500 cTnI (Diagnostics Products Corporation), and Elecsys 2010 cTnT (Roche Diagnostics) assays and related to the 1-year mortality. The primary cutoff concentrations were based on the 99th percentile upper reference limits and an imprecision (CV) < or =10%. RESULTS: The sensitivities of the AccuTnI and Architect cTnI assays in identifying patients who died within 1 year were equal and were significantly higher (P <0.05) than those of the Immulite 2500 cTnI and the Elecsys cTnT assays. The concordance between the AccuTnI and Architect cTnI assays was 97%, but concordances between the Architect cTnI and the Elecsys cTnT assays were 89%-92% with more at-risk patients (P <0.01 to P <0.001) identified by the Architect cTnI assay. CONCLUSIONS: The Architect cTnI assay has clinical performance similar to that of the AccuTnI, probably as a result of the inclusion of a monoclonal antibody against troponin I epitope 41-49 in the assay.     

Improved early risk stratification and diagnosis of myocardial infarction, using a novel troponin I assay concept

BACKGROUND: We evaluated the clinical performance of a novel cardiac troponin I (cTnI) assay specifically designed to improve the very early risk stratification in acute coronary syndromes. SUBJECTS AND METHODS: Serum and plasma samples (taken 0, 6-12 h and 24 h after admission) from 531 patients with suspected acute coronary syndrome were studied using a novel investigational cTnI assay, reference cTnI assay and myoglobin. The lowest cTnI concentration giving a total assay imprecision of 10% was used as the positive myocardial infarction (MI) cut-off value. RESULTS: At the time of admission, the investigational assay was positive in 27.9% of the patients, the reference cTnI assay was positive in only 17.5% (P < 0.001) and myoglobin in 24.1% (P = 0.067). Receiver operating characteristic (ROC) curve analysis for the detection of myocardial injury on admission gave area-under-curve (AUC) values of 0.937, 0.775 and 0.762, respectively (P < 0.001). Of those MI patients who presented within 3 h of symptom onset, 50.0% were identified by the investigational assay at the time of presentation, compared with 44.2% by myoglobin (P = 0.791) but only 11.5% by the reference assay (P < 0.001). CONCLUSIONS: The novel cTnI assay considerably improves the performance of cTnI as an early rule-in biomarker for MI.     

Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology

BACKGROUND: Spurious increases in serum troponins, especially troponin T, have been reported in patients with and without acute myocardial syndromes. METHODS: We studied 78 autopsied patients without clinical myocardial infarction (MI) and correlated histologic cardiac findings with antemortem serum creatine kinase (CK), its MB isoenzyme (CK-MB), cardiac troponin I (cTnI), and cardiac troponin T (cTnT). RESULTS: There was no significant myocardial pathology in 15 patients. Cardiac pathologies were in five groups: scarring from previous MI or patchy ventricular fibrosis (n = 9), recent MI (n = 27), healing MI (n = 7), degenerative myocyte changes consistent with congestive heart failure (CHF; n = 12), and other cardiac pathologies (n = 8). The median concentrations in the five groups were not significantly different for either CK or CK-MB. Compared with the no-pathology group, only the MI group was significantly different for cTnI, and the MI and other pathology groups were significantly different for cTnT. For patients with MI, 22%, 19%, 48%, and 65% had increased CK, CK-MB, cTnI, and cTnT, respectively; for CHF and other cardiac pathologies combined, the percentages were 28%, 17%, 22%, and 50%. For patients with increased cTnI, 72% and 28% had MI and other myocardial pathologies, respectively; patients with increased cTnT had 64% and 36%, respectively. Patients without myocardial pathology had no increases in CK-MB, cTnI, or cTnT. CONCLUSIONS: All patients with increased serum CK-MB, cTnI, and cTnT had significant cardiac histologic changes. The second-generation cTnT assay appears to be a more sensitive indicator of MI and other myocardial pathologies than the cTnI assay used in this study.     

Comparative study of cardiac troponin I and T measurements in a routine extra-cardiological clinical setting.

This study compared troponin I (cTnI) to troponin T (cTnT) in a population admitted to General Medicine Divisions in whom acute myocardial infarction (AMI) was suspected; 98 consecutive patients were included. Diagnoses were made without knowledge of troponin results: 51 patients had AMI, and 47 (including 8 with unstable angina) had no AMI. Patients were considered to be troponin positive if the marker concentration was >99th percentile value of the reference population. Both troponins were associated with an almost absolute sensitivity for AMI (100% for cTnI and 98.0% for cTnT), while the specificity was marginally higher for cTnI (78.7% vs. 68.1%). Increased cTnI and/or cTnT were observed in 15 patients out of 39 without acute coronary syndromes. Simultaneous positivity was seen in 8 patients with severe disorders and complications. Discordances were more frequent in favor of increased cTnT (n = 5) than the opposite (n = 2), even if this difference did not achieve statistical significance. cTnI and cTnT detected AMI with comparable efficiency. Cases without coronary syndrome positively concordant for troponins confirmed the ability of these biomarkers to detect myocardial injury undetectable by conventional diagnostic approaches.     

Effect of elevated concentration of alkaline phosphatase on cardiac troponin I assays.

Troponin I is the regulatory subunit of troponin complex associated with the actin thin filament within muscle cells. Cardiac troponin I (cTnI) is a good marker for diagnosis of myocardial damage. Several immunoassays are available for determination of cTnI in serum. The Stratus cTnI fluorometric enzyme immunoassay (Dade International) uses alkaline phosphatase (ALP) substrate. The microparticle enzyme immunoassay (MEIA) for cTnI (Abbott Laboratories) also uses ALP conjugate. On the other hand, the chemiluminescent assay (CLIA) for cTnI (Bayer Diagnostics) does not use ALP. ALP activity may frequently be elevated in serum of patients being evaluated for suspected myocardial infarction. Therefore, we studied the potential interference of ALP in cTnI assays. Serum pools were prepared from patients, and various concentrations of ALP solution were added to different aliquots. The cTnI concentrations were measured by the Stratus, MEIA, and CLIA assays. We observed no interference of ALP in the MEIA and CLIA assay for cTnI. On the other hand, we observed significant positive interference of ALP when cTnI concentrations were measured using the Stratus.     

Frequency histograms of three high‐sensitivity cardiac troponin assays in a reference population

BackgroundCardiac troponin (cTn) values above the 99th percentile upper reference limit (URL) indicate myocardial injury. We established 99th percentile URLs for three high‐sensitivity cTn (hs‐cTn) assays (Beckman Coulter Access hs‐cTnI, Abbott STAT hs‐cTnI, and Roche Elecsys hs‐cTnT) using a healthy population in Korea.MethodsEach cTn value was measured by three assays and analyzed by dividing by gender and age.ResultsThe frequency histograms of log‐transformed cTn values for Beckman and Abbott assays exhibited a bell‐shaped distribution. The 99th percentile URLs were 9.8, 17.4, and 17.3 ng/L in the total population; 10.9/9.0, 18.9/17.0, and 18.9/17.7 ng/L in the male/female population (p < 0.001 for all three assays); and 11.2/7.2, 19.9/14.5, and 22.7/9.3 ng/L in the older/younger population (p < 0.001 for all three assays) for Beckman, Abbott, and Roche assays, respectively.ConclusionAmong the three assays, bell‐shaped distributions were observed in a frequency histogram of log‐transformed cTn values for healthy population in Beckman and Abbott assays. Also, our findings show that the 99th percentile URLs for cTn levels vary not only by gender but age.     

心肌肌钙蛋白Ⅰ和肌钙蛋白T对急性缺血性心脏病预后相关性分析

目的探讨心肌肌钙蛋白I(cTnI)和肌钙蛋白T(cTnT)对急性缺血性心脏病转归的影响。方法对就诊的急性缺血性心脏病患者定性测定入院时及距胸痛发作间隔10h的cTnI和定量测定相同时点的cTnT。同时随访患者发病后1、3、6、12个月的疾病转归,以心绞痛、心肌梗死、心力衰竭、心源性猝死为终点评价指标。结果cTnI或cTnT异常患者与正常者相比较,不稳定型心绞痛、心肌梗死、心力衰竭、心源性猝死的发生率具有显著性差异(P<0.01)。cTnI或cTnT异常与终点事件(不稳定型心绞痛、心肌梗死、心力衰竭、心源性心源性猝死)发生率呈正相关。结论cTnI或cTnT对急性心肌梗死,尤其是微小心肌坏死诊断具有高度的敏感性和特异性,并与急性缺血性心脏病的预后密切相关。     

Reference values for cardiac troponins T and I in healthy neonates

OBJECTIVES: Cardiac troponins T (cTnT) and I (cTnI) are the most sensitive biochemical parameters in the detection of myocardial damage. In neonates, in utero exposure to tocolytic therapy results in detectable values of cardiac troponins after delivery. Additionally, some preliminary results suggest that the upper reference limits for healthy newborns are higher than those for adults but definitive reference limits for newborns are not available. Our objective was to determine those limits. DESIGN AND METHODS: In this study we investigated the distribution of cTnT and cTnI in cord blood of 869 healthy newborns. cTnT was determined with the 3rd generation assay and cTnI with the Dade Behring assay on a Dimension RxL. For data analysis Student's t test and the Mann-Whitney U test were used. RESULTS: Using the 99th percentile, the upper reference limit in healthy termed newborns was 0.097 microg/l for cTnT and 0.183 microg/l for cTnI. Compared to the adult values, the newborn upper limit was tripled for cTnT and doubled for cTnI. Statistically significant differences were found between males and females for cTnT and between natural childbirth and caesarean section for cTnI. CONCLUSION: Healthy-termed newborns have a higher upper reference limit for both cTnT and cTnI compared to adults. This circumstance must be taken into account when interpreting slightly "elevated" cTnT and cTnI values in newborns.     

A New Time-Saving Apparatus for Paper Electrophoresis

Abstract

Background. Although troponin is a cornerstone biomarker in the assessment and management of patients with acute coronary syndrome, much remains to be learned about the biology of this widely used biomarker, including its post-release modification. Degradation of troponin following release in patients with acute coronary syndrome has been described; however whether such post-release modification occurs in other non-acute coronary syndrome states remains unknown. The aim of this study was to define troponin degradation in patients with acute ischemic stroke. Materials and methods. Troponin I (cTnI) was measured daily during the first 5 days of admission in 244 patients with acute ischemic stroke. Western blot analysis was performed using anti-cTnI antibodies and compared with serum concentrations of cTnI in seven patients and one patient with myocardial infarction (positive control). Results. Elevated levels of troponin were detected in 25 (10 %) patients; in all, both intact cTnI and cTnI degradation products were detected, with up to seven degradation fragments found. Samples with the highest total cTnI levels gave the strongest and most numerous western-blotting bands. All fragments were comparable with the degradation pattern of the positive control in terms of position. Conclusions. Immunoblotting of blood samples from patients with acute ischemic stroke reveals similar degradation patterns of cTnI as has been described in patients with acute myocardial infarction. The biological ramification and potential clinical impact of this finding bears further scrutiny.     

Diagnostic performance of four point of care cardiac troponin I assays to rule in and rule out acute myocardial infarction

ObjectiveThis study evaluated the diagnostic performance of four point-of-care (POC) cardiac troponin I (cTnI) assays compared to a central laboratory cTnI assay for detecting myocardial injury and diagnosing acute myocardial infarction (AMI).Design and methodsPlasma obtained at admission, 3 h, and 6 h post-admission in 169 patients presenting with symptoms suggestive of acute coronary syndrome (ACS) was studied. cTnI concentrations were measured on the Instrumentation Laboratory prototype GEM Immuno, Radiometer AQT90, Mitsubishi PATHFAST, Abbott i-STAT and the Ortho-Clinical Diagnostic Vitros assays. MI was determined based on 99th percentiles according to Universal MI guidelines.ResultsFor ruling in MI at presentation (0 h), the GEM Immuno (sensitivity 63%, specificity 85%) and PATHFAST (sensitivity 53%, specificity 86%) were comparable to the OCD (sensitivity 68%, specificity 81%), and significantly better (p < 0.05) than the AQT90 (sensitivity 26%, specificity 93%) and i-STAT (sensitivity 32%, specificity 92%). cTnI concentrations and serial rising patterns after MI differed by each assay. Negative predictive values were > 90% and ROC AUCs were > 0.90 after 6 h for all assays. Detection of myocardial injury in non-ischemic pathologies accounted for lower than 100% specificity for MI.ConclusioncTnI is a sensitive biomarker for detection of myocardial injury. The analytical variability that exists between POC cTnI assays demonstrates substantial diagnostic differences for ruling in and ruling out MI in patients presenting with symptoms suggestive of ACS.     

血清心型脂肪酸结合蛋白联合心肌肌钙蛋白I在低血糖后心肌损害中的诊断价值

目的研究血清心型脂肪酸结合蛋白(H-FABP)联合心肌肌钙蛋白I(cTnI)在低血糖心肌损害中的诊断价值。方法将2013年5月至2015年5月在该院治疗并出现低血糖的糖尿病患者80例纳入本研究;同期体检且一般资料与研究组匹配的80例健康志愿者为对照组。采集两组受试者的血清并测定H-FABP和cTnI水平。结果心肌损伤组患者0~2h H-FABP出现明显升高,以0~2h各指标水平为标准对心肌损伤进行诊断发现H-FABP+cTnI的诊断效能较高,诊断的灵敏度、特异度、阳性预测值、阴性预测值均明显高于单用H-FABP和cTnI进行诊断的患者。H-FABP+cTnI阳性作为诊断标准的阳性患者48h心肌酶谱水平明显高于单cTnI阳性和H-FABP单阳性作为诊断标准的患者,差异有统计学意义(P0.05)。结论联合HFABP和cTnI诊断心肌损伤,有助于减少心肌损伤的漏诊。     

Lack of concordance between a rapid bedside and conventional laboratory method of cardiac troponin testing: impact on risk stratification of patients suspected of acute coronary syndrome

OBJECTIVES: This study was designed to test the usefulness of a bedside assay as compared to a laboratory method of troponin testing to predict adverse cardiac outcome of chest pain patients. METHODS: We studied 358 ER visits of patients suspected of a non ST-elevation acute coronary syndrome. cTnI (Immulite, DPC) on a lab analyser and cTnT (Cardiac Reader, Roche) at bedside were measured at baseline. The between-assay level of concordance, reporting turnaround times and clinical outcomes during 180 days of follow-up were assessed. Death and myocardial infarction were then evaluated according to troponin result, either concordant negative, discordant or concordant positive. RESULTS: Discordance occurred in 11.4% (41/358) of cases. The proportion of patients with a positive cTnI and negative cTnT result (8.9%) versus the reverse (2.5%) differed significantly (p<0.001). The median time gained using the rapid test was 72 min. The rate of death and/or MI was 25% (10/40) among patients with discordant results as compared to 7.5% (17/228) with a concordant negative result (p<0.001). All patients from the discordant group with an event had a positive cTnI result, while cTnT was negative. CONCLUSION: Patients with a discordant reading were at high risk of adverse cardiac outcome, which was only identified by the laboratory cTnI assay. Markedly, the use of the rapid assay saved time at the expense of clinical sensitivity.     

Serial and single time-point measurements of cardiac troponin T for prediction of clinical outcomes in patients with acute ST-segment elevation myocardial infarction

Background  Cardiac troponins are the preferred biomarkers to predict infarct size in patients (pts) after acute myocardial infarction (AMI). Less information is currently available to verify the prognostic value of such a biomarker surrogate. Methods  We included 82 pts with acute STEMI and compared all single time point and serial cardiac troponin T (cTnT) values (peak and area-under-the-curve) from admission until day 4 to predict future major adverse cardiac events (MACE). Results  Pts who had suffered any MACE during follow-up had higher cTnT values (median (25th/75th percentiles) on day 4 (3.16 μg/l (2.71/5.20) Vs. 2.1 μg/l (1.19/3.96), P = 0.0304), and higher peak cTnT values (5.11 μg/l (3.31/9.47) Vs. 2.92 μg/l (1.81/5.63), P = 0.0234). The likelihood to develop a composite of MACE was twofold higher in the intermediate cTnT tertile (1.66–3.04 μg/l, n = 23), and in the upper cTnT tertile (3.35–20.68 μg/l, n = 23) for cTnT on day 4. For cTnT peak the risk was 1.7-fold higher in the intermediate cTnT peak tertile (2.55–5.01 μg/l, n = 28) and 2.4-fold in the upper cTnT peak tertile (5.11–18.93 μg/l, n = 27). The optimal ROC cutoff for cTnT to predict the composite of MACE was 2.69 μg/l measured on day 4 and 2.85 μg/l for the cTnT peak. Conclusions  A single measurement of cTnT after STEMI is an independent predictor for MACE, performs as effective as serial cTnT sampling and may be useful to assess future events.     

Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction

Background: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of acute myocardial infarction. Serum cTnT is also slightly elevated in patients with severe heart failure and is associated with left ventricular hypertrophy (LVH) in patients treated with haemodialysis. In this study serum cTnT concentrations and echocardiographic findings were investigated in heart failure patients without acute coronary syndrome. cTnT was also compared with other cardiac markers and plasma levels of brain natriuretic peptide (BNP). Methods: Twenty-six patients hospitalized with heart failure were included in the study. Echocardiographic measurements and blood sampling were carried out 12-36?h after admission. Serum cTnT (3rd generation assay), cardiac troponin I (cTnI), creatine kinase MB (CKMB) and CK were measured. Plasma BNP was analysed using the Shionoria assay. LVH was defined as left ventricular mass index (LVMI)&;gt;125?g/m&;lt;formula&;gt;²&;lt;/formula&;gt; for males and&;gt;110?g/m&;lt;formula&;gt;²&;lt;/formula&;gt; for females. Left ventricular systolic function was estimated from the mitral annulus motion (AV-mean LV). Results: Median cTnT was 0.012 (&;lt;0.010-0.032)?μg/L. Sixty-two percent of the patients (16 of 26) had elevated serum cTnT≥0.010?μg/L. cTnT was positively correlated with CKMB (ρ=0.40, p=0.04) and BNP (ρ=0.43, p=0.03), but not with cTnI and CK. A negative correlation was found between cTnT and AV-mean LV (ρ=?0.58, p=0.007), and there was a positive correlation between cTnT and LVMI (ρ=0.44, p=0.03). No other analyte was correlated to LVMI. Conclusions: Serum cTnT but not cTnI was associated with left ventricular dysfunction and LVH in patients hospitalized with heart failure. This explains why cTnT tends to be slightly elevated in patients with heart failure without symptoms of acute myocardial ischaemia.     

Differentiating type 1 and 2 acute myocardial infarctions using the N-terminal pro B-type natriuretic peptide/cardiac troponin T ratio

Purpose

Differentiation of type 1 (T1MI) from type 2 myocardial infarction (T2MI) is important as recommended treatments for each differ. Patients with T2MI may have more/earlier cardiac wall stress resulting in an increased N-terminal pro B-type natriuretic peptide (NT-proBNP)/cTnT generation 5 ratio (cTnT Gen 5).

A sensitive method to quantify human cell-free circulating DNA in blood: relevance to myocardial infarction screening

Objectives

Human cell-free circulating DNA (cf-DNA) derived mainly from cell apoptosis and necrosis can be measured by a variety of laboratory techniques, but almost all of these methods require sample preparation. We have developed a branched DNA (bDNA)-based Alu assay for quantifying cf-DNA in myocardial infarction (MI) patients.

Design and methods

A total of 82 individuals were included in the study; 22 MI and 60 normal controls. cf-DNA was quantified using a bDNA-based Alu assay.

Results

cf-DNA was higher in serum compared to plasma and there was a difference between genders. cf-DNA was significantly higher in MI patients compared to the controls. There was no correlation between cf-DNA and creatine kinase-MB (CK-MB), troponin I (cTnI) or myoglobin (MYO). In serial specimens, cf-DNA was sensitive and peaked earlier than cTnI.

Conclusions

The bDNA-based Alu assay is a novel method for quantifying human cf-DNA. Increased cf-DNA in MI patients might complement cTnI, CK-MB and MYO in a multiple marker format.     

心肌型脂肪酸结合蛋白在急性心肌梗死早期诊断中的价值

目的定量分析心肌型脂肪酸结合蛋白(H-FABP)在早期急性心肌梗死(AMI)诊断中的临床应用价值。方法选择因胸痛而就诊的患者120例,最后将确诊AMI患者69例作为AMI组,非AMI患者51例作为对照组,按胸痛发作距就诊时间分为小于3h、3~6h、6h以上3组。采用免疫比浊法定量测定各组H-FABP的水平,同时检测肌酸激酶同工酶(CK-MB)和超敏肌钙蛋白T(hs-cTnT),比较各指标在诊断AMI早期的敏感度和特异度。结果 AMI组入院后不同胸痛发作时间段的H-FABP水平均高于对照组,差异均有统计学意义(P0.05);AMI组CK-MB和hs-cTnT在胸痛发作3h内检测结果与对照组比较差异无统计学意义(P0.05);在3~6h和6h以上组的检测结果均高于对照组,差异有统计学意义(P0.05)。H-FABP的敏感度在发病3h内和3~6h分别为74.1%与87.5%,高于CK-MB(18.5%、54.1%)和hs-cTnT(14.8%、58.3%),差异有统计学意义(P0.05);发病6h后H-FABP的敏感度为83.3%,低于CK-MB(88.9%)和hs-cTnT(94.4%),但差异无统计学意义(P0.05)。结论 H-FABP定量检测在AMI早期诊断中有较高的敏感度,与其他高特异度指标联合检查可提高AMI的早期诊断准确率。     

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

Objectives

ST-elevation and non-ST-elevation myocardial infarction (STEMI, NSTEMI) are considered two distinct pathophysiologic entities. We evaluated cardiac troponin I (cTnI) release in STEMI and NSTEMI using a “contemporary” (CV > 10 to 20% at the 99th percentile concentration) cTnI assay for patients undergoing early percutaneous coronary intervention (PCI).

Design and methods

856 patients with suspected acute coronary syndrome consecutively admitted to the Emergency Department of the Maggiore Hospital of Novara (225 STEMI and 135 NSTEMI) were selected according to: 1) early (≤ 4 h from admission) and successful PCI; and 2) cTnI measurements at ED presentation and within 24 h. The influence of the MI type on cTnI concentrations at baseline and after PCI as well as the velocity of cTnI [cTnI V = absolute increase (after log conversion of cTnI measurements) / delay between the two measurements] was studied by multiple regression analysis, adjusting for patient parameters.

Results

A statistically significant interaction between MI type and time from symptoms was reported on cTnI concentrations (p < 0.0001): STEMI and NSTEMI differed for cTnI releases at admission and after revascularization. Higher cTnI V in STEMI was detectable in patients admitted within 6 h from symptoms. Baseline cTnI concentrations were lower in patients with a history of coronary artery disease (CAD) and increased with aging (p < 0.0001). In the elderly (> 75 years), the cTnI V was significantly increased.

Conclusion

STEMI and NSTEMI patients have different patterns and dynamics of cTnI release influenced by the interaction with time from symptoms, by aging and history of CAD.