Comparison of Troponin T to creatine kinase and to radionuclide cardiac imaging infarct size in patients with ST-elevation myocardial infarction undergoing primary angioplasty

Troponin is used mainly for detection of minor myocardial damage, whereas repeated measurements of creatine kinase (CK) and myocardial band (CK-MB) are used for assessing infarct size in patients with myocardial infarction. The purpose of this study was to correlate peak level and area under the curve (AUC) of troponin T to that of CK and CK-MB and with single-photon emission computed tomographic infarct size and left ventricular function in patients with ST elevation myocardial infarction. In this multicenter study (29 centers, 5 countries), we included 267 patients who underwent primary coronary intervention within 6 hours of onset of symptoms. All had repeated measurements of troponin T, CK, and CK-MB. Infarct size and left ventricular function were assessed by single-photon emission computed tomography performed on days 7 and 30. Mean infarct sizes were 14% on day 7 and 10% on day 30, and mean ejection fractions were 42% on day 7 and 45% on day 30 after the acute infarct. Very high correlation (r >0.85, Spearman correlation) was found between peak level and AUC of troponin T, CK, and CK-MB. Similar high correlation was found between peak level and AUC of troponin, CK, and CK-MB with single-photon emission computed tomographic infarct size (r >0.70). In conclusion, based on the results of this multicenter study, we suggest that peak levels and AUC of troponin are as accurate as CK and CK-MB in estimating myocardial infarct size.     

急性ST段抬高心肌梗死患者白细胞计数与肌酸激酶同工酶及肌钙蛋白T峰值的相关分析

目的探讨急性ST段抬高心肌梗死(ST-elevation myocardial infarction,STEMI)患者入院即刻WBC计数与肌酸激酶同工酶(CK-MB)及肌钙蛋白T(cTnT)峰值的相关性,及WBC作为心肌坏死面积大小指标的可靠性。方法连续入选2010年1月～2011年6月就诊于北京友谊医院的初发STEMI患者212例,按入院即刻外周血WBC水平分为正常组(WBC<10×10~9/L)120例,升高组(WBC≥10×10~9/L)92例。比较2组患者CK-MB及cTnT峰值的差异,并分析WBC与CK-MB、cTnT峰值的相关性。结果与正常组比较,升高组患者舒张压、TG、CK MB及cTnT峰值明显升高,差异有统计学意义(P<0.05,P<0.01);多元逐步回归分析显示,WBC与CK-MB和cTnT峰值呈正相关(r=0.636,r=0.539,P<0.05)。结论 STEMI的入院即刻WBC水平与CK-MB及cTnT峰值升高程度呈显著线性正相关,WBC是反应STEMI患者心肌坏死面积大小的良好指标。     

Biomarker assessment for early infarct size estimation in ST-elevation myocardial infarction

BackgroundHigh-sensitivity cardiac troponin T (hs-cTnT) represents the biomarker of choice for infarct size (IS) estimation in patients with acute ST-elevation myocardial infarction (STEMI). However, admission values of hs-cTnT are only weakly associated with IS. The aim of this study was to investigate the incremental value of different biomarkers measured on admission for IS estimation in STEMI patients.MethodsIn this prospective observational study, we included 161 consecutive STEMI patients treated with primary percutaneous coronary intervention (pPCI). The following biomarkers were assessed on admission: hs-cTnT, N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) and neutrophil/lymphocyte ratio (NLR). IS was determined by cardiac magnetic resonance (CMR) imaging 3 (Interquartile range [IQR] 2 to 4) days after the index event.ResultsPatients with large IS (>19% of left ventricular myocardium) showed significantly higher levels of admission hs-cTnT (399.6 vs. 53.4 ng/L, p < .001), NT-pro-BNP (140 vs. 86 ng/L, p = .008) and NLR (6.4 vs. 4.1, p < .001). The combination of hs-cTnT, NT-pro-BNP and NLR on admission resulted in a significantly higher area under the curve (0.78; 95% CI 0.704 to 0.838, (p = .01)) for the prediction of large IS than admission hs-cTnT alone (0.69; 95% CI 0.619 to 0.767).ConclusionsIn STEMI patients undergoing pPCI, a comprehensive biomarker approach on admission including hs-cTnT, NT-pro-BNP and NLR was significantly better for immediate infarct severity estimation as compared to hs-cTnT alone.     

Scintigraphic quantification of myocardial necrosis in patients after intravenous injection of myosin-specific antibody

The Fab fragments of antimyosin antibodies, labeled with 99mTc, were used in the scintigraphic examination of 30 patients with myocardial infarction. The ability to detect necrosis and determine its extent from the antimyosin scan were compared with the results of quantitative regional wall motion analysis by contrast ventriculography at 10 to 14 days and 99mTc-pyrophosphate imaging. Antimyosin images recorded by planar and single photon-emission computed tomography (SPECT) delineated areas of myocardial necrosis in 27 of 30 patients (90%) compared with a 91% sensitivity of pyrophosphate in 21 of 23 patients. Infarct size was determined by both antimyosin and pyrophosphate SPECT images. Results by both techniques showed a significant correlation with computer-derived hypokinetic segment length (r = .79 for both, p = .002) and peak creatine kinase (r = .9 for both, p less than .01). Although sensitivity for and correlations with markers of necrosis were similar with both techniques, infarct size by pyrophosphate SPECT was 1.7 times larger than infarct size by antimyosin SPECT (p less than .01). Certain zones in the infarct area were differentially labeled; the nature and irreversibility of injury within these zones remains to be clarified.     

Cardiac troponin T at 96 hours after acute myocardial infarction correlates with infarct size and cardiac function.

OBJECTIVES: In clinical practice, myocardial infarct size can be estimated non-invasively by nuclear imaging techniques or contrast-enhanced magnetic resonance imaging (CE-MRI). Due to limited availability and high costs, serologic tests are frequently used as an alternative. BACKGROUND: We examined the ability of a single value of cardiac troponin T (cTnT) 96 h after onset of ST-/non-ST-segment elevation myocardial infarction (STEMI/NSTEMI) to estimate absolute infarct mass. METHODS: Functional and CE-MRI were conducted on a 1.5-T whole-body system 4 days after STEMI/NSTEMI using gadolinium (0.2 mmol/kg/bw). Infarct sizes were measured employing a specified software (Philips Medical Systems, Best, the Netherlands) and correlated with TnT measurements 96 h after onset of STEMI/NSTEMI. RESULTS: We enrolled 23 STEMI and 21 NSTEMI patients. Median time delay from onset of symptoms to balloon angioplasty was 6.25 and 9.9 h for STEMI/NSTEMI patients, respectively. Contrast-enhanced magnetic resonance imaging (median 4 days) revealed an absolute mean infarct size of 16.2 g (7.7 to 30.1 g) with a mean ejection fraction of 58% (53% to 63%) and mean stroke volume of 84 ml (75 to 107 ml). Absolute infarct sizes and median cTnT values were larger in STEMI than in NSTEMI (29.3 g [interquartile range (IQR) 16.0 to 53.0] and 1.88 microg/l [IQR 0.7 to 2.57] vs. 8.8 g [IQR 3.3 to 16.4] and 0.83 microg/l [IQR 0.4 to 1.3], both p < 0.02). Linear regression analysis was excellent for STEMI (r = 0.910) and moderate albeit still significant for NSTEMI (r = 0.575). CONCLUSIONS: A single 96-h cTnT value provides an accurate estimate of absolute infarct mass in myocardial infarction. The ability to quantify and the potential to distinguish effects of novel drug regimens on infarct size make cTnT attractive for routine practice and as a clinical end point.     

Possible reasons for the prognostic value of troponin-T on admission in patients with ST-elevation myocardial infarction

BACKGROUND: In patients with acute myocardial infarction and ST-segment elevation, increased troponin-T (TnT) on admission implies an increased mortality. OBJECTIVE: To elucidate the underlying mechanisms of the prognostic value of TnT. METHODS AND RESULTS: One hundred and one patients were included and all received thrombolytic treatment. The patients were compared according to TnT level on admission (cut-off 0.1 microg/l). Elevation of TnT was associated with long-term mortality and also with longer delay, more episodes of chest pain during the last 24 h and fewer noninvasive signs of reperfusion at 90 min. In the group with elevated TnT, the coronary angiography at 24 h showed a strong trend towards lower patency in the infarct-related artery. TnT was also associated with increased infarct size if a higher cut-off level (0.43 microg/l) was used. In univariate analysis, elevated TnT, longer delay, repeated chest pain, Q-waves on admission and reduced left ventricular (LV) function were significantly associated with long-term mortality. In multivariate models, only reduced LV function and less than TIMI (thrombolysis in myocardial infarction) grade 3 flow turned out to be significant independent risk factors. CONCLUSIONS: The prognostic value of TnT level on admission regarding long-term mortality was confirmed and seems mainly to be explained by its association with longer delay and recent myocardial damage, but its association with reduced effect of thrombolytic treatment, larger infarct size and impaired LV function might also be of importance.     

Frequency and significance of troponin T elevation in acute ischemic stroke

Elevated levels of troponin have been reported in patients with acute ischemic stroke. In this prospective study, the prevalence and characteristics of troponin elevation were examined in 244 patients with acute ischemic stroke but without overt ischemic heart disease. Troponin T (TnT) and creatine kinase-MB (CK-MB) concentrations were measured and 12-lead electrocardiograms obtained daily during the first 5 days of admission. Myocardial perfusion scintigraphy was performed in patients with TnT levels of 0.10 micro g/L and in comparable controls without elevation of TnT. Patients were followed for a mean of 19 +/- 7 months, with all-cause mortality as the clinical end point. Elevated levels of TnT (>0.03 micro g/L) and creatine kinase-MB (> or =10 micro g/L) were observed in 10% and 9% of patients, respectively. Patients with elevated TnT had higher frequencies of heart and/or renal failure. Perfusion abnormalities on myocardial perfusion scintigraphy at rest were not more frequent or pronounced in patients with TnT levels of > or =0.10 micro g/L than in the control group. Only 7 patients (3%) had elevations of TnT or creatine kinase-MB and electrocardiographic changes suggesting acute myocardial infarctions. According to univariate and multivariate analyses, elevation of TnT was significantly associated with mortality. In conclusion, elevated levels of TnT are rare in patients presenting with ischemic stroke but without overt ischemic heart disease. Heart and renal failure rather than myocardial infarction are the most likely causes. When present, elevation of TnT seems to be useful in identifying patients who are at increased risk of dying within the following 2 years.     

Takotsubo cardiomyopathy has a unique cardiac biomarker profile: NT-proBNP/myoglobin and NT-proBNP/troponin T ratios for the differential diagnosis of acute coronary syndromes and stress induced cardiomyopathy

Background

Takotsubo cardiomyopathy (TC) usually is not recognized until heart catheterization reveals typical wall motion abnormalities in the absence of significant coronary artery disease. It was our aim to identify TC by its unique cardiac biomarker profile at an early stage and, preferably, with non-invasive procedures only.

Methods

Ratios of N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and myoglobin, NT-proBNP and troponin T (TnT), NT-proBNP and creatinekinase-MB (CK-MB) were compared in patients with TC (n = 39), patients with ST-elevation myocardial infarction (STEMI, n = 48) and patients with non-ST-elevation myocardial infarction (NSTEMI, n = 34). Biomarkers were recorded serially at admission and at the three consecutive days. Optimal cut-off values to distinguish TC from STEMI and NSTEMI were calculated with receiver operator characteristic (ROC) curves.

Results

At admission a NT-proBNP (ng/l)/myoglobin (μg/l) ratio of 3.8, distinguished TC from STEMI (sensitivity: 89%, specificity: 90%), while a NT-proBNP (ng/l)/myoglobin (μg/l) ratio of 14 separated well between TC and NSTEMI (sensitivity: 65%, specificity: 90%). Best differentiation of TC and ACS was possible with the ratio of peak levels of NT-proBNP (ng/l)/TnT (μg/l). A cut-off value of NT-proBNP (ng/l)/TnT (μg/l) ratio of 2889, distinguished TC from STEMI (sensitivity: 91%, specificity: 95%), while a NT-proBNP (ng/l)/TnT (μg/l) ratio of 5000 separated well between TC and NSTEMI (sensitivity: 83%, specificity: 95%).

Conclusions

TC goes along with a singular cardiac biomarker profile, which might be useful to identify patients with TC among patients presenting with acute coronary syndromes (ACS).     

Comparison of MB fraction of creatine kinase mass and troponin I serum levels with necropsy findings in acute myocardial infarction

Serum levels of troponin and heart-related fraction of creatine kinase (CK-MB) mass are used as diagnostic and prognostic criteria in myocardial infarction, but the relation between those levels and the necropsy-determined size of necrosis has not been tested in human beings. In this retrospective study, 1-cm-thick transverse sections of the ventricles were cut from the base to the apex in the necropsy hearts of 27 patients aged 47 to 86 years (mean 66, median 69; 19 men). Total and necrotic areas were measured using a computer-linked image analysis system. The weights of the necrotic areas were also calculated. The correlations of the areas and weights of necrotic myocardium with the highest serum values of CK-MB mass and troponin I, which had been quantified during life by chemiluminescence immunoassays, were verified by Pearson's test; results were considered significant at p相似文献   

Cardiac magnetic resonance imaging study for quantification of infarct size comparing directly serial versus single time-point measurements of cardiac troponin T.

OBJECTIVES: We compared single-point cardiac troponin T (cTnT) measurements with parameters from serial sampling during 96 h after acute myocardial infarction with magnetic resonance imaging measured infarct mass. BACKGROUND: Contrast-enhanced magnetic resonance imaging (CE-MRI) allows exact quantification of myocardial infarct size. Clinically, measurement of cardiac biomarkers is a more convenient alternative. METHODS: The CE-MRI infarct mass was determined 4 days after primary percutaneous coronary intervention in 31 ST-segment elevation myocardial infarction (STEMI) and 30 non-ST-segment elevation myocardial infarction (NSTEMI) patients. All single-point, peak, and integrated area under the curve (AUC) cTnT values were plotted against CE-MRI infarct mass. RESULTS: All single-point and serial cTnT values were significantly higher in STEMI than in NSTEMI (p < 0.01) patients. Except for the admission values, all single-point values on any of the first 4 days, peak cTnT and AUC cTnT were found to correlate comparably well with infarct mass. Among single-point measurements, cTnT on day 4 (cTnTD4) showed highest correlation and performed as well as peak cTnT or AUC cTnT (r = 0.66 vs. r = 0.65 vs. r = 0.69). Receiver-operator characteristic analysis demonstrated that cTnTD4 >0.84 microg/l predicted infarct mass above median as well as peak cTnT >1.57 microg/l or AUC cTnT (receiver-operator characteristic for AUC: 0.839 vs. 0.866 vs. 0.893). However, estimation of infarct mass with cTnTD4, peak cTnT, and AUC cTnT was worse in patients with NSTEMI (r = 0.36, r = 0.5, r = 0.36) than in STEMI (r = 0.75 vs. r = 0.65 vs. r = 0.76). CONCLUSIONS: All single-point cTnTs, except on admission, give a good estimation of infarct size and perform as well as peak cTnT or AUC cTnT. Infarct estimation by single-point measurements, particularly cTnTD4, may gain clinical acceptance because the measurement is easy and inexpensive.     

急性心肌梗死溶栓疗效判断中血清酶测定时间的合理选择

目的　适时合理选择急性心肌梗死 (AMI)溶栓疗效判断中血清酶学指标。方法　回顾性分析 145例AMI溶栓患者血清酶学及心肌肌钙蛋白T(TnT)资料 ,其中男 10 7例 ,女 38例 ,平均年龄 (6 1 9± 9 3)岁。以无创指标判断溶栓成功者 110例 ,未成功者 35例。 6 5例行冠脉造影 ,梗死相关血管 (IRA)开通者 44例 ,未开通者2 1例。 5 9例同时测定TnT。结果　 (1)TnT首次异常检出率 84 7% ,高于肌酸磷酸激酶 (CK)同功酶 (CK -MB)(4 9 2 % ) (P <0 0 5 )。 (2 )溶栓成功、IRA开通者与溶栓未成功、IRA未开通者间CK/CK -MB峰值无显著性差异 (P >0 0 5 )。结论　 (1)TnT用于AMI心肌损伤早期诊断优于CK -MB。 (2 )CK/CK -MB峰值前移与溶栓成功与否、IRA开通与否有关 ,而CK/CK -MB峰绝对值与此无直接关系。对早期溶栓的AMI患者不必过早取血测定CK/CK -MB ,而在发病后 16～ 2 0h间取血测定即可满足判断酶峰是否前移的需要 ,从而减轻病人痛苦和经济负担。     

Kinetics of C-reactive protein release in different forms of acute coronary syndrome

INTRODUCTION AND OBJECTIVES: Better knowledge of C-reactive protein (CRP) kinetics could lead to improved clinical application of this biomarker. METHODS: We studied 110 patients: 42 had ST-elevation acute myocardial infarction (STEMI), 35 had non-ST-elevation acute myocardial infarction (NSTEMI), and 33 had unstable angina. Patients were admitted to our institution within 6 hours of symptom onset. The levels of CRP, troponin-I, and creatine kinase MB fraction (CK-MB) were measured on admission and every 6 hours during the first 48 h. The CRP level was also measured daily until hospital discharge. RESULTS: The median (interquartile range) CRP level increased relative to baseline from 6 hours after admission, from 5 (2-9) mg/L to 6 (3-10) mg/L (P=.004). Although, CRP levels on admission were similar in all groups, there was a significant difference in peak CRP level: it was 67 (36-112) mg/L in the STEMI group, 29 (20-87) mg/L in the NSTEMI group, and 18 (12-36) mg/L in the unstable angina group. The maximum CRP level was observed 49 (38-53) hours after the onset of symptoms, but occurred later in patients with STEMI. Although there was only a weak non-significant correlation between CRP and troponin levels (r=0.135) at admission, the maximum CRP level was found to be influenced by the degree of myocardial damage (r=0.496; P< .001). CONCLUSIONS: The pattern of CRP release observed was clearly different in different forms of acute coronary syndrome. Although the CRP level measured at admission was similar in all patient groups, it was influenced by the degree of early myocardial tissue necrosis. This variation in CRP kinetics should be taken into consideration when designing future studies.     

Impact of duration of ischemia on left ventricular diastolic properties following reperfusion for acute myocardial infarction

We sought the correlation between duration of myocardial ischemia and severe left ventricular (LV) diastolic dysfunction (restrictive filling pattern [RFP]) in patients with acute ST-elevation myocardial infarction (STEMI). Duration of ischemia determines infarct size and survival after STEMI. However, the impact of duration of ischemia on LV diastolic function has not been previously studied. Ninety-five consecutive patients with first-ever STEMI underwent transthoracic echocardiography 3 days after primary percutaneous coronary intervention (PCI). RFP was defined as a mitral inflow E/A ratio >2.0 and/or E-wave deceleration time <140 ms. Composite major adverse cardiovascular events (death, reinfarction, heart failure, revascularization) were determined at 12 months. Twenty patients (21%) had RFP on day 3. Symptom-to-reperfusion time in the RFP group was 413 ± 287 versus 252 ± 138 minutes in the non-RFP group (p = 0.014). Peak troponin T levels were higher in the RFP group (12.2 ± 8.4 vs 5.7 ± 3.6 ng/ml, p = 0.002). Logistic regression identified symptom-to-reperfusion time (hazard ratio 1.02, 95% confidence interval 1.01 to 1.03, p = 0.010) and infarct size by peak troponin T levels (hazard ratio 1.54, 95% confidence interval 1.14 to 2.10, p = 0.005) as independent predictors of RFP. Major adverse cardiovascular events occurred in 10 patients (50%) in the RFP group and 6 patients (8%) in the non-RFP group. On multivariate Cox proportional hazards analysis, RFP was an independent predictor of major adverse cardiovascular events at 12 months (hazard ratio 5.43, 95% confidence interval 1.52 to 19.39, p = 0.001). In conclusion, delayed reperfusion after STEMI was associated with severe LV diastolic dysfunction, which in turn independently predicted adverse long-term outcomes. LV diastolic dysfunction represents a significant pathophysiologic link among duration of myocardial ischemia, infarct size, and outcomes.     

ST段抬高型急性心肌梗死患者入院时心电图表现的临床意义

目的:评价ST段抬高型急性心肌梗死(STEMI)患者入院时心电图缺血程度(ST段抬高和QRS波终末扭曲)对梗死范围和住院期间病死率判断的价值。方法:入选STEMI患者122例,发病时间均在12h以内,根据入院时心电图表现分为非QRS波终末扭曲组(n=73)和QRS波终末扭曲组(n=49),住院期间记录一般临床特征、动态监测肌酸激酶(CK)和肌酸激酶同工酶(CK-MB)水平,并记录住院期间死亡例数。结果:QRS波终末扭曲组发病年龄较大(P=0.001),ST段抬高导联数多(P=0.025)及入院时Killp分级>1者例数多(P=0.044),有较高的CK[(1526.5±1180.4)IUvs(2129.7±1414.1)IU,P=0.012]和CK-MB[(137.1±109.0)IUvs(184.9±117.0)IU,P=0.023]水平。2组住院期间病死率分别为6.8%vs20.4%,Logistic回归证实住院期间病死率与QRS波终末扭曲呈明显的相关性(OR值7.14,95%可信区间1.17～43.60,P=0.016)。结论:入院时心电图QRS波终末扭曲对STEMI患者梗死范围大小和住院期间病死率有独立的预测价值。     

Grade 3 ischemia on the admission electrocardiogram is associated with severe microvascular injury on cardiac magnetic resonance imaging after ST elevation myocardial infarction

Background

Grade 3 ischemia during ST elevation myocardial infarction (STEMI) is defined as ST elevation with distortion of the terminal portion of the QRS on electrocardiogram (ECG). The aim of this study was to evaluate the effect of ischemic grade on cardiac magnetic resonance (CMR) imaging infarct characteristics such as infarct size, microvascular obstruction (MVO), intramyocardial hemorrhage (IMH), and myocardial salvage.

Methods

Patients with STEMI treated with primary percutaneous coronary intervention had a 12-lead ECG on presentation for analysis of ischemic grade. Gadolinium-enhanced CMR imaging was performed within 7 days to assess infarct size, MVO, IMH, and myocardial salvage.

Results

Of the 37 patients enrolled in the study, grade 3 ischemia was present in 32%. Those with grade 3 ischemia had higher peak troponin I levels (P = .013), more MVO (P < .001), more IMH (P < .001), larger infarct size (P = .025), and less myocardial salvage (P = .012). Regression analysis found that grade 3 ischemia, infarct size, and peak troponin I level were significantly associated with MVO and IMH.

Conclusion

Grade 3 ischemia on the admission ECG during STEMI is closely associated with the development of severe microvascular damage on CMR imaging.     

Early positive biomarker in relation to myocardial necrosis and impaired fatty acid metabolism in patients presenting with acute chest pain at an emergency room.

BACKGROUND: Measurement of circulating biomarkers has enabled early diagnosis and risk assessment of acute coronary syndrome. This study sought diagnostic values of the first single-point data of biomarkers obtained soon after patient arrival by comparing with scintigraphically quantified myocardial injury in patients presenting with acute chest pain at an emergency room. METHODS AND RESULTS: Serial blood samples were taken soon after arrival in an emergency department in 74 patients with suspected acute coronary syndrome to quantify blood levels of troponin-T (TnT), heart-type fatty acid-binding protein (H-FABP), myocardial-bound creatine kinase (CK-MB), and myoglobin. Myocardial perfusion and metabolic defects were scintigraphically quantified. The first single-point data had high positive predictive values for detecting the defects (80-100%) but low negative predictive values (15-41%). CK-MB and TnT had higher specificities (73-100%) but significantly lower positive rates (22-27%) than the others (61-68%), resulting in greater sensitivities of H-FABP and myoglobin (75-80%) than those of CK-MB and TnT (29-35%). Among biomarkers, TnT peak concentrations most closely correlated with scintigraphic abnormalities. CONCLUSION: H-FABP can contribute to early detection of myocardial injury and TnT is most likely to correlate with injured myocardial mass. The differential features of biomarkers are complementary in patients with acute chest pain presenting at an emergency room.     

Impact of Changing Definitions for Myocardial Infarction: A Report from the AMIS Registry

Background

To assess the impact of the new definitions of myocardial infarction, we retrospectively analyzed 9190 patients from 63 hospitals with reported peak troponin values included between 2001 and 2007 in the Swiss AMIS (Acute Myocardial Infarction in Switzerland) Plus registry.

Methods

Patients were classified as belonging to the “classic” myocardial infarction group (peak total CK or CK-MB above the upper limit of normal, or troponin T [TnT] >0.1 μg/L or troponin I [TnI] >0.1-0.8 μg/L [depending on the assay]) or “new” myocardial infarction group (TnT >0.01 μg/L or TnI >0.01-0.07 μg/L).

Results

There were 489 patients in the “new” group who were similar to the 8701 “classic” patients in terms of age, sex, and prevalence of both diabetes and renal failure, but more frequently had a history of prior coronary artery disease, hypertension, and hyperlipidemia. At admission, they less frequently had ST elevation on their electrocardiogram, were more frequently in Killip class I, and received less primary percutaneous coronary intervention. Hospital mortality was 3.5% in the “new” and 6.7% in the “classic” myocardial infarction group (P = .004). In a subset of patients with a longer follow-up, mortality at 3 and 12 months was 1% and 5.6%, respectively, for “new” and 1.6% and 4%, respectively, for “classic” myocardial infarction (NS).

Conclusions

Patients with minimal elevation of serum troponin have smaller infarctions, less aggressive treatment, fewer early complications, and a better early prognosis than patients with higher serum biomarker levels. After discharge, however, their prognosis currently appears no different from that of patients with a “classic” myocardial infarction event.     

Prehospital troponin T testing in the diagnosis and triage of patients with suspected acute myocardial infarction

Prehospital electrocardiographic (ECG) diagnosis has improved triage and outcome in patients with acute ST-elevation myocardial infarction. However, many patients with acute myocardial infarction (AMI) present with equivocal ECG patterns making prehospital ECG diagnosis difficult. We aimed to investigate the feasibility and ability of prehospital troponin T (TnT) testing to improve diagnosis in patients with chest pain transported by ambulance. From June 2008 through September 2009, patients from the central Denmark region with suspected AMI and transported by ambulance were eligible for prehospital TnT testing with a qualitative point-of-care test (cutpoint 0.10 ng/ml). Quantitative TnT was measured at hospital arrival and after 8 and 24 hours (cutpoint 0.03 ng/ml). A prehospital electrocardiogram was recorded in all patients. Prehospital TnT testing was attempted in 958 patients with a 97% success rate. In 258 patients, in-hospital TnT values were increased (≥0.03 ng/ml) during admission. The prehospital test identified 26% and the first in-hospital test detected 81% of patients with increased TnT measurements during admission. A diagnosis of AMI was established in 208 of 258 patients with increased TnT. The prehospital test identified 30% of these patients, whereas the first in-hospital test detected 79%. Median times from symptom onset to blood sampling were 83 minutes (46 to 167) for the prehospital sample and 165 minutes (110 to 276) for the admission sample. In conclusion, prehospital TnT testing is feasible with a high success rate. This study indicates that prehospital implementation of quantitative tests, with lower detection limits, could identify most patients with AMI irrespective of ECG changes.     

Fibrinogen and C-reactive protein on admission as markers of final infarct size after primary angioplasty for acute myocardial infarction.

BACKGROUND: In acute myocardial infarction (AMI) treated conservatively or with thrombolysis, marked increases of C-reactive protein (CRP) and fibrinogen have been observed. No data are however available concerning a possible relation between CRP and fibrinogen levels on admission and markers of infarct size after obtaining thrombolysis in myocardial infarction (TIMI) flow III by primary angioplasty. METHODS: We studied 34 patients with a first AMI (29 men, mean age 54+/-11 years) who were treated with primary angioplasty (TIMI flow III in all patients, no concomitant treatment with glycoprotein IIb-IIIa antagonists) within 6 h of onset of pain. CRP and fibrinogen levels on admission were determined and related to the following markers of infarct size: peak creatine kinase MB (CKMB) levels, radionuclide left ventricular ejection fraction (LVEF) at discharge and thallium-201 single-photon emission computed tomography (SPECT) infarct size at 1 month. RESULTS: Median CRP levels were 0.4 mg/dl (range 0.09-3 mg/dl), median fibrinogen levels 412 mg/dl (range 198-679 mg/dl), mean CKMB was 178+/-151 U/l, mean LVEF 52+/-8% and mean thallium-201 infarct size 7+/-6%. Although CRP levels were related to fibrinogen levels on admission (r=0.56, P=0.002), only fibrinogen levels were related to markers of infarct size (r=0.58, P=0.001 for CKMB, r=-0.44, P=0.01 for LVEF and r=0.64, P=0.001 for thallium-201 infarct size). No relation was found between CRP or fibrinogen levels on admission and the extent of coronary artery disease or the myocardial area at risk. In multiple regression analysis, the relation between fibrinogen and markers of infarct size was independent of CRP levels and the duration of pain on admission. CONCLUSIONS: These findings indicate a relation between fibrinogen levels on admission and myocardial infarct size in patients treated with primary angioplasty for AMI. This relation seems to be independent of CRP levels and the duration of pain on admission. If confirmed in larger patient populations, fibrinogen levels on admission could have an important value for risk stratification and more aggressive reduction of infarct size in patients who are treated with primary angioplasty.     

Troponin I concentrations following primary percutaneous coronary intervention predict large infarct size and left ventricular dysfunction in patients with ST-segment elevation acute myocardial infarction

The aim of this study was to investigate the ability of troponin I (cTnI) levels to predict myocardial infarction size in patients with ST-segment elevation acute myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). In 87 patients with STEMI undergoing primary PCI, serial plasma concentrations of cTnI and alpha-hydroxybutyrate deshydrogenase (HBDH) were measured before PCI and over the following 72 h. Enzymatic infarct size was estimated by the cumulative release of HBDH during the 72 h following PCI (QHBDH72). Delayed radionuclide left ventricular ejection fraction (LVEF) was measured in 63 patients. While cTnI concentrations at admission did not correlate with QHBDH72 or with LVEF, from the 3rd to the 72nd h following PCI, they did correlated with QHBDH72 (P<0.001; R: 0.76-0.86) and with LVEF (P<0.001; R: -0.42 to -0.50). Receiver-operator characteristic (ROC) curve analysis showed that admission concentrations of cTnI could not predict either a large infarct size (i.e., QHBDH72>10 g-eq l(-1)) or a low LVEF (i.e., LVEF<40%). However, 6 h and up until 72 h after PTCA, cTnI concentrations were predictive of large enzymatic infarct size (sensitivity: 91 and 95%, specificity: 90 and 87%, respectively) and of LVEF under 40% (sensitivity: 75 and 77%, specificity: 90 and 78%, respectively). Thus, our study suggests that in contrast with admission cTnI concentration, cTnI levels following primary PCI represent a reliable tool for predicting large enzymatic infarct size and may help in selecting patients with a high risk of low LVEF at 1 month.