The prognostic significance of serial myoglobin,troponin I,and creatine kinase-MB measurements in patients evaluated in the emergency department for acute coronary syndrome

STUDY OBJECTIVE: We sought to determine the value of serial measurements of myoglobin, cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB) to predict 30-day adverse events in patients evaluated in the emergency department (ED) for possible acute coronary syndrome. METHODS: Serum myoglobin, cTnI, and CK-MB levels were measured at presentation, 90 minutes, 3 hours, and 9 hours in patients evaluated in the ED for possible acute coronary syndrome. In 764 consecutive patients, the ability of each individual marker and combination of markers to predict a 30-day adverse event (death or myocardial infarction) over time was calculated. RESULTS: There were 109 (14%) patients with an adverse event at 30 days (84 myocardial infarctions and 43 deaths). The sensitivities of initial measurements of myoglobin, cTnI, and CK-MB for identifying adverse events were 60%, 47%, and 52%, respectively. The combined sensitivity of myoglobin and cTnI measurements during a 9-hour period was 94%; specificity was 50%. Measurement of CK-MB did not improve sensitivity. CONCLUSION: The measurement of both myoglobin and cTnI during a 9-hour period was the most predictive of subsequent adverse events in patients evaluated in the ED for possible acute coronary syndrome.     

The role of cardiac troponin t and other new biochemical markers in evaluation and risk stratification of patients with acute chest pain syndromes

Background and hypothesis: Increased serum creatinine kinase (CK) and CK-MB enzyme levels have been used for years to detect myocardial infarction (MI). However, serum myoglobin and CK-MB mass or protein levels may indicate MI earlier; cardiac troponin T is the most specific marker of myocardial injury and it can detect even minor myocardial necrosis. The diagnostic and prognostic utility of the traditional and new markers of cardiac injury in the emergency evaluation of patients with acute chest pain syndromes were therefore compared. Methods: One hundred and fifteen consecutive patients with an acute coronary syndrome, and 64 controls recruited during the same period, were examined. The time elapsed from onset of symptoms to blood collection was recorded. Cardiac markers were measured in specimens collected upon arrival (0 h), and 2 and 5–9 h, and later in cases of longer observation. The major cardiac events occurring up to 40 months after the index examination were recorded. Results: cTnT levels provided unique information: they were the most specific indicators of myocardial damage and identified unstable angina patients at high risk of future major events. Up to 6 h after the onset of chest pain, the new markers were elevated more frequently than the traditional ones and permitted earlier MI recognition. The worst prognosis (nonfatal myocardial infarction or death) was noted in subjects with chest pain at rest within 48 h before the index examination and elevated cTnT levels. Conclusions: The new markers, particularly cardiac troponin T, offer considerable advantages and they should be more widely used in the diagnosis and risk stratification of acute coronary syndromes.     

急性ST段抬高型心肌梗死直接PCI术后ST段回落的临床研究

目的：通过观察急性ST段抬高型心肌梗塞（STEMI）直接经皮冠状动脉介入治疗（PCI）术后,梗塞相关动脉（IRA）达心肌梗塞溶栓（TIMI）血流3级患者心电图ST段回落程度,探讨ST段回落与心肌损伤及心脏收缩功能的关系。方法：选择在发病12h内接受直接PCI治疗后TIMI血流达到3级的STEMI患者115例,PCI术前、术后行心电图检查,观察ST段回落情况,术前、后测定患者肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）及肌钙蛋白T（cTnT）,术后测定左室射血分数（LVEF）;按照ST段回落幅度（∑STR）不同,患者被分为两组：A组：∑STR〈50%,21例,为心肌灌注不良组,B组：∑STD≥50%,94例,为心肌灌注良好组;分析两组患者ST段回落程度与CK、CK-MB、cTnT及LVEF的关系。结果：（1）两组患者IRA部位、病变血管支数,PCI治疗前TIMI血流分级、cTnT水平,发病到PCI时间等差异均无显著性（P〉0.05）;（2）两组患者术前、后CK、CK-MB水平差异无显著性（P〉0.05）;（3）术后A组cTnT水平明显高于B组[（1.30±0.43）μg/L∶（1.0±0.45）μg/L,P〈0.05];（4）术后A组LVEF明显低于B组[（44.13±4.83）%∶（47.93±5.23）%,P〈0.05]。结论：急性ST段抬高型心肌梗塞直接PCI术后,TIMI血流达到3级,ST段回落良好的患者,心肌组织水平灌注程度较好,心肌损伤程度轻,左心收缩功能较好。     

Myocardial damage in falciparum malaria detectable by cardiac troponin T is rare

OBJECTIVES: To estimate the prevalence of myocardial damage in falciparum malaria by serum concentration of cardiac troponin T. METHODS: Retrospective study of stored sera and patient files; assessment of acute myocardial damage by serum concentration or activity of cardiac troponin T, creatine kinase, creatine kinase MB and myoglobin and by routine electrocardiography. RESULTS: A total of 161 patients with falciparum malaria were included in the study; troponin T was elevated in one case (0.6%), no CK-MB elevations were found, myoglobin was elevated in 10 of 161 patients (6.2%), all of whom were elderly and had concomitant elevated serum concentration levels of cystatin C; ECG abnormalities were seen in 23 patients. CONCLUSION: Assessed by troponin T, myocardial damage in falciparum malaria is rare.     

Long-term prognostic value of serial troponin T bedside tests in patients with acute coronary syndromes

The early presence of troponin T in serum strongly predicts short-term mortality and myocardial infarction in patients with acute coronary syndromes. We investigated the long-term outcome of the prognostic significance of the troponin T rapid bedside assay (TROPT) and compared this with the quantitative troponin T assay (cTnT enzyme-linked immunosorbent assay), myoglobin and creatine kinase-MB (CK-MB) mass. One hundred sixty-three patients with chest pain and suspected acute coronary syndromes were studied and followed prospectively for 3 years. Serial blood specimens were obtained at admission and at 3, 6, 12, 24, 48, 72, and 96 hours after admission. Patients were classified as having acute myocardial infarction in 99 patients (61%), unstable angina in 34 patients (21%), and no evidence for acute cardiac ischemia in 30 patients (18%). At 3 years, 28 patients (17%) had died of which 25 deaths (15%) were for cardiac reasons. Twenty-one patients (13%) had a nonfatal (recurrent) myocardial infarction. At admission 29% of the patients were TROPT positive (> or = 0.2 microg/L), another 31% became positive within 12 hours, and 39% remained negative. When adjusted for baseline variables, a positive TROPT (any sample 0 to 12 hours) was independently associated with a higher risk of cardiac mortality (RR 4.3, 95% confidence interval [CI] 1.3 to 14.0). Because troponin T stays elevated up to 2 weeks, later TROPT results between 24 and 96 hours remained significantly predictive for mortality. The cTnT enzyme-linked immunosorbent assay (any sample 0 to 12 hours; cutoff > or = 0.2 microg/L) was similarly predictive (RR 2.9, 95% CI 1.0 to 8.6). Early myoglobin results were significantly prognostic for cardiac mortality up to 12 hours after admission (RR 3.7; 95% CI 1.0 to 12.0). In contrast, serial CK-MB mass measurements were not predictive of mortality. Thus, a combination of a baseline TROPT and an additional TROPT 12 hours or later identifies a subgroup of patients at high risk for subsequent mortality and reinfarction, both at short-term but also at long-term.     

Comparison of different cardiac markers in monitoring percutaneous coronary interventions with frequent use of stents and gpIIbIIIa-antagonists

Studies from the early 1990s found elevations of creatine kinase (CK) and its isoform CK-MB in 5-30% of patients after PCI, indicating minor myocardial damage. Less is known about the influence of modern improved PCI-techniques on the frequency of elevated cardiac markers and the correlation between different commonly used markers, especially cardiac troponins. From 1997 to 2001, 1486 patients undergoing PCI during the regular working hours were included in the prospective "Ludwigshafen Infarctlet Registry". Myocardial infarction in the past 48 hours was an exclusion criterion. Clinical and procedural data were documented. Follow-up data were obtained from discharge up to one year. PCI-related elevations of troponin T were found in 18%, of total-CK in 11%, of CK-MB in 33% and of myoglobin in 23% of cases. The correlation between the different markers was poor. Compared with troponin T, other markers showed low sensitivity (total-CK 58%, CK-MB 27%, myoglobin 22%) and, especially total-CK, low specificity. Stenting, side branch occlusion or major dissection, complex lesion morphology, gpIIbIIIa-antagonist application, proximal stenosis and unstable angina were independent predictors of an elevated troponin T in multivariate analysis. Due to this weak correlation between more specific and sensitive troponins and the other markers, troponins are preferred in monitoring after PCI. In addition to lesion characteristics, particularly stenting is associated with an increased rate of elevated troponin.     

Risk stratification in acute coronary syndrome

BACKGROUND: The spectrum of symptoms of patients with active ischemic heart disease ranges from silent ischemia to acute myocardial infarction and the extent of myocardial damage from reversible myocardial injury to extensive necrosis. The term "acute coronary syndrome" comprises this continuum. In particular the evaluation of patients without ST-segment elevation is difficult, for clinical symptoms, ECG criteria and CK-MB measurements appear insufficient for appropriate risk stratification. TROPONIN MEASUREMENT: Serial measurements of either troponin T or I reliably detect minor myocardial damage in those patients, who are known to be at a higher risk for adverse cardiac events comparable to the risk of patients with acute myocardial infarction. Hence determination of troponins allow superior risk stratification contributing to early triage and therapeutic decision making. Without elevation of troponins the cardiac risk for death or myocardial infarction will not exceed 1%. CONCLUSION: Patients with elevated troponins should be early hospitalized and further evaluated in order to begin efficacious therapy as soon as possible. These patients represent a high-risk subgroup of patients clinically classified as unstable angina, who might benefit from potential antithrombotic treatment such as low-molecular weight heparin or glycoprotein IIb/IIIa antagonists without or with revascularization strategies.     

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.     

A prospective study of an algorithm using cardiac troponin I and myoglobin as adjuncts in the diagnosis of acute myocardial infarction and intermediate coronary syndromes in a veteran's hospital

BACKGROUND: Accurate and cost-effective evaluation of acute chest pain has been problematic for years. The high prevalence of missed myocardial infarctions (MI) has led to conservative triage behavior on the part of physicians, leading to expensive admissions to coronary care units. New algorithms are sorely needed for more rapid and accurate triage of patients with chest pain to appropriate treatment settings. HYPOTHESIS: We sought to test an algorithm for rapid diagnosis of MI and acute coronary syndromes using cardiac troponin I (cTnI) and myoglobin as adjuncts to creatine kinase (CK)-MB. We hypothesized our algorithm would be both sensitive and specific at early time points, and would allow safe stratification of patients not ruling in by conventional CK-MB criteria. METHODS: This was a 6-month prospective study of 505 consecutive patients who presented with chest pain at a university-affiliated veteran's hospital. The percentage of MIs at various time points was identified using combinations of markers. Safety outcomes were assessed by follow-up of patients discharged home. Cost savings analysis was assessed by surveying the physicians as to whether the use of the algorithm affected their disposition of patients. Forty-nine patients ruled in for MI. Using the combination of cTnI, 2-h doubling of myoglobin, and CK-MB, 37 (76%) ruled in at the time of presentation, 43 (88%) at 2 h, and 100% by 6 h. RESULTS: Cardiac troponin I plus a 2-h myoglobin was as accurate as the combination of all three markers and performed better than CK-MB in detecting patients presenting late and as a predictor for complications when CK-MB was normal. Of the 456 patients with normal markers after 6 h, only 140 were sent to the coronary care unit (CCU), and 176 were sent home. A 3-month follow-up showed minimal adverse events. One-half of physicians completing a survey stated the use of markers changed their disposition of patients, leading to an estimated 6-month cost savings of a half-million dollars. CONCLUSIONS: We developed an algorithm using troponin I and myoglobin as adjuncts to usual CK-MB levels that allowed for rapid and accurate assessment of patients with acute MI. It also afforded physicians important input into their decision making as to how best to triage patients presenting with chest pain. Their comfort in sending home certain subgroups of patients who otherwise would have been admitted to the CCU was rewarded with a good short-term prognosis and a large cost savings to the hospital.     

Evaluation of "new" cardiac markers for ruling out myocardial infarction after coronary artery bypass grafting

STUDY OBJECTIVES: This study was conducted to evaluate the value of serum troponin T, myoglobin, and creatine kinase (CK)-MB mass concentrations for ruling out perioperative myocardial infarction (poMI) early after cardiac surgery. DESIGN: Retrospective study. SETTING: Cardiothoracic surgery department in a university hospital. PATIENTS: One hundred eighty-one patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass were included. METHODS: Serum concentrations of troponin T, myoglobin, and CK-MB mass were measured preoperatively (baseline), on arrival at the cardiosurgical ICU (CICU), and at 2, 4, 8, 12, 16, and 20 h after arrival at the CICU. The strength of markers studied for ruling out poMI was studied using receiver operating characteristics curves. Based on these curves, the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for each marker at every time point were calculated. RESULTS: poMI developed in 14 patients. On arrival at the CICU, all markers were significantly increased from baseline concentrations in both patient groups. In patients with poMI, serum concentrations of troponin T, myoglobin, and CK-MB mass were significantly higher than in control patients from 8, 2, and 0 h after arrival on the CICU, respectively. CK-MB mass was the earliest marker, and its NPV reached 98.6% 12 h after arrival at the CICU. On arrival at the CICU, the NPV for CK-MB mass already reached 96.7%. The NPV for myoglobin reached 98.4% 12 h after arrival at the CICU. Troponin T was not an early marker for ruling out poMI, with an NPV reaching 98.6% 12 h after arrival on the CICU. During the first 8 h after arrival at the CICU, sensitivity, specificity, PPV, and NPV of CK-MB mass exceeded those of myoglobin and troponin T. In later measurements (until 20 h after arrival at the CICU), troponin T gave the most sensitive definition of poMI. CONCLUSIONS: For ruling out poMI on the CICU after CABG, CK-MB mass is a better marker than myoglobin and troponin T during the first 12 h after arrival on the CICU. Using these markers, postoperative treatment of cardiac surgical patients might be further improved.     

Clinical impact of the troponin 99th percentile cut-off and clinical utility of myoglobin measurement in the early management of chest pain patients admitted to the Emergency Cardiology Department

OBJECTIVE: To verify the clinical impact of different low cut-offs for troponin I/cardiac troponin I (99th percentile to 10% CV) and for myoglobin, in early risk stratification of patients with suspected acute coronary syndrome. METHODS: A total of 516 consecutive non-ST-elevation patients admitted to hospital were followed. The first measurement of cardiac markers was performed at the point-of-care in the Emergency Cardiology Department, using Stratus CS. The lowest cardiac troponin I concentration with a CV0.07 microg/l in the Emergency Cardiology Department (P>0.05). Using lowering cut-off values, the difference between the fraction of patients that was positive compared with the diagnosis according to European Society of Cardiology and American College of Cardiology criteria and had remained statistically significant (P<0.05) up to 0.03 microg/l (99th percentile upper reference limit) was considered (85 patients, 16.5%, n.s.). Relative operating characteristic analysis confirmed that the best clinical cut-off was related to the cardiac troponin I concentration that meets the 99th percentile upper reference limit. The diagnostic accuracy of myoglobin in detecting the minimum cardiac damage was significantly lower, independently from the cut-offs considered. CONCLUSION: The diagnostic accuracy in detecting myocardial damage early in the Emergency Cardiology Department improves when the 99th percentile is used as a decisional value of cardiac troponin I; the use of this cut-off makes the measurement of myoglobin unnecessary.     

Acute myocardial infarction spurred by myopericarditis in a young female patient: Coxsackie B2 to blame

Myocardial virus infection may mimic but also trigger acute myocardial infarction.The present paper reports an exceedingly rare presentation of an acute myocardial infarction in a very young female associated with Coxsackie B2 virus infection. A 17-year-old woman with no prior medical history presented to the Cardiac Intensive Care unit with chest pain, ST segment elevation and increased cardiac troponin with pericardial effusion one week after experiencing febrile viral gastroenteritis. Given the age and health of the patient, myocarditis was initially presumed. Coronary angiography and cardiac magnetic resonance imaging studies, however, demonstrated an acute posterior myocardial infarction related to a right coronary artery thrombosis. Serological studies disclosed a concurrent Coxsackie B2 virus infection. The patient made a successful recovery with subsequent minor left ventricular dysfunction at long-term follow-up. Coxsackie B2 myocarditis might have triggered a coronary artery spasm and subsequent thrombosis.     

Sialic acid or troponin T to detect perioperative myocardial damage in patients undergoing elective coronary artery bypass grafting.

Sialic acid (SA), a family of acetylated derivatives of neuraminic acid, is elevated in patients with coronary heart disease. Cardiac troponin T (cTnT), myoglobin (Mb), and creatine kinase-MB (CK-MB) are specific markers of myocardial injury and are, at present, widely used to detect perioperative myocardial damage during coronary artery bypass grafting (CABG) surgery. The present study investigated the net myocardial release of SA and the cardiac markers (cTnT, Mb, CK-MB) during reperfusion after hypothermic cardioplegic cardiac arrest in 25 patients undergoing elective CABG. Additional paired arterial, central venous, and coronary sinus blood samples were obtained after atrial cannulation before aortic cross-clamping (preischemic sample) and at 1 and 10 min after aortic declamping (reperfusion samples). There were no increase in the SA, cTnT, Mb and CK-MB concentrations before aortic cross-clamping, but there was considerable release of these markers within 10 min after aortic declamping: cTnT release was significantly higher compared with baseline values before aortic cross-clamping. In contrast to SA, Mb, and CK-MB, the difference between baseline and release values for cTnT at 1 min after aortic declamping was not significant. The rate of increase for SA was significantly higher than for Mb, CK-MB and cTnT. SA is a unique and novel marker that could be particularly useful in assessing myocardial cell damage in patients undergoing cardiac surgery.     

Enzymatische Marker der Reperfusion bei akutem Myokardinfarkt

Despite advances in therapy acute myocardial infarction is associated with a mortality rate of up to 30%. Early and complete reperfusion of the infarct related artery (defined as TIMI flow 3 at 90 minutes following therapy) as obtained with thrombolytic therapy in 50 to 80% of patients improves survival and enhances ventricular function. Failure to achieve recanalization should prompt further intervention (second attempt of thrombolysis or rescue-PTCA). Various cardiac markers known from diagnosing acute myocardial infarction or risk stratification in unstable angina pectoris have been assessed in their ability to predict successful reperfusion/failure of therapy. Following reperfusion creatinkinase (CK) and its isoform CK-MB, troponin and myoglobin show an early and rapid rise to a high maximum value with rapid normalization. For creatinkinase time to peak values of less than 9 hours or rates of increase of > 50 U/h (> or = 10 U/h for CK-MB activity) within the first 2.5 hours following thrombolysis have been suggested as useful indicators of successful reperfusion. The same applies for a troponin (T)slope > 0.5 ng/ml/h within the first hour (Table 5). The major limitation in applying either creatinkinase, troponin or even lactatdehydrogenase (LDH) is their comparatively late release (4 to 6 hours) following myocardial infarction. In that respect myoglobin (though not specific for cardiac injury) seems ideal for guidance of intervention after failed thrombolysis. The I.S.A.M. study included 1,741 patients with acute myocardial infarction of less than 6 hours duration being given either streptokinase or placebo. Serial blood samples for measurement of cardiac enzymes were drawn within the first 50 hours. In the streptokinase group the time to peak concentration of CK-MB activity was significantly lower (mean 10.9 hours vs 16.1 hours following initiation of treatment) as was the area under the CK-MB curve indicating reduction of infarct size (Table 2). A substudy investigating the myoglobin release in 120 patients having received streptokinase or placebo demonstrated higher maximum values in the streptokinase group (mean 3008 vs 2097 ng/ml), a shorter time to peak interval following treatment (3.4 vs 6.5 hours) and a reduction in infarct size as suggested by a smaller area under the myoglobin curve (17,377 vs 23,240 ng/ml x h) (Table 3). For LDH/alpha-HBDH the reduction in time to peak intervals was less impressive (Table 4). In angiographic studies with TIMI flow 3 at 90 minutes in the infarct related artery in 22 patients (Figure 5) the maximum myoglobin value was reached in less than 4.2 hours (mean value plus SEM) following treatment (9.5 hours for CK-MB activity). Therefore, myoglobin seems to be the preferred marker in reperfusion assessment.     

Relation of minor cardiac troponin I elevation to late cardiac events after uncomplicated elective successful percutaneous transluminal coronary angioplasty for angina pectoris.

There is little information about the relation between mild cardiac troponin I (cTn-I) increase after coronary interventions and late outcome. We therefore focused on the long-term outcome and the clinical, morphologic, and procedural correlates of elevation of cTn-I compared with cardiac troponin T, creatine kinase (CK), CK-MB activity and mass, and myoglobin in 105 patients with successful elective percutaneous transluminal coronary angioplasty (PTCA) for stable or unstable angina. Patients with myocardial infarction and those with unstable angina who had a detectable increase in serum markers before PTCA were excluded. Markers were measured before and after the procedure and for 2 days. Patients were followed up to record recurrent angina, myocardial infarction, cardiac death, repeat PTCA, or elective coronary artery bypass graft surgery. Procedure success was achieved in all cases. Elevation in cTn-I (> or =0.1 microg/L) was observed in 23 of 105 patients (22%) (median peak: 0.25 microg/L); 18% had cardiac troponin T (cTn-T) release (> or = 0.1 microg/L, median peak 0.21); 11.4% CK-MB mass (> or =5 microg/L), and 7.6% myoglobin (> or =90 microg/L) release. Five and 2 patients had elevated CK and CK-MB activity, respectively. Fourteen of 18 patients with cTn-T elevation had a corresponding elevation in cTn-I (kappa 0.68; p = 0.001). Patients positive for cTn-I had more unstable angina (p = 0.042) and heparin before PTCA (p = 0.046), and had longest total time (p = 0.004) and single inflation (p = 0.01). By multivariate logistic regression, predictors of postprocedure cTnI elevation were maximum time of each inflation (odds ratio 9.2; p = 0.0012), type B lesions (odds ratio 6.6; p = 0.013), unstable angina (p = 0.041), and age > or =60 years (p = 0.032). Clinical follow-up was available in 103 patients (98%) (mean 19+/-10 months). Kaplan-Meier survival analysis showed that cTn-I elevation was not an important correlate of cardiac events (p = 0.34, by log-rank analysis). The incidence of recurrent angina, myocardial infarction, cardiac death, and repeat revascularization after 12 months was not different in patients positive or negative for cTn-I. We conclude that cTn-I elevation after successful PTCA is not associated with significantly worse late clinical outcome. Levels of cTn-I allow a much higher diagnostic accuracy in detecting minor myocardial injury after PTCA compared with other markers, but there is no association with periprocedural myocardial cell injury and late outcome when cTn-I and other markers are considered.     

New cut-off values of cardiac markers for risk stratification of angina pectoris

BACKGROUND: The aim of this present prospective study was to investigate the accuracy of cardiac markers for the prediction of subsequent cardiac events (cardiac death, acute myocardial infarction and recurrent ischemia requiring coronary revascularization). METHODS: Fibrinogen, cardiac troponin T, troponin I, creatine phosphokinase myocardial fraction, C-reactive protein and myoglobin at baseline and after 6 h were measured on 154 patients (109 male, 63+/-11 years) with chest pain. Receiver operator characteristic analyses were performed to determine cut-off points of cardiac markers in prediction of adverse events. RESULTS: The following cut-off values for prediction of cardiac events were calculated: troponin I at baseline 0.3 ng/ml (predictive accuracy=0.870), troponin I at 6 h 0.50 ng/ml (p.a.=0.909); troponin T at baseline 0.05 ng/ml (p.a.=0.643), troponin T at 6 h 0.05 ng/ml (p.a.=0.612), creatine phosphokinase myocardial fraction at baseline 2.0 ng/ml (p.a.=0.721), creatine phosphokinase myocardial fraction at 6 h 2.5 ng/ml (p.a.=0.734), myoglobin at baseline 23 ng/ml (p.a.=0.623), myoglobin at 6 h 26 ng/ml (p.a.=0.617), C-reactive protein at baseline 0.31 mg/dl (p.a.=0.662), C-reactive protein at 6 h 0.55 mg/dl (p.a.=0.682), and fibrinogen at baseline 360 mg/dl (p.a.=0.701). The combination of baseline troponin I with different parameters resulted in a higher sensitivity of up to 98%, with a similar predictive accuracy, but a lower specificity. Additive measurements of cardiac troponin I at 6 h to baseline cardiac troponin T and I proved to be the best combination for prediction of subsequent cardiac events. CONCLUSIONS: Changes in cut-off levels of cardiac markers and inflammatory parameters results in a high accuracy of risk stratification in patients with chest pains. Combination of these measurements might further help in the identification of patients who would benefit from early coronary revascularization.     

Superiority of combined CK-MB and troponin I measurements for the early risk stratification of unselected patients presenting with acute chest pain

BACKGROUND: Recent studies have suggested that positive troponin I tests are associated with an increased risk of cardiac death during short-term follow-up. However, it is unknown if troponin I tests alone or in addition to CK-MB measurements are superior to predict unfavorable outcome during long-term follow-up. PATIENTS AND METHODS: In a prospective, double-blind study we assessed the prevalence and prognostic value of combined troponin I and CK-MB tests in an unselected cohort of patients (n = 292) admitted to the emergency department for acute chest discomfort. Patients were grouped according to the diagnosis on discharge in those with acute myocardial infarction (1), unstable angina (2), and noncardiac chest pain (3). Six months after enrollment, death rates were obtained and follow-up interviews were performed with respect to survival, recurrence of chest pain, and myocardial infarction. RESULTS: In patients with evidence of coronary heart disease, the mortality rate for abnormal troponin I and normal CK-MB levels was 5.0%. Baseline troponin I and elevated CK-MB levels were associated with a mortality rate of 4.0%. However, the mortality rate was significantly higher (11.1%) in patients presenting with elevated troponin I and CK-MB values. In patients without myocardial infarction on admission, 10.5% with positive troponin I tests died compared to 1.6% with negative tests. The mortality rate in patients without myocardial infarction was 2.7% for patients with elevated CK-MB but normal troponin I values. In patients with both markers elevated a significantly higher mortality rate (16.7%) was found, representing a 6-fold increase in the death event rate. With the additional knowledge of troponin I values, it could be demonstrated that certain cases were misclassified as having noncardiac chest pain. At least some of the latter patients with above-normal values of troponin I were retrospectively to be reclassified as unstable angina. Acute non-Q-wave myocardial infarctions were occasionally misdiagnosed as either angina pectoris or nonischemic chest pain. CONCLUSIONS: Our data suggest the superiority of combined CK-MB and troponin I measurements in clinical practice for the early risk stratification of patients presenting with acute chest pain. In nonmyocardial infarctions, both CK-MB and troponin I convey independent prognostic information with regard to fatal outcome. Troponin I tests in addition to CK-MB measurements contribute to a lower rate of misdiagnoses.     

Cardiac troponin T in acute coronary syndrome with renal insufficiency

Cardiac troponin levels are frequently elevated in patients with chronic renal failure, hence diagnosis of myocardial necrosis is difficult. The prevalence of elevated serum troponin T was determined and its diagnostic value in acute coronary syndrome was assessed in patients with chronic renal insufficiency. A retrospective cross-sectional analysis was performed in 227 patients with chronic renal insufficiency and a diagnosis of unstable angina, non-ST or ST-segment elevation myocardial infarction. All patients had baseline serum troponin T levels measured at previous visits; the baseline troponin T level was raised in 53.3%. Cardiac troponin T levels did not correlate with creatinine levels, and were not affected by dialysis. Mortality after an acute coronary event was high (46.3%). Because of the elevated baseline cardiac troponin T levels, detection of acute coronary syndrome in patients with chronic renal failure requires evaluation of serial cardiac enzyme measurements and serial 12-lead electrocardiograms. Early and definitive cardiac interventions may contribute towards decreasing the mortality rate in this group of patients.     

Lack of cardioprotective efficacy of allopurinol in coronary artery surgery.

OBJECTIVE--To examine the cardioprotective efficacy of allopurinol in patients undergoing elective coronary artery surgery. DESIGN--Prospective randomised trial. SETTING--London teaching hospital. PATIENTS--Twenty patients with at least moderately good left ventricular function undergoing elective coronary artery surgery and requiring at least two bypass grafts. INTERVENTIONS--Patients were randomised to receive allopurinol (1200 mg in two divided doses) or to act as controls. MAIN OUTCOME MEASURE--The primary determinant of the efficacy of myocardial protection was serial measurement (preoperatively and subsequently at one, six, 24, and 72 hours after the end of cardiopulmonary bypass) of cardiac troponin T (cTnT) a highly sensitive and specific marker of myocardial damage. Additional evidence was provided by serial measurement of the MB-isoenzyme of creatine kinase (CK-MB) and myoglobin, ECG changes, and clinical outcome. RESULTS--There was no significant difference in age, ejection fraction, number of grafts, bypass times, or cross clamp times between the two groups. In both groups there was a highly significant (p < 0.01) rise in cTnT, CK-MB, and myoglobin. Peak concentrations were reached between one (CK-MB and myoglobin) and six hours (cTnT) after the end of cardiopulmonary bypass. At 72 hours cTnT concentrations were six times higher than baseline concentrations whereas CK-MB and myoglobin were approximately double baseline concentrations. There was no significant difference in cTnT, CK-MB, or myoglobin between the allopurinol and control groups at any time. There was no diagnostic ECG evidence of perioperative infarction in any patient. CONCLUSION--Unlike previous reports this study did not show that allopurinol had a cardioprotective effect in patients with good left ventricular function undergoing elective coronary artery surgery.     

Use of biochemical markers of infarction for diagnosing perioperative myocardial infarction and early graft occlusion after coronary artery bypass surgery.

STUDY OBJECTIVES: Perioperative myocardial infarction (PMI) during coronary artery bypass grafting (CABG) is an important clinical problem because it is closely associated with increased morbidity and mortality. The diagnosis of PMI is, however, associated with several problems. Due to the surgical trauma, the usual indicators of myocardial infarction (pain, ECG changes, and elevated biochemical markers of infarction) have uncertain diagnostic value. The primary aim of this study was to illustrate the levels of the biochemical markers after uncomplicated bypass surgery defined as no clinical or ECG evidence of PMI, and no graft occlusion at 7 days by repeat angiography; and secondarily, to establish biochemical diagnostic discrimination limits for detection of in-hospital graft occlusion. METHODS AND RESULTS: One hundred three patients undergoing elective CABG were closely monitored by serial measurements of creatine kinase (CK)-MB mass, myoglobin, troponin T, and troponin I, and underwent a repeat angiography before discharge. Seven patients had ECG evidence of PMI. Peak troponin T and CK-MB values were significantly higher in these seven patients, although the diagnostic performances of the optimally chosen cutoff levels for diagnosing AMI were fair. Twelve patients had at least one occluded graft shown by repeat angiography. Peak values of CK-MB and troponin T were significantly higher in patients with graft occlusion (52.2 microg/L vs 24.7 microg/L, p = 0.01; and 3.7 microg/L vs 1.0 microg/L, p = 0.05, respectively). By multivariate analysis, a diagnostic discrimination level of 30 microg/L for CK-MB did not reach statistical significance; however, the independent diagnostic value of a cutoff level for troponin T at 3 microg/L reached a level of significance (p = 0.06). DISCUSSION: We have suggested normal values of four different biochemical markers of infarction after uncomplicated coronary bypass surgery. Patients with in-hospital graft occlusion had higher peak CK-MB and troponin T values. However, the overlap with patients without graft occlusion is substantial, and the patency status in the individual cannot be reliably predicted from these noninvasive tests.