心肌坏死标志物联合检测在急性心肌梗死早期诊断及鉴别中的意义

目的探讨心肌坏死标志物联合检测在急性心肌梗死早期诊断及鉴别中的意义。方法选取20lO年12月至2013年5月我院收治的90例患者,其中45例被确诊为急性心肌梗死,设为观察组,其余45例疑似急性心肌梗死的患者经过心电图、彩色多普勒超声心动图检查未见异常,最终确定为非急性心肌梗死患者,设为对照组。对两组患者进行酶活性、心肌蛋白及同工酶电泳检查。采用免疫抑制法测定肌酸激酶（CK）、肌酸激酶同工酶（CK—MB）,采用电化学发光法检测肌钙蛋白l（cTnI）和肌红蛋白（MYO）,记录CK、CK—MB、cTnI和MYO等含量,比较观察组患者心肌标志物不同时间的变化并进行统计学分析。结果与对照组比较,观察组患者血清CK、CK—MB、cTnI及MYO含量升高明显,其中CK、MYO含量升高最为显著（P〈0．05）。CK、CK—MB在发病3-6h后快速升高,均于24h左右达高峰,经治疗3-5天后恢复;cTnI前24h与CK—MB同步,但在血中维持时间较长;MYO在发病后12h发生异常,12h内达到峰值（P〈0．05）。结论心肌坏死标志物联合检测可以提高急性心肌梗死检出率,有助于急性心肌梗死早发现、早诊断和早治疗。     

Serum CK-MB isoenzyme after aortic and mitral valve replacements

A release of the MB fraction of creatine kinase (CK) enzyme into the serum due to myocardial manipulation and trauma occurs in patients undergoing cardiac surgery. Thus, the appearance of CK-MB activity as such is not sufficient to indicate of perioperative myocardial infarction. The mean (+/- SD) serum CK-MB isoenzyme level was 95 +/- 103 U/l 18 hours after aortic or mitral valve replacement in 76 patients. Thirteen patients undergoing closure of an atrial septal defect served as controls. They had a significantly lower (p less than 0.01) isoenzyme level postoperatively: 45 +/- 39 U/l. Two patients had the ECG changes of definite myocardial infarction after valve replacement and they also showed high CK-MB values, while the other patients with high enzyme level had no ECG signs suggesting acute infarction. CK-MB values correlated with the aortic cross-clamping time (r = 0.39, p less than 0.001) and weakly with the precordial ECG voltage of SV1 + RV5 (r = 0.25, p less than 0.01). While these findings may reflect the sensitivity of a thick myocardial wall to ischaemia during surgery, the postoperative recovery was not related to the serum CK-MB level.     

Utility of Troponin I in Patients with Cocaine-associated Chest Pain

Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine-associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. OBJECTIVE: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. METHODS: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule-in protocol that included serial sampling of creatine kinase (CK), CK-MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK-MB MI (CK-MB >or= 8 ng/mL with a relative index [(CK-MB x 100)/total CK] >or= 4, cardiac death, and significant coronary disease (>or=50%). RESULTS: Of the 246 admitted patients, 34 (14%) met CK-MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI-positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK-MB criteria for MI, and the other had a peak CK-MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK-MB MI and cTnI and were not significantly different. CONCLUSIONS: Most patients with cTnI elevations meet CK-MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK-MB for diagnosing necrosis in patients with cocaine-associated chest pain and suspected MI.     

Diagnosis of perioperative myocardial infarction by considering relationship of postoperative electrocardiogram changes and enzyme increases after coronary bypass operation

We report the results of enzyme determinations in sera from 88 patients, 65 of whom showed inconspicuous reconvalescence, 14 who had myocardial infarction within 24 h (MI 1) after bypass surgery, and nine with myocardial infarction between 24 and 48 h postoperatively (MI 2). We wanted to determine whether the consequent measurement of activities of total creatine kinase (CK), CK isoenzyme MB (CK-MB), lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase, conducted as a part of routine laboratory diagnostics, provided meaningful information for diagnosing infarcts besides that obtained from the electrocardiogram. The postoperative mean values of the enzyme activities in blood were significantly different among the three groups; however, only a combined evaluation of CK and CK-MB by means of a discriminant analysis allowed the prediction of MI (sensitivity: MI 1 = 98.5%, MI 2 = 95.4%; specificity: MI 1 = 71.4%, MI 2 = 81.8%). CK greater than 600 U/L or CK-MB greater than 45 U/L supports the diagnosis of acute MI.     

IgA-CK-BB complex with CK-MB electrophoretic mobility can lead to erroneous diagnosis of acute myocardial infarction

This patient, on admission, presented with a tentative diagnosis of myocardial infarction: the electrocardiogram showed a nonspecific ST-segment and T-wave abnormalities, and total creatine kinase (CK; EC 2.7.3.2) activity was slightly increased (238 U/L). However, a high electrophoretic value for CK-MB (50% of total CK activity) and the electrophoretic pattern of lactate dehydrogenase (EC 1.1.1.27) isoenzymes ruled out myocardial infarction. The isoenzyme migrating as CK-MB was found later to contain no immunologically normal CK-M subunits, and it was bound to IgA. A mixture of the patient's serum and a human serum control containing all CK isoenzymes showed altered electrophoretic mobility only for CK-BB, indicating that the patient's serum contained antibodies to the B unit of CK. Elution from a Sephadex G-200 column showed that the peak at which most of the anodic CK was eluted corresponded to a molecular mass of approximately 200 kDa. Evidently this atypical isoenzyme was an IgA-CK-BB complex. Because this macro CK type 1 can mimic CK-MB, it may therefore be a source of confusion.     

The value of serum CK-MB and myoglobin measurements for assessing perioperative myocardial infarction after cardiac surgery

In 41 patients who underwent coronary bypass surgery, creatine kinase (CK)-MB mass concentration was repeatedly measured in serum during and after the intervention using a new two-site immunoenzymetric assay (IEMA). Serum CK-MB activity was determined with the use of four different techniques: immunoinhibition, immunoinhibition-immunoprecipitation, column chromatography and electrophoresis. Myoglobin (Mb) was also measured in each specimen by radioimmunoassay. In the 33 patients who followed a completely uneventful postoperative course, the cumulated CK-MB release was, on the average, 12.2-fold less than after acute myocardial infarction. The CK-MB peak concentrations using the IEMA were 33 +/- 3 micrograms/l (X +/- SEM) and occurred 6.4 +/- 0.5 h after the intervention was started; CK-MB levels had decreased to 2.9 +/- 0.4 micrograms/l at the end of the first postoperative day. The evolution of the CK-MB concentration was parallel to that of the enzyme activity. The serum Mb maximum concentrations (518 +/- 39 micrograms/l) were reached after 3.3 +/- 0.1 h. The other eight patients developed perioperative myocardial infarction (PMI); in this group, the cumulated CK-MB release was higher, and the serum CK-MB postoperative curves were of three different types. The patients with delayed CK-MB peaks (type I pattern) or sustained elevations (type III) of this isoenzyme also showed increased serum Mb levels at the end of the first postoperative day. The PMI patients with early (10 h) CK-MB elevations (type II) did not demonstrate abnormal serum Mb levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Macro creatine kinase type 1 with electrophoretic mobility identical to that of the MB isoenzyme

We describe the case of an elderly woman whose symptoms and electrocardiographic pattern initially suggested acute myocardial infarction. The value for total serum creatine kinase (EC 2.7.3.2; CK) was 737 U/L (reference interval: 22-269 U/L), and electrophoresis for CK isoenzymes demonstrated two bands, the more anodal migrating to the CK-MB region and the second migrating between the CK-MB and CK-MM regions. The above-normal total CK and electrophoretic pattern persisted during her 11-day hospital course. The QuiCK-MB (International Immunoassay Labs.) and Tandem-E CK-MB (Hybritech) immunoassays, however, showed CK-MB mass measurements within the normal range. In further investigation with a mixture of patient's serum and human-serum-based control containing all CK isoenzymes, the electrophoretic mobility of only CK-BB was altered, proving that the patient had antibody to the B unit of CK in her serum. Immunofixation revealed the more anodal band to be a CK-IgA lambda complex, and the more cathodal band, a CK-IgG kappa complex. Mixing the patient's serum with polyclonal antibody specific for CK-B slowed the electrophoretic mobility of only the more anodal band. Polyclonal antibody specific for CK-M had no effect on either band. Evidently, this patient had two different types of macro CK type 1, both containing CK-BB. We conclude that macro CK type 1 can mimic CK-MB and be a source of confusion.     

新生儿缺氧缺血性脑病合并心肌损害相关因素分析

目的 :探讨新生儿缺氧缺血性脑病 (NHIE)伴心肌损害的心电图、血清心肌酶学改变与HIE分度的相互关系 ,心肌损害与窒息恢复时间的关系。方法 :对 16 5例HIE伴心肌损害的患儿出生后 4 8h以内的血清LDH(乳酸脱氢酶 )、CK (肌酶激酶 )、CK -MB (肌酶激酶同功酶 )、HBDH (a -羟丁酸脱氢酶 )的含量进行测定 ,并作心电图检查。结果 :心肌损害与窒息恢复时间呈明显正相关 ,P <0 0 1。 83例 (83/16 5 )患儿心电图出现改变 ,重度组改变分别大于轻、中度组 ,轻度组大于中度组。经方差分析显示 :心肌酶中CK、CK -MB变化与HIE的分度呈正相关性 ,差异显著 (P <0 0 5 ) ;12例 (12 /16 5 )病人于出生后 12h内出现心肌酶谱变化 ,而其中 8例的酶谱变化出现于生后 6h内。结论 :心肌损害和窒息恢复时间密切相关 ,常规检测心肌酶、心电图对HIE伴心肌损害的程度及预后判断 ,以及指导临床治疗有较大参考价值 ;生后 12小时内即可监测心肌酶学变化     

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.     

Creatine kinase MB in cases of skeletal muscle trauma

Fifty-eight patients admitted through our emergency room with severe skeletal muscle injury but no obvious cardiac contusions were evaluated for creatine kinase isoenzyme MB (CK-MB). When such patients show an above-normal value for total CK, it is a question of whether or not myocardial injury has been sustained along with skeletal muscle injury when (a) there are no obvious chest contusions or (b) the patient is unconscious and unable to complain of chest pain. Whenever there is doubt concerning the cardiac status of a patient, lactate dehydrogenase (LD) isoenzymes, serial electrocardiograms, and CK isoenzymes are ordered. Our study revealed that serum of 8.6% of the trauma victims had CK-MB values exceeding 5.0 EU/L (reflecting abnormal CK-MB concentrations) as part of their increased total CK. All patients had normal electrocardiographic patterns along with negative results for LD isoenzymes; none had sustained any demonstrable myocardial injury. The CK-MB value must be interpreted together with the total CK value for appropriate diagnosis in patients with skeletal muscle trauma.     

肌酸激酶同工酶检测在急性心肌梗死中的临床价值

目的 探讨肌酸激酶（CK）MB和MM同工酶（CK-MB和CK-MM）亚型在急性心肌梗死（AMI）患者中的变化规律与其预后的关系,评价CK同工酶的亚型检测在AMI心肌早期再灌注、梗死延迟或再梗死诊断中的临床价值。方法 采用琼脂糖凝胶电泳系统将血清CK同工酶亚型分离为CK-MM3、CK-MM2、CK-MM1、CK-MB2和CK-MB1,并分析比较21例AMI患者血清CK同工酶亚型在发病后0～6小时、24小时和72小时的动态变化。结果 AMI患者血清CK-MB和CK-MM在发病后6h开始升高,其中以CK-MB2和CK-MM3升高为主,MB2／MB1〉1．36,MM3／MM1〉0．7;12-24小时达峰值,CK-MB／CK〉30％。15例早期再灌注的AMI患者血清CK、CK-MB和CK-MM在72小时下降至正常,但6例无早期再灌注患者仍处于较高水平,其中MB2／MB1〉1．29,MM3／MM1〉0．65。结论 CK同工酶的亚型检测能反映AMI患者心肌组织损伤的动态过程,可作为一项较灵敏的生化指标,有助于诊断AMI心肌早期再灌注、梗死延迟或再梗死。     

肠道病毒71型IgM阳性手足口病患儿70例心肌酶谱的临床观察

目的了解肠道病毒71型（EV71）IgM阳性手足口病患儿心肌酶谱的改变及其临床意义。方法对我市2009年3—4月收治的EV71IgM阳性的足口病患儿进行心肌酶谱：天门冬氨酸氨基转移酶（AST）、乳酸脱氢酶（LDH）、肌酸激酶（CK）、肌酸激酶同工酶（CK—MB）进行检测并分析其临床意义。结果70例EV71IgM阳性手足口病患儿有66例有一项或多项心肌酶谱异常,占94．3％;其中CK～MB单项异常24例,占34．28％;LDH、CK—MB两项项异常25例,占35．71％;CK、CK—MB两项项异常5例,占7．14％;AST、LDH、CK、CK—MB四项项异常5例,占7．14％：LDH、CK、CK—MB三项异常6例,占8．6％;AST、LDH、CK—MB三项异常1例,占1．42％;四项全正常者4例,占5．7％。结论EV71IgM阳性手足口病患儿大部分心肌酶谱异常,可能存在心肌损害。     

Value of a single troponin T at the time of presentation as compared to serial CK-MB determinations in patients with suspected myocardial ischemia

BACKGROUND: Prior studies with cardiac markers have focused predominantly on subjects presenting to the emergency department with chest pain or unstable angina, and have relied on serial markers for the diagnosis of acute myocardial infarction. We evaluated the diagnostic utility of a single cardiac troponin T (cTnT) determination at the time of presentation as compared to serial creatine kinase (CK) MB determinations in a broad spectrum of patients with suspected myocardial ischemia. METHODS: A total of 267 consecutive patients presenting to the emergency department with suspected myocardial ischemia had a single, blinded cTnT determination drawn at the time of presentation to the emergency department in addition to routine serial electrocardiographic and CK-MB determinations. RESULTS: The specificity (93.7% vs. 87.1%; p<0.05) and positive predictive value (80.0% vs. 69.4%; p<0.05) of a single cTnT determination were superior to that of serial CK-MB determinations without compromising sensitivity. Forty-six percent of patients with confirmed myocardial infarction and an abnormal cTnT at presentation had a normal initial CK-MB determination. Conversely, 20% of patients without acute coronary syndromes had an abnormal CK-MB determination in the setting of a normal cTnT. The initial cTnT was abnormal in all patients with confirmed myocardial infarction and a symptom duration of at least 3.5 h. CONCLUSIONS: In a heterogeneous population of patients with suspected myocardial ischemia, the initial cTnT determination drawn at the time of presentation is a powerful diagnostic tool that, when used in context with symptom duration, allows for more rapid and accurate triage of patients than serial CK-MB determinations.     

Comparison of ASAT, CK, CK-MB, and LD for the estimation of acute myocardial infarct size in man

The purpose of this study was to set up a simple and reliable procedure for estimating acute myocardial infarct (AMI) size by measuring serum enzymes in a few daily blood samples. Peak enzyme values and estimated infarct size from one, two, or three daily samples of aspartate aminotransferase (ASAT), creatine kinase (CK), CK-MB, and lactate dehydrogenase (LD) were compared with the extent of myocardial necrosis measured at autopsy in 22 patients who died from AMI. The correlation between the extent of the necrosis measured and peak serum enzymes from one daily blood sample was highest for CK-MB (r = 0.78) and LD (r = 0.73) compared to CK (r = 0.68) and ASAT (r = 0.67). To obtain a significant correlation, however, two patients had to be excluded from the ASAT and LD analyses. No significant improvement was obtained by more frequent blood sampling. Estimation of infarct size did not improve the correlation significantly for any enzyme, although the coefficient of correlation for CK-MB increased slightly (r = 0.83). Serum CK-MB determination provides a semiquantitative estimate of infarct size, but the other enzymes may give erroneous estimates owing to lesser cardiospecificity.     

Predictive value of serum enzyme determinations in acute myocardial infarction

The prognostic significance of serum enzyme measurements in acute myocardial infarction was studied in 146 patients hospitalized shortly after the attack. Creatine kinase (CK), CK-MB, aspartate aminotransferase (ASAT) and lactate dehydrogenase (LDH) were serially determined every four hours during the first three days following admission.Peak enzyme levels correlated well with the cumulated CK release (r = 0.95, 0.74, 0.70 for CK, ASAT and LDH respectively). Among all enzyme measurements, LDH levels determined when CK reached its peak value provided the best discrimination between acute phase survivors (15 days) and non-survivors. LDH was also the best measurement for identifying patients with ventricular impairment. LDH and ASAT peak levels were more powerful predictors of the patient's risk than CK peak levels. CK levels determined later in the course of myocardial infarction were more discriminant, indicating prolonged CK elevation in non-survivors. There was no significant difference in CK-MB levels, nor in cumulated CK-MB amounts for survivors and non-survivors.It is concluded that serum LDH activity is a better predictor of the short term evolution of myocardial infarction than CK levels or infarct size estimations from serial CK determinations.     

The serum selenium concentration of patients with acute myocardial infarction

Serum selenium concentration was determined in 49 patients with acute myocardial infarction within 4 hours after the beginning of the symptoms. The mean serum selenium concentration of the patients was significantly lower than that of healthy controls (55 +/- 15 micrograms/l vs. 78 +/- 11 micrograms/l). Among the 49 patients with acute myocardial infarction 20 (41%) had serum selenium concentration below the 95% percentile of the healthy control group. It is concluded that the low serum selenium concentration was present in these patients before the acute event and was not a consequence of the myocardial infarction. No relationship was found in this study between the serum selenium concentration and the severity of myocardial infarction if the number of coronary vessels occluded is taken as the criterion of severity. Serum selenium concentration was similar in patients with 1 or more coronary vessels occluded. Patients with anterior or posterior myocardial infarction had similar serum selenium concentrations. A positive correlation was observed between serum selenium concentration and total serum creatine kinase (CK) activity and serum myoglobin (MB). The serum selenium concentration correlated negatively with the ratio CK-MB/total CK activity, which can be interpreted as minor injury of mitochondria during infarction in patients with normal serum selenium concentration.     

Increased activity of creatine kinase isoenzyme MB in a theophylline-intoxicated patient

A 78-year-old woman had increased activities of creatine kinase (CK; EC 2.7.3.2) and CK-MB isoenzyme in her serum, associated with severe theophylline intoxication. The time course for CK-MB activity was similar to that from an acute myocardial infarction. Clinical findings, however, including electrocardiograms, did not support the diagnosis of myocardial infarction. We suggest caution in interpreting CK-MB results in severe theophylline intoxication.     

Release patterns of CK-MB and mitochondrial CK following myocardial ischaemia

Following myocardial damage as in acute myocardial infarction (AMI) or open heart surgery, the tissue damage might result in a release of mitochondrial CK (CK-MIT). The presence of this CK isoenzyme in serum may be detected after chromatographic separation of CK-activity on Sephacryl S-200. By combining chromatographic separation of CK-MB with immunologic inhibition of CK-M, both CK-MB and CK-MIT can be estimated in serum. Using this procedure changes in enzyme activities were studied in ten patients with AMI and twelve patients subjected to open heart surgery using cardioplegia. Following AMI CK-MB peaked about 24 h after onset of ischaemic symptoms. CK-MIT increased similarly and reached a plateau after 24 h where it remained during an additional 24-36 h. At peak CK-MB concentration, the corresponding CK-MIT activity was about 22% of the CK-MB activity. Following cardiac surgery there was a rapid release of CK-MB with a peak about 5 h after release of aortic cross-clamping, and with a simultaneous CK-MIT activity amounting to 19% of the CK-MB activity. In conclusion, CK-MIT is released into serum following myocardial ischaemia. Its appearance has time characteristics similar to that of other mitochondrial enzymes. The CK-B method does not specifically determine CK-B, but non-CK-M, which in cardiac ischaemia at peak serum CK-MB concentrations includes about 20% CK-MIT.     

Acute coronary syndrome and myocardial infarct--new definitions

Until recently a general consensus existed for the clinical entity diagnosed as myocardial infarction using the world health organisation (WHO) definition. According to the WHO definition myocardial infarction was defined by a combination of two of three typical characteristics: typical symptoms, rise of cardiac enzymes (CK, CK-MB), and a typical ECG pattern involving the development of Q waves. New insights into the development of acute myocardial infarction, the superiority of the biochemical characteristics of cardiac troponin assays over CK and CK-MB measurements in blood, and new therapeutic concepts made a new definition of myocardial infarction, e.g. of the acute myocardial infarction, necessary. Timing of the diagnosis of myocardial necrosis is of outmost importance relative to the time of observation (acute, evolving, healing, healed MI), as is the classification of the extent of myocardial damage (microscopic, small, medium or large). The term "acute coronary syndrome" (ACS) has been established as a working diagnosis for choosing the appropriate therapeutic strategy. In patients with ACS and ST elevation ischemia (STEMI ACS, true posterior ischemia inclusive) as well as in patients with presumably new LBBB, immediate reperfusion therapy should be performed (primary PTCA or thrombolytic therapy), whereas in patients with ECG changes other than ST elevation or new LBBB (NSTEMIACS) additional antiplatlet therapy on top of aspirin and heparin is indicated. In contrast to the acute phase of infarction when troponin in blood often is not detectable yet, the diagnosis of definitive myocardial infarction is based primarily on troponin elevation. Hard criteria for established infarction are the development of pathologic Q waves or healing or healed myocardial necrosis in pathology; troponin may be normal then, depending of time relapsed.     

Creatine kinase MM isoforms in serum after cardiac surgery

We evaluated creatine kinase (CK; EC 2.7.3.2) MM3:MM1 isoform ratios in the serum of cardiac patients immediately after cardiac surgery for the diagnosis of perioperative myocardial injury. The mean ratio was 4.8 (range, 1.4-10.7) in 22 patients who had postoperative myocardial complications and 4.6 (1.3-9.6) in 66 patients who did not. By the first postoperative day the ratio had decreased substantially in both groups of patients. The isoform ratio did not correlate with the concentration of total CK, CK-MB, total lactate dehydrogenase (LD), or the incidence of LD1:LD2 or LD5:LD2 ratio reversal. Of these measurements, CK-MB and LD concentrations differed most between the groups of patients; parallel testing of CK-MB and LD showed an optimized sensitivity and specificity of 77% and 87%, respectively. We conclude that analysis for CK-MM isoforms does not add information in the period immediately after cardiac surgery; concentrations of CK-MB and LD correlate with myocardial injury, but the sensitivity and specificity of these measurements may not be high enough for clinical utility.