Activity of serum aspartate aminotransferase isoenzymes in patients with acute myocardial infarction

Activities of aspartate aminotransferase (AST) isoenzymes were determined in serial serum samples from 40 cases of acute myocardial infarction, and compared with activities of creatine kinase, CK-MB isoenzyme, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase for temporal changes. Cytosolic (soluble) AST (s-AST) and mitochondrial AST (m-AST) respectively increased 6.6 and 9.0 h after onset of chest pain. The median time at which serum m-AST activity peaked (15.8 U/L, range 6.4-53.5 U/L) was 47.8 h after the onset of infarction, 19.8 h later than the peak s-AST activity (171 U/L, range 53-517 U/L) and m-AST also disappeared from the serum more slowly than s-AST (p less than 0.001). Serum m-AST values were above normal for at least six days after the infarct. The ratio of m-AST to total AST in serum increased after myocardial infarction, being greatest (20%, range 11-32%) on the third day after onset. For individuals, peak activities of s-AST correlated well with total CK (r = 0.91) and CK-MB (r = 0.86) peak activities, indicating that s-AST also reflects the infarct size. However, m-AST correlated poorly with the enzymes commonly used in infarct diagnosis; it apparently provides different biological information.     

Clinical effectiveness of the Du Pont aca measurement of creatine kinase MB in serum from patients in a coronary-care unit

We evaluated the clinical effectiveness of measuring creatine kinase (CK; EC 2.7.3.2) isoenzyme MB and lactate dehydrogenase (LD; EC 1.1.1.27) isoenzymes in diagnosis of acute myocardial infarction. We used an agarose electrophoresis method to measure CK and LD isoenzymes and the Du Pont aca column method to measure CK-MB. Serial blood specimens were drawn from 100 patients consecutively admitted to our Coronary Care Unit. Because of the low diagnostic specificity for CK-MB measurements by both agarose electrophoresis and the discrete-analysis method, as compared with reported values, we re-evaluated our isoenzyme data by using Receiver Operating Characteristic curves. Such analysis of the data established optimal decision levels of greater than or equal to 25 U/L and greater than or equal to 18 U/L plus greater than or equal to 6% of total CK for serum CK-MB measured by the agarose electrophoresis and the aca methods, respectively, and an optimal decision level of greater than or equal to 0.92 for the ratio of LD 1/2 measured after agarose electrophoresis. At these decision levels we obtained a sensitivity of 100%, 100%, and 95% and a specificity of 94%, 92%, and 90% for CK-MB (agarose electrophoresis), CK-MB (aca), and the LD 1/2 ratio, respectively.     

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.     

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.     

Evaluation of ck-mb isoform analysis for early diagnosis of myocardial infarction

Measurement of CK-MB and its isoforms by high-voltage electrophoresis has been proposed as a sensitive test for early detection of myocardial infarction (MI). We performed a prospective study of this test in 231 patients presenting to the Emergency Department with symptoms consistent with ischemic chest pain. Blood specimens were obtained at 0, 1, and 3 h following presentation, and plasma was immediately frozen and analyzed within 1 week by high-voltage electrophoresis for total CK-MB and isoforms. The test was considered positive whenever total CK-MB was elevated (>6 U/L) or the cardiac isoform MB₂ was relatively increased (MB₂ > 2 U/L and MB₂/MB₁ > 1.7). This test had a sensitivity of 68% overall and 55% for specimens collected within 3 h of symptom onset. It was positive within 3 h of presentation in 36/39 (92%) of patients with confirmed MI. Specificity was 92% overall and did not vary with time after symptoms. The CK-MB alone, at the cutoff of 6 U/L, had lower sensitivity overall (56%; p = 0.01) and within 3 h of onset (39%; p = 0.03), and higher specificity overall (98%; p < 0.001). Lowering the cutoff for CK-MB alone to match the sensitivity of the isoform test caused a greater loss of specificity. It is concluded that analysis of CK-MB by high-voltage electrophoresis is an effective method for rapid diagnosis of MI, with the isoform analysis enhancing early sensitivity.     

Serum enzymes in acute myocardial infarction after intracoronary thrombolysis

Serum kinetics of total creatine kinase (CK), CK-MB isoenzyme, aspartate aminotransferase (AST), lactate dehydrogenase (LD) and alpha-hydroxybutyrate dehydrogenase (HBD) activities were studied in twenty patients with acute myocardial infarction randomly assigned to receive either intracoronary urokinase (group A) or conventional (control) therapy (group B). The temporal characteristics of enzyme changes described were the time lag from onset of chest pain until maximum catalytic concentration value, the rate at which enzymes are released into blood, the peak value of the serum enzyme curves and (d) the fractional disappearance rate (Kd) for each enzyme considered. Thrombolytic treatment induced earlier peak times in group A: for CK, 10.8 vs 27.0 h, for CK-MB, 10.4 vs 23.1, for AST, 13.9 vs 31.3, for LD, 24.4 vs 49.1, and for HBD, 20.5 vs 48.5 (for all enzymes, p less than 0.001). The maximal rate of release for the enzymes was at least twofold greater in group A. Enzyme peak activities and Kd were not significantly different between the groups. The most significant discrimination between the two groups was obtained with AST peak time (Hartz overlap index (Oi) = 0.11) and CK-MB peak time (Oi = 0.12).     

Cardiac enzyme changes in myxedema coma

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.     

高功率脉冲微波对心肌酶谱的影响

目的研究高功率脉冲微波( high power pulse microwave ,HPPM)辐照对心肌酶谱的影响. 方法以实验犬 30只和离体培养原代乳鼠心肌细胞为对象,检测 HPPM辐照后不同时间点动物血清和细胞培养液中天门冬氨酸氨基转移酶、乳酸脱氢酶、乳酸脱氢酶同工酶、肌酸激酶、肌酸激酶同工酶、羟丁酸脱氢酶和碱性磷酸酶活性的变化. 结果HPPM辐照后,出现以酶活性显著降低为主的心肌酶谱紊乱.实验犬以肌酸激酶的变化最为敏感,于辐照后 6 h～ 1个月 [辐照后 6, 24 h,3 d,1, 2周, 1个月实验犬的肌酸激酶分别为( 796.9± 756.70) ,(287.8± 274.87),(367.2± 241.16),(324.4± 128.81),(336.5± 152.36),(257.5± 105.86),(165.8± 99.00) mmol/L]一直显著降低( t=2.67～ 4.77,P< 0.01);细胞培养液心肌酶多于辐照后 0～ 1 h下降到最低水平, 24 h时大多恢复到正常水平, 48 h时酶活性出现显著性增高. 结论HPPM辐照可明显影响实验动物和心肌细胞的心肌酶活性.     

Analytical and clinical evaluation of creatine kinase MB mass assay by IMx: comparison with MB isoenzyme activity and serum myoglobin for early diagnosis of myocardial infarction.

We analytically and clinically evaluated Abbott's IMx assay for creatine kinase (CK) isoenzyme MB (CK-MB) in serum. Over a 1-year period, the method was more specific but less precise than catalytic isoenzyme measurements by electrophoresis or immunoinhibition. Sera from different individuals without electrophoretic evidence of CK-MB but containing macro CK type 1 (n = 20), mitochondrial CK (n = 5), or CK-BB (n = 5) were scored as CK-MB negative by the IMx. Likewise, CK-MB-negative by the sera remained so after addition of purified human CK-MM (< or = 7600 U/L) or CK-BB (< or = 8100 U/L). For 39 patients admitted for suspicion of uncomplicated acute myocardial infarction (precordial pain for < or = 4 h), the diagnostic performance of the IMx CK-MB assay on admission and 4 h later was superior to that of total CK activity and compared well with that of CK-MB activity measured by electrophoresis or immunoinhibition. An admission, myoglobin showed a higher diagnostic sensitivity, specificity, and predictive value than did CK-MB and was the most informative test. Diagnostic performance on admission and 4 h later was further improved by considering positivity for myoglobin and for CK-MB by IMx and for the change in each over the first 4 h of hospitalization as criteria. Twelve hours after admission, diagnostic performance was further improved for all CK and CK-MB methods but began to decline for myoglobin.     

"Flipped" patterns of lactate dehydrogenase isoenzymes in serum of elite college basketball players

We kinetically measured total lactate dehydrogenase (LD, EC 1.1.1.27), total creatine kinase (CK, EC 2.7.3.2), and aspartate aminotransferase (AST, EC 2.6.1.1.) in 16 elite college basketball players, before the competition season and not in close temporal relation to near-maximal exercise, and in 17 healthy non-athlete controls. LD isoenzymes were determined by both electrophoretic and immunoprecipitation methods. CK-MB isoenzyme was measured electrophoretically. We found significantly higher mean LD-1 values and LD-1/LD-2 ratios in the players than the controls: 31.6 (SD 3.7)% vs 25.8 (SD 3.2)% (P less than 0.005) and 1.1 (SD 0.13) vs 0.87 (SD 0.16) (P less than 0.001), respectively. A "flipped" LD pattern (LD-1 greater than LD-2) was found in half the players and in six of the eight black athletes, but in only two of the control group and in none of the black controls. Mean CK activity in serum exceeded normal values in the serum of the athletes and was higher in comparison with the control group [274 (SD 156) vs 103 (SD 82) U/L]. Mean CK was significantly higher in the eight athletes with the flipped LD pattern than in those with LD-1 less than LD-2 [322 (SD 163) vs 180 (SD 98) U/L; P = 0.05], and also in comparison with CK in the two controls with flipped LD pattern. We saw no significant difference in mean CK between the nine players with normal immunochemical LD-1/LD ratios and the seven players with above-normal ratios. CK-MB was not detected in either athletes or controls. None of the players had any clinical or electrocardiographic evidence for myocardial ischemia or infarction. Evidently the flipped LD pattern usually found in patients with acute myocardial infarction and reported in some athletes after extreme exercise such as ultra-marathon running may also be found in athletes who are in their "basal fitness shape" but who are not involved in competitive physical activity.     

Creatine kinase:aspartate aminotransferase activity ratio as an indicator of the source of an increased creatine kinase activity

Although measurements of creatine kinase isoenzyme 2 (CK-MB) are often used to diagnose acute myocardial infarction, their sensitivity and specificity are less than 100%. Because skeletal muscle contains more CK and less aspartate aminotransferase (AST) than cardiac muscle, the CK/AST ratio might provide a useful adjunct in evaluating the source of a supranormal value for CK. I established the following decision levels in a retrospective study of 342 patients: ratios less than 14 (if total CK was 300-1200 U/L), less than 20 (CK 1201-2000 U/L), or less than 25 (CK greater than 2000 U/L) suggested myocardial infarction, with a sensitivity of 95% and a specificity of 65%. In a validation study with 277 additional patients, liver disease and alcohol abuse caused erroneous results, leading to exclusion of 22% of these patients. In the remaining cases, sensitivity was 94%, specificity 90%. The CK/AST ratios changed little with time, suggesting that a single value would be adequate for evaluating patients with increased CK.     

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.     

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.     

Lactate dehydrogenase isoenzyme 1: Its usefulness as a screening test in diagnosis of myocardial infarction

Immunological assay of LD-1 activity provides a quantitative measurement of the type of lactate dehydrogenase (LD, EC 1.1.1.27) activity characteristic of myocardial origin. Using this test, a laboratory diagnosis of myocardial infarction can be either ruled out or confirmed in approximately 75% of patients in whom this diagnosis is suspected, without electrophoretic separation of creatine kinase (CK, EC 2.7.3.2.) and LD isoenzymes. Normal total CK and LD activities cannot be used to rule out myocardial infarction since CK-MB and LD-1 may have increased although total activities remain within their reference ranges. LD-1 activity increases as quickly as CK-MB following the onset of pain in the majority of patients but it remains elevated longer giving a greater period of time during which the diagnosis of myocardial infarction can be confirmed.     

Immunochemical extraction and automated measurement of plasma creatine kinase MB isoenzyme and creatine kinase MB2 isoform

Measurement of creatine kinase MB (CK-MB) and its isoforms CK-MB₂ and CK-MB₁ are now applied in the diagnosis of acute myocardial infarction (AMI). The most common approach for analysis includes RIA, IRMA, and electrophoresis, all of which may be time-consuming. This study examines determination of CK-MB and CK-MB₂ by a rapid immunochemical extraction method followed by an automated measurement for both analytes. The automated method was sensitive to 2 U/L, linear to 180 U/L, and gave excellent interassay precision (<10% CV). Interference studies indicated that bilirubin, hemolysis, and lipemia caused analytical problems as did the presence of high activities of other CK isoenzymes, notably CK-MM and CK-BB, requiring dilution of samples prior to analysis. Application of immunochemical extraction gave a reference interval of CK-MB (0–2.5 U/L) and CK-MB₂ (0.1–1.4 U/L) for blood donors (20–60 years), peak levels for ruled-out AMI patients of CK-MB (0.5–7.3 U/L) and CK-MB₂ (0.3–4.9), peak levels for ruled-in AMI patients of CK-MB (80–174 U/L) and CK-MB₂ (80–155 U/L). Coronary artery bypass patients (n = 24) and all trauma patients (n = 14) also demonstrated elevations in CK-MB and CK-MB₂, whereas only five of the trauma patients demonstrated increased CK-MB by IRMA. In patients (n = 7) having increased total CK and normal CK-MB by IRMA, the extraction assay for CK-MB and CK-MB₂ yielded increased values in all patients. This new approach to CK-MB and CK-MB₂ analysis can be performed within 30 minutes of sample receipt. J. Clin. Lab. Anal. 11:163–168, 1997. © 1997 Wiley-Liss. Inc.     

Differentiating muscle damage from myocardial injury by means of the serum creatine kinase (CK) isoenzyme MB mass measurement/total CK activity ratio

We immunoenzymometrically measured creatine kinase (CK) isoenzyme MB in extracts of myocardium and in homogenates of five different skeletal muscles. CK-MB concentrations in the former averaged 80.9 micrograms/g wet tissue; in the skeletal muscles it varied widely, being (e.g.) 25-fold greater in diaphragm than in psoas. CK-MB in skeletal muscles ranged from 0.9 to 44 ng/U of total CK; the mean for myocardium was 202 ng/U. In sera from 10 trauma and 36 burn patients without myocardial involvement, maximum ratios for CK-MB mass/total CK activity averaged 7 (SEM 1) ng/U and 18 (SEM 6) ng/U, respectively. Except for an infant (220 ng/U), the highest ratio we found for serum after muscular damage was 38 ng/U. In contrast, the mean maximum ratio determined in 23 cases of acute myocardial infarction exceeded 200 ng/U. Among seven determinations performed 8 to 32 h after onset of symptoms, each infarct patient demonstrated at least one ratio greater than or equal to 110 ng/U. Ratios observed after infarct were unrelated to treatment received during the acute phase. We propose a CK-MB/total CK ratio of 80 ng/U as the cutoff value for differentiating myocardial necrosis from muscular injury.     

N末端脑钠肽前体与心肌酶谱联合检测在心力衰竭诊断及预后分析中的应用

目的探讨N末端脑钠肽前体(NT-proBNP)与心肌酶谱联合检测在心力衰竭(HF)诊断中的应用价值。方法选择2019年5月-2020年1月徐州医科大学附属第三医院收治的76例HF患者作为HF组,另外选择同期76例健康体检者作为健康对照组。比较两组的血清NT-proBNP、乳酸脱氢酶(LDH)、α-羟丁酸脱氢酶(HBD)、肌酸激酶(CK)和肌酸激酶同工酶(CK-MB)水平。根据美国纽约心脏病学会(NYHA)心功能分级划分HF患者的病情严重程度等级,并对患者进行随访,观察预后,比较不同NYHA分级和不同预后患者的血清NT-proBNP、LDH、HBD、CK、CK-MB水平,分析上述指标与HF患者NYHA分级和不良预后的相关性。结果 HF组NT-proBNP、LDH、HBD、CK、CK-MB水平均明显高于健康对照组〔NT-proBNP(ng/L):534.02±73.24比68.91±8.29,LDH(μmol·s^-1·L^-1):5.81±0.79比2.67±0.53,HBD(U/L):319.82±41.08比95.31±13.29,CK(U/L):286.61±57.18比90.34±15.07,CK-MB(U/L):58.82±6.05比12.06±3.04,均P<0.05〕;NYHA分级≥Ⅲ级患者的NT-proBNP、LDH、HBD、CK、CK-MB水平均明显高于NYHA分级<Ⅲ级的患者〔NT-proBNP(ng/L):718.04±74.52比345.39±61.05,LDH(μmol·s^-1·L^-1):7.52±1.03比4.15±0.76,HBD(U/L):398.35±48.67比224.08±26.71,CK(U/L):388.26±61.08比179.74±30.43,CK-MB(U/L):78.61±9.07比39.34±5.82,均P<0.05〕;预后不良患者的NT-proBNP、LDH、HBD、CK、CK-MB水平均明显高于预后良好患者〔NT-proBNP(ng/L):759.35±79.17比291.24±56.82,LDH(μmol·s^-1·L^-1):8.04±1.12比3.79±0.67,HBD(U/L):410.04±51.81比209.18±24.86,CK(U/L):411.95±63.72比158.63±28.54,CK-MB(U/L):86.05±10.82比35.08±5.29,均P<0.05〕。Pearson相关性分析显示,NT-proBNP、LDH、HBD、CK、CK-MB与HF患者NYHA分级和不良预后均呈正相关(均P<0.05)。结论 NT-proBNP、LDH、HBD、CK、CK-MB联合检测在HF诊断中具有较高的应用价值,并能为患者病情及预后分析提供指导。     

Lactate dehydrogenase isoenzyme-1 in serum for detection of peri-operative myocardial infarction after cardiac surgery

We prospectively studied changes in serum lactate dehydrogenase isoenzyme-1 (LD-1, EC 1.1.1.27) in 99 consecutive patients after either coronary artery bypass grafting (CABG, n = 61), isolated cardiac-valve replacement (n = 24), or the two procedures combined (n = 14); 86 of these had no clinical evidence of peri-operative myocardial infarction (MI). Blood was sampled immediately after surgery and at 6-h intervals for up to 42 h thereafter. LD-1 was isolated by using the LD M-subunit antiserum. Samples from the non-MI patients were used to establish the reference intervals for LD-1. By 24 h after surgery, mean serum LD-1 values were higher (P less than 0.001) in non-MI patients who underwent isolated valve replacement (222 +/- 74 U/L) or combined CABG and valve replacement (266 +/- 58 U/L) than in 50 non-MI patients who underwent CABG alone (134 +/- 42 U/L). Separate reference intervals were determined for CABG and other patients at each sampling time. By 24 h after operation, LD-1 exceeded these reference intervals in the 10 CABG and two combined-procedure patients in whom other evidence of MI was present. Measurement of LD-1 24 to 42 h after cardiac surgery appears to be a useful test for the diagnosis of perioperative MI.     

Mass concentration of creatine kinase MB isoenzyme and lactate dehydrogenase isoenzyme 1 in diagnosis of perioperative myocardial infarction after coronary bypass surgery

Recent advances in methodology allow the mass concentration of creatine kinase MB isoenzyme (CK-MB), and of lactate dehydrogenase isoenzyme 1 (LD1) to be determined quickly and easily as routine, emergency tests. We evaluated these tests as diagnostic criteria of perioperative myocardial infarction (PMI) after coronary bypass surgery. These tests were compared with the usual measurements of CK-MB activity by immunoinhibition and LD1 by electrophoresis and with other biological markers of myocardial infarction such as total CK, total LD, and aspartate aminotransferase. Sixty-one patients who underwent coronary bypass grafting were followed pre- and postoperatively by enzyme determinations and electrocardiography; a subgroup was monitored by myocardial scintigraphy. CK-MB mass appeared to be the best marker of PMI during the first 48 h, although LD1 was the marker of choice from days 2 to 4.     

Vigorous response in plasma N-terminal pro-brain natriuretic peptide (NT-BNP) to acute myocardial infarction

Acute myocardial infarction (MI) results in activation of neurohormonal systems and increased plasma concentrations of myocardial enzymes and structural proteins. We hypothesized that plasma levels of N-terminal pro-brain natriuretic peptide (NT-BNP) would respond more vigorously after MI than those of other natriuretic peptides. We also sought to compare this response with that of the established myocardial injury markers troponin T (TnT), myoglobin and creatine kinase MB (CK-MB). We obtained multiple blood samples for measurement of atrial natriuretic peptide (ANP), N-terminal pro-ANP, brain natriuretic peptide (BNP) and NT-BNP along with CK-MB, TnT and myoglobin in 24 patients presenting to the Coronary Care Unit within 6 h of onset of MI. Multiple samples were obtained in the first 24 h, then at 72 h, 1 week, 6 weeks and 12 weeks. NT-BNP increased rapidly to peak at 24 h and exhibited greater ( P <0.001) absolute increments from baseline compared with BNP and ANP, whereas NT-ANP did not change from baseline. Proportional increments in NT-BNP were also greater than those for the other natriuretic peptides ( P <0.05). Natriuretic peptide levels reached their peak around 24 h, later than peak TnT, CK-MB and myoglobin (peak between 1-10 h), and NT-BNP and ANP remained elevated on average for 12 weeks. Our present results, with detailed sampling of a cohort of acute MI patients, demonstrate greater absolute and proportional increments in NT-BNP than ANP or BNP with sustained elevation of these peptides at 12 weeks.