Serum creatine kinase and creatine kinase-MB isoenzyme activities in perinatally asphyxiated newborns

Serum creatine kinase (CK) and creatine kinase-MB isoenzyme (CK-MB) activities were studied prospectively in serial blood samples obtained from 23 perinatally asphyxiated negroid newborns and 12 healthy controls during the first 100 h of life. The asphyxiated infants had significantly elevated mean CK and absolute CK-MB but no fractional CK-MB activities. Peak mean CK and CK-MB values (U.l-1) were 789.17 (+/- 220), P less than 0.01 and 16.36 (+/- 3.0) P less than 0.001 respectively at the 6-8 post-partum period. The healthy controls, on the other hand, showed a steady decline in the activities of these enzymes from birth. The vaginally and operatively delivered asphyxiated infants showed significantly higher CK and CK-MB activities than their respective non-asphyxiated controls, but no increase in fractional CK-MB was recorded in any of the groups. The elevation in absolute and fractional CK-MB 42.0 U.l-1 (5.1%) in respect of the infants with TTI (transient tricuspid incompetence) was significant (P less than 0.05) when compared with the controls with features of TTN (transient tachypnoea of the newborn) in the 6-8 h post-partum period. One of the infants with TTI at autopsy had hypoxic myocardial injury. The specificity of CK-MB, as a marker of myocardial injury in asphyxiated negroid neonates, is plausible but remains uncertain. Until the lack of rise of CK and CK-MB in healthy negroid newborns is confirmed in a larger series with further studies on MM, BB and MB isoenzymes, caution is urged in the interpretation of elevated CK and CK-MB activities in asphyxiated negroid newborns.     

Serum creatine kinase and creatine kinase MB isoenzyme responses of post-infarction patients after a graded exercise test.

The response of total creatine kinase (CK) and the creatine kinase isoenzyme (CK MB) was studied in 22 male post-infarction patients (three to six months after myocardial infarction) after a functional graded exercise test, before entering a rehabilitation programme. Eleven subjects (group A) completed the test without developing significant electrocardiographic abnormalities. Eleven subjects (group B) showed changes that necessitated premature termination of the test. No significant differences were observed before the functional graded exercise test between the groups in serum concentration of CK, CK MB, and the percentage of CK MB to CK (MB/ CK%). The two groups were significantly different (p less than 0.01) 24 hours after the graded exercise test in CK MB and MB/CK%, but not in CK. In group B, CK and CK MB rose significantly after the graded exercise test (p less than 0.05) as did MB/CK% (p less than 0.01). In group A only CK showed a significant rise (p less than 0.05). It is probable that increases in CK MB after exercise arise from myocardial tissue efflux, reflecting reversible ischaemia. It is concluded from this study that CK MB appears to be a specific indicator of myocardial ischaemia and could, therefore, be of significant assistance in the clinical and functional assessment of the post-infarction patient.     

Creatine kinase and its isoenzyme MB in patients after open heart surgery.

Total serum creatine kinase (CK) and its isoenzyme MB (CKMB) were measured before and 4, 24, 48 and 72 hours after termination of cardiopulmonary bypass in patients undergoing (I) atriotomy, (II) ventriculotomy and (III) coronary artery bypass surgery. All patients were free of postoperative complications and myocardial infarction as defined by clinical course, 12 lead ECG and 2D echocardiography. Peak elevation of CK occurred at 24th hour and CKMB at 4th hour and then gradually declined. There was no relation between the peak level of rise of CK or CKMB with cross clamp time or bypass time. The 96th percentile values of absolute CKMB level at 4, 24, 48 and 72 hours may suggest perioperative myocardial infarction with specificity of 95%. In addition, the rising value of CKMB beyond 24 hours after the termination of bypass may also suggest occurrence of myocardial infarction.     

Mortality risk conferred by small elevations of creatine kinase-MB isoenzyme after percutaneous coronary intervention

OBJECTIVES: The aim of this study was to assess whether small creatine kinase-MB isoenzyme (CK-MB) elevations after percutaneous coronary intervention (PCI) affect the subsequent mortality risk. BACKGROUND: Several studies have evaluated the relationship of CK-MB levels after PCI with the subsequent risk of death. While there is consensus that elevations exceeding 5 times the upper limit of normal increase mortality significantly, there is uncertainty about the exact clinical impact of smaller CK-MB elevations. METHODS: We performed a meta-analysis of seven studies with CK-MB measurements and survival outcomes on 23230 subjects who underwent PCI. Data were combined with random effects models. RESULTS: Mean follow-up was 6 to 34 months per study. By random effects, 19% (95% confidence interval [CI], 16% to 23%) had one- to five-fold CK-MB elevations, while only 6% (95% CI, 5% to 9%) had >5-fold elevations. Compared with subjects with normal CK-MB, there was a dose-response relationship with relative risks for death being 1.5 (95% CI, 1.2 to 1.8, no between-study heterogeneity) with one- to three-fold CK-MB elevations, 1.8 (95% CI, 1.4 to 2.4, no between-study heterogeneity) with three- to five-fold CK-MB elevations, and 3.1 (95% CI, 2.3 to 4.2, borderline between-study heterogeneity) with over five-fold CK-MB elevations (p < 0.001 for all). CONCLUSIONS: Any increase in CK-MB after PCI is associated with a small, but statistically and clinically significant, increase in the subsequent risk of death.     

非体外循环冠状动脉旁路移植术围术期cTnI、CK及CK-MB的变化

目的 :通过对非体外循环冠状动脉旁路移植术 （OPCABG）患者 ,围手术期血清心肌肌钙蛋白 I（c Tn I）、肌酸磷酸激酶 （CK）、肌酸磷酸激酶同工酶 MB（CK- MB）变化的观察 ,探讨 OPCABG围手术期心肌损伤的情况。方法 :选择 2 0例全麻常温下进行 OPCABG患者及 2 0例同期行肺叶切除术患者 （对照组 ） ,麻醉诱导气管插管后以微量输液泵持续输注异丙酚、利多卡因复合液 ,并间断静脉注射芬太尼和哌库溴铵维持麻醉。在麻醉诱导前、术后 1h、2 4h、4 8h4个时间点抽取血样测定 c Tn I、CK、CK- MB值。结果 :所有患者手术经过及术后恢复顺利 ,OPCABG组无一例转为体外循环。两组患者术前 CK、CK- MB均在正常范围 ,术后 1h开始升高 ,术后 2 4 h达峰值 ,与麻醉前比较 ,均 P<0 .0 1;术后 4 8h明显下降 ,但仍高于麻醉前水平 （P<0 .0 1）。 4个时间点两组 CK、CK- MB值相比 ,差异无显著性。OPCABG组 c Tn I值与术前比较 ,术后 1h开始升高 （P<0 .0 1） ,2 4 h达峰值 （P<0 .0 1） ,术后 4 8h有所下降 ,但仍高于麻醉前水平 （P<0 .0 1） ;而肺叶切除组术后 c Tn I值始终不高。术前、术后 1h两组 c Tn I值差异无显著性 ,但 OPCABG组术后 2 4 h、4 8h值均明显高于肺叶切除组 （P<0 .0 1）。手术全程及术后 4 8h动态心电图未发现心肌梗死 ,血?     

Significance of elevated MB isoenzyme with normal creatine kinase in acute myocardial infarction

The significance of elevated levels of the MB isomer of creatine kinase (CK-MB) when creatine kinase (CK) level is normal was studied in 400 patients with suspected acute myocardial infarction (AMI). In 350 patients both CK and CK-MB were elevated (group 1), in 21 only CK-MB was elevated (group 2), in 24 neither enzyme was elevated (group 3) and in 5 only CK was elevated (group 4). In 57% of patients in group 2 the CK level was doubled, with a characteristic enzyme curve, within the normal range, suggesting that an increase in CK had been missed because arbitrary definitions of "normal" were used. The median CK increase (60 IU/liter) in group 2 was greater than that in group 3 (23 IU/liter) (p less than 0.001). Patients in group 1 with small AMIs had a relative increase in CK similar to that in group 2. However, patients in group 2 had a lower baseline CK level so that peak CK did not become abnormally high despite a 5-fold increase in some patients. In patients in group 1 with small AMIs, CK was elevated in fewer samples than CK-MB. If only 2 samples were obtained in all patients, elevation of CK levels would have been missed in 63 group 1 patients, erroneously increasing the number of patients in group 2 fourfold (to 84 of 400, or 21%, instead of 21 of 400, or only 5%). Conversely, if patients in group 2 with a doubling of CK are excluded, the prevalence of elevated CK-MB with normal CK would be only 9 of 400 (2%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Creatine kinase MB isoenzyme studies in diagnosis of myocardial infarction.

Serial measurements of the MB isoenzyme of creatine kinase, total creatine kinase, aspartate mainotransferase, and urea stable lactate dehydrogenase have been made in the serum of a series of 139 patients admitted with a diagnosis of suspected myocardial infarction. Serum MB isoenzyme measurements have also been made on postoperative surgical patients and patients with medical disorders known to have caused raised serum total creatine kinase activity. All these enzymes were abnormal in at least one specimen from all patients with electrocardiographically proved acute myocardial infarction. The magnitude of the MB isoenzyme rise was 2 to 3 times greater than that of any of the other enzymes. The duration of its rise was relatively short. The MB isoenzyme was more specific for myocardial infarction than other enzymes and no increases were found in postoperative patients, except in those after cardiac bypass surgery. The MB isoenzyme seems the most sensitive and specific test for myocardial infarction available, though there are technical problems in its accurate measurement.     

Creatine kinase MB isoenzyme studies in diagnosis of myocardial infarction.

Serial measurements of the MB isoenzyme of creatine kinase, total creatine kinase, aspartate mainotransferase, and urea stable lactate dehydrogenase have been made in the serum of a series of 139 patients admitted with a diagnosis of suspected myocardial infarction. Serum MB isoenzyme measurements have also been made on postoperative surgical patients and patients with medical disorders known to have caused raised serum total creatine kinase activity. All these enzymes were abnormal in at least one specimen from all patients with electrocardiographically proved acute myocardial infarction. The magnitude of the MB isoenzyme rise was 2 to 3 times greater than that of any of the other enzymes. The duration of its rise was relatively short. The MB isoenzyme was more specific for myocardial infarction than other enzymes and no increases were found in postoperative patients, except in those after cardiac bypass surgery. The MB isoenzyme seems the most sensitive and specific test for myocardial infarction available, though there are technical problems in its accurate measurement.     

Evaluation of creatine kinase and creatine kinase-MB for diagnosing myocardial infarction. Clinical impact in the emergency room

We prospectively studied the performance of emergency room strategies using a single sampling of total creatine kinase (CK) only and total CK with, if total CK levels were elevated, CK-MB levels in 639 patients with acute chest pain, including 386 patients who were admitted and 253 patients who were discharged. Acute myocardial infarction was diagnosed in 104 patients and excluded in 535. An elevated total CK level had a sensitivity of only 38% and specificity of only 80%, whereas a CK-MB level over 5% of an elevated total CK level had a sensitivity of only 34% and specificity of 88%. The sensitivities of both CK and CK-MB were higher in patients who arrived more than four hours after the onset of symptoms, and, in this population, the strategy using CK-MB performed significantly better than the strategy using total CK alone. Since a very positive CK-MB in a low-risk patient can greatly raise the probability of myocardial infarction, future strategies using CK-MB may have a role in selected subsets in determining which patients should not be sent home. However, the sensitivity of a single sampling of CK and CK-MB is too low for these assays to be used to exclude myocardial infarction in the emergency room or to be used as the rationale for deciding not to admit a patient.     

Serum creatine kinase MM isoenzyme sub-bands after acute myocardial infarction in man

Using an isoelectric-focusing (IEF) method developed to quantitate MM isoenzyme-creatine kinase (CK) sub-band activity, we identified a reproducible time-varying pattern of these sub-bands in the serum of eight patients with acute myocardial infarction (MI). Our observations are consistent with the view that MM3-CK (the M2-CK dimer, the pure gene product) is converted intravascularly to MM2-CK, and then to MM1-CK (the M1-CK dimer, the pure postsynthetic sub-band). The MM3-CK reaches a peak first, 16 hours after infarction, followed by MM2-CK, and then by MM1-CK. The MM3-CK is the dominant sub-band in normal myocardium; there is much less MM2-CK and virtually no MM1-CK. The MM3-CK sub-band peak may indicate the time at which enzyme ceases to be released from the injured myocardium. The ratio MM3-CK:MM1-CK rises within 6 hours after onset of chest pain from a baseline of 0.38 and peaks 10 hours after MI. The peak ratio was between 1.1 and 4.2, and the value correlated with the time when total CK activity peaked after MI. The 10-fold change in the MM3:MM1 ratio after MI, as well as the early period at which this ratio peaks (10 hours), makes this an earlier and more sensitive indicator of enzyme release.     

Reduction of creatine kinase and creatine kinase-MB indexes of infarct size by intravenous verapamil

In a prospective, controlled study, 29 patients were randomly allocated to receive intravenous verapamil, 5 to 10 mg/hour, for 2 days starting at a mean of 8 hours after the onset of myocardial infarction. Twenty-five patients received no specific treatment and served as control subjects. Left ventricular (LV) filling pressure in all patients was initially less than 15 mm Hg. Age, infarct localization and hemodynamic values on admission (Swan-Ganz catheter) were comparable in both groups. Maximal creatine kinase (CK) and creatine kinase-MB (CK-MB) values were markedly lower in the verapamil group than in the control group (CK 547 vs 703 U/liter, p less than 0.05; CK-MB 51 vs 68 U/liter, p less than 0.025), as was infarct weight (48 vs 65 g-Eq, p less than 0.03; CK-MB 31 vs 49 g-Eq, p less than 0.005). Arterial blood pressure was 10% lower in the verapamil group than in the control group. Systemic vascular resistance and LV filling pressure remained unchanged. Verapamil reduced myocardial infarction size by about 30% in patients without LV failure and the arterial pressure was reduced.     

Creatine kinase-MB mass concentration versus creatine kinase-B activity for the detection of acute myocardial infarction in patients with slightly elevated total creatine kinase activity in serum

Abstract. Objective . The diagnostic value of creatine kinase-MB mass concentration (CK-MB mass) was compared with that of creatine kinase-B (CK-B) activity in patients with suspected acute myocardial infarction (AMI) but with total serum CK activity only slightly above the reference range. Design . One hundred consecutive blood samples with total CK activity between 120 and 360 U I^-1 and CK-B activity ≥ 9 U I^-1 were analysed. Electrophoresis of CK isoenzymes was also performed. Setting . Patients from all departments of the hospital were included. About half of the patients originated from the coronary care unit. Subjects . The blood samples derived from 49 patients. Thirteen patients had at least one serum sample with total CK activity above 360 U I^-1. These and another three patients were omitted from the study. Results . Acute myocardial infarction had been diagnosed clinically (with CK and CK-B methods) in 12 of 33 patients. However, using the CK-MB mass concentration of the reference method, five of these 12 patients did not have myocardial infarction whereas nine patients with small infarctions were undetected. A good correlation was seen between the results from CK-MB mass concentration and CK isoenzyme electrophoresis, but there was a poor correlation between these methods and CK-B activity including the CK-B/CK ratio. A relatively high proportion (24%) of the selected patients had increased levels of macro CK. Conclusion . CK-B activity was inaccurate for the detection of probable myocardial infarction in patients with slightly elevated total CK activity. Increased levels of macro CK interfering with the CK-B assay was one explanation for this observation.     

Weak diagnostic performance of troponin,creatine kinase and creatine kinase-MB to diagnose or exclude myocardial infarction after successful resuscitation

Background

The aim of this study is to evaluate the diagnostic accuracy of the cardiac injury markers troponin (TNT), creatine kinase (CK) and creatine kinase-MB (CK-MB) to diagnose or exclude acute myocardial infarction after cardiac arrest.

Methods

226 patients who underwent diagnostic coronary angiography after sudden cardiac arrest were analyzed retrospectively. Levels of TNT, CK and CK-MB on admission and 6 h, 24 h and 36 h later were retrieved from the files and compared with the results of coronary angiography.

Results

Acute myocardial infarction (AMI) as well as non-AMI patients showed increasing levels of TNT and CK after resuscitation, although the AMI group showed significantly higher TNT and CK levels. Receiver operator curves were calculated to determine the diagnostic precision of TNT, CK and CK-MB to differentiate AMI and non-AMI patients. All analyzed markers yielded mediocre diagnostic precision with an area under the ROC curve of 0.7020, 0.6802 and 0.6508 for 6 h TNT, CK and CK-MB, respectively. Applying a modified cut-off of 1 μg/l the 6 h TNT measurement had a sensitivity of 70.9% and specificity of 61.2% to diagnose AMI after cardiac arrest. Using CK 800 U/l as cut-off level resulted in a sensitivity of 62.5% and specificity of 73.7%, CK-MB levels higher than 100 U/l yielded a sensitivity of 58.8% and specificity of 72.7%.

Conclusion

Cardiac injury markers cannot be used to reliably diagnose or rule out AMI after resuscitation. Consequently we propose that indication for coronary angiography should be extended to all patients without a certain alternative diagnosis explaining the occurrence of cardiac arrest.     

Creatine kinase MB isoenzyme of noncardiac origin in elderly patients

Increased activity of creatine kinase MB (CKMB) isoenzyme is regarded as highly diagnostic for acute myocardial infarction. We report two cases of elderly patients with increased levels of CKMB but no evidence of cardiac injury. We conclude that numerous factors influence CKMB activity and that the suitability of this test for the diagnosis of cardiac muscle damage in the elderly should be viewed with caution.