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.     

急性心肌梗死患者血浆N-末端脑钠肽前体水平检测及其临床意义

目的探讨急性心肌梗死(AMI)患者住院早期血浆N-末端脑钠肽前体(NT-proBNP)水平与梗死面积、心功能及住院期心脏事件的关系。方法采用ELISA法测定41例AMI患者住院后48小时内血浆NT-proBNP水平,并与患者肌酸激酶(CK)和肌酸激酶同功酶(CK-MB)峰值浓度、左室射血分数(LVEF)、住院期主要不良心脏事件(MACE)对比分析。结果AMI患者血浆NT-proBNP水平明显高于正常对照组(699.44±386.28pg/ml vs 41.75±24.26pg/ml,P<0.001)。血浆NT-proBNP水平与CK、CK-MB峰值浓度呈正相关(r=0.817,P=0.001;r=0.772,P=0.001),与LVEF呈负相关(r=-0.661,P<0.01)。住院期发生MACE患者的血浆NT-proBNP水平明显高于未发生MACE者(971.50±367.01pg/ml vs 393.60±261.16pg/ml,P<0.001)。结论AMI患者血浆NT-proBNP水平与CK、CK-MB峰值呈正相关,与LVEF呈负相关。检测血浆NT-proBNP水平可预测AMI患者梗塞面积、心功能及住院期心血管事件。     

Serum interferon-gamma-inducible protein 10 level was increased in myocardial infarction patients, and negatively correlated with infarct size

OBJECTIVES: We examined the serum levels of interferon-gamma-inducible protein 10 (IP-10), an inflammation-induced chemokine, in acute myocardial infarction (AMI). DESIGN AND METHODS: The subjects were 33 AMI patients, 20 stable angina pectoris patients (AP) and 20 normal subjects. In AMI patients, blood samples were collected before percutaneous coronary intervention (PCI) and on days 3, 7 and 28. RESULTS: Patients with AMI showed significantly higher serum IP-10 levels (137.5+/-79.8 pg/mL) than control subjects (91.2+/-40.1 pg/mL) and patients with AP (93.3+/-41.1 pg/mL). The serum IP-10 level before PCI was negatively correlated with infarct size, as indicated by cumulative release of creatine kinase (CK) and peak CK and its isoenzyme CK-MB. Stepwise multiple regression analysis revealed that the serum IP-10 level before PCI was an independent predictor of cumulative CK release. CONCLUSIONS: The serum IP-10 level was increased in AMI, and a higher level of serum IP-10 before PCI may be informative regarding infarct size.     

Activities of key enzymes in the energy metabolism of human myocardial and skeletal muscle

Summary. Activities of total creatine kinase (CK), its isoenzyme MB (CK-MB), total lactate dehydrogenase (LD) and its isoenzyme LD₁, phosphofructokinase (PFK), asparate aminotransferase (ASAT) and citrate synthase (CS) were determined in skeletal muscle biopsies obtained from physically trained and untrained men and in myocardial biopsies from patients subjected to open heart surgery because of valve disease. The LD₁, ASAT and CS activities were higher in trained than in untrained skeletal muscle and still higher in heart muscle than in either trained or untrained skeletal muscle. The CK-MB activity was higher in trained than untrained skeletal muscle and the myocardial CK-MB activity was similar to that in trained skeletal muscle. Total CK activity was slightly lower in trained than in untrained skeletal muscle and the myocardial CK activity was approximately one third of the skeletal muscle CK. Both the PFK and the total LD activity was of similar magnitude in the different muscle types. In conclusion, as estimated by enzyme activities, the oxidative capacity is 2–3 times larger in myocardial than in skeletal muscle, while the glycolytic capacity as estimated by PFK appears to be the same.     

The diagnostic value of different enzymes and standard ECG in acute myocardial infarction

Serum (S) enzyme activity of aspartate aminotransferase (ASAT, E.C. 2.6.1.1.), heat stable lactate dehydrogenase (LD, E.C. 1.1.1.27.), creatine kinase (CK, E.C. 2.7.3.2.) and CK-B subunit and the respective standard electrocardiograms (ECG) were compared in 463 patients with suspected acute myocardial infarction (MI) in order to evaluate sensitivity and specificity. Serum ASAT was analysed daily for 3 days, S-heat stable LD every 12 h for 48-108 h, S-CK and S-CK-B every 6 h for 48 h and ECG once daily for 3 days. All four enzymes had a high sensitivity, varying from 99% for LD to 97% for CK-B. The highest specificity was observed for CK-B and CK (98%) as compared with heat stable LD (91%) and ASAT (74%). Standard ECG showed a high specificity (96%) and a low sensitivity (80%).     

Differential diagnosis of patients with abnormal serum creatine kinase isoenzymes

For the diagnosis of myocardial injury, particularly AMI, CK-MB has become the gold standard. Changing CK-MB activities in serially collected blood from patients with suggestive signs and symptoms of AMI is almost pathognomonic for infarction. Nevertheless, an increased CK-MB cannot be equated with AMI owing to the many other types of inflammatory, traumatic, and miscellaneous forms of injury to the heart and the trace activities of CK-MB in skeletal muscle. Other enzyme tests for AMI are less efficient. In order of decreasing efficiency, the tests are CK-MB, CK, LD1 greater than LD2 or LD1/LD2 greater than 0.76, AST and LD; the latter two tests are not cost effective and add little or nothing when results for CK-MB, CK, and LD isoenzymes are available. The value of the isoforms of CK-MM and CK-MB remains to be established. Early evidence suggests that they could be helpful in the diagnosis of AMI; however, owing to the greater technical difficulties in performing these tests, their use is necessarily more restricted. Enzyme testing on admission and then every 12 hours for 2 days is sufficient and effective in making the initial diagnosis. In patients presenting early after an attack, CK and CK-MB are often normal. Decisions on AMI cannot be made on blood tests collected in the emergency department. Clot-lysing agents like streptokinase, urokinase, and tPA have changed the therapy of AMI dramatically. Enzyme tests clearly separate patients with and without successful therapeutic or spontaneous reperfusion. With successful reperfusion, the uniform finding has been a "washout" phenomenon with significantly earlier peaking times for CK and CK-MB. The isoforms of CK and myoglobin give the earliest peaks after successful reperfusion. With faster turnaround times for these tests, they may become important tools in patient management.     

Creatine kinase and myoglobin determination in myocardial infarction

Summary In order to evaluate the diagnostic and prognostic impertance of serum myoglobin (Mb) determination during acute myocardial infarction (AMI) we determined the time of first rise of both CK and Mb, that is the time in hours between the onset of pain and the last normal myoglobin and enzyme determination (TFR for Mb=2.2±1.5 h; TFR for CK=4.0±2.5 h). We also attempted to evaluate infarct size by mathematical analysis of the serum concentrations of Mb. The average percentage difference between the infarct size calculated from the CK concentrations and Mb concentrations was 35.8±35.2%. The results show that the determination of serum myoglobin is a useful and sensitive test for the early diagnosis of AMI. On the other hand, the serum myoglobin cannot be utilized to evaluate infarct size. The main limitation in the determination of infarct size from the serum Mb concentrations lies in the extreme variability of the disappearance rate (Kd), mainly resulting from the renal elimination of the substance.     

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).     

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.     

Single-point cardiac troponin T at coronary care unit discharge after myocardial infarction correlates with infarct size and ejection fraction

BACKGROUND: One of the major concerns in replacing creatine kinase MB (CK-MB) with cardiac troponins is the lack of evidence of the ability of troponins to estimate the size of acute myocardial infarction (AMI). We investigated the ability of a single measurement of cardiac troponin T (cTnT) at coronary care unit (CCU) discharge to estimate infarct size and assess left ventricular (LV) function in AMI patients. METHODS: We studied 65 AMI patients in whom infarct size was estimated by CK-MB peak concentrations and gated single-photon emission computed tomography (SPECT) myocardial perfusion using technetium-99m sestamibi and LV function by SPECT imaging. Measurements of cTnT and SPECT were performed 72 h (median) after admission (range, 40-160 h). SPECT was also repeated 3 months later. RESULTS: We found a significant correlation between cTnT and both the peak CK-MB concentrations (r = 0.76; P <0.001) and the perfusion defect size at SPECT (r = 0.62; P <0.001). cTnT was inversely related to LV ejection fraction (LVEF) assessed both early (r = -0.56; P <0.001) and 3 months after AMI (r = -0.70; P <0.001). cTnT >2.98 micro g/L predicted a LVEF <40% at 3 months with a sensitivity of 86.7%, specificity of 81.4%, and a likelihood ratio for a positive test of 4.7 (95% confidence interval, 4.0-5.4). CONCLUSIONS: A single cTnT measurement at CCU discharge after AMI is useful as a noninvasive estimate of infarct size and for the assessment of LV function in routine clinical setting.     

急性心肌梗塞患者白细胞计数与梗塞范围的相关性研究

目的:探索白细胞计数(WBC)与急性心肌梗塞(AMI)梗塞范围的关系。方法:358例AMI患者,男168例, 女190例,年龄35～80岁,按WBC水平分为6组,分别统计并比较各组肌酸磷酸激酶同工酶MB(CK MB)值,并 确定其与不同WBC水平间的相关关系。结果:各组间CK-MB水平差别显著(P<0.05),各组不同的CK MB水 平与其WBC水平呈显著正相关关系(r=0.89,P=0.018)。结论:AMI急性期WBC与梗塞范围)呈正相关。     

Enhanced cardiac enzyme profile

A protocol for an enhanced Cardiac Enzyme Profile is proposed based on an admission, or initial, serum specimen and a second specimen 16 hours after onset of symptoms as minimal baseline serum samples in order to accomplish several simultaneous goals: 1. Detecting CK2MB at its average peak for maximal assurance of diagnosis when release is small and for prognosis in all cases of increased serum CK2MB 2. Detection of laboratory evidence of myocardial injury when admission is delayed after onset by the collection of an admission sample for declining CK2MB, and for assays of other enzymes with longer time curves after myocardial injury such as LD isoenzymes and ASAT/ALAT activities and ratio 3. Establishment of decision limits and criteria for the determination of laboratory evidence of myocardial injury 4. Providing cost-effective procedures other than limitation of the number of samples; these include establishing thresholds and criteria for total CK, total LD, and ASAT so that isoenzymes and ALAT are only performed when thresholds are exceeded and criteria are met; performing only CK and, if the threshold is exceeded, CK isoenzymes on the 16-hour sample; collecting additional samples after the first two only when indicated by positive or suspicious (borderline) results and only on routine morning or afternoon rounds rather than specifically timed specimens (except in cases involving thrombolytic therapy); and termination of the protocol once peak positive CK2MB activity and requisite diagnostic consensus confirmation (such as positive LD isoenzymes) is obtained whether or not thrombolytic therapy is involved. Tissue localization of the enzymes has been outlined in some detail with particular reference to the amount of CK2MB in skeletal muscle. Pathophysiological factors discussed in more depth in a previous article have been amplified here with particular reference to the role of increased synthesis as a response to myocardial injury by surrounding prehypertrophic and hypertrophic myocardium as a possible major source of increased serum enzymes in myocardial infarction. ASAT and especially the ASAT/ALAT ratio are useful tests in the protocol, particularly in cases tested late after onset of symptoms when CK2MB has declined into the borderline or usual range, and ASAT/ALAT may be helpful in evaluating LD isoenzyme results. Codes for interpretive comments are provided to serve as guidelines.     

Rapid determination of brain natriuretic peptide in patients with acute myocardial infarction.

We evaluated a rapid brain natriuretic peptide (BNP) assay (Triage BNP, Biosite Diagnostics) as indicator of infarct size, left ventricular (LV) dysfunction, and longterm survival in patients with acute myocardial infarction (AMI) during the coronary care unit stay. We studied 64 AMI patients in whom infarct size was estimated by creatine kinase isoenzyme MB (CK-MB) peak concentrations and single-photon emission computed tomography (SPECT) myocardial perfusion using technetium-99m sestamibi, and LV function by gated SPECT imaging. Measurements of BNP and SPECT were performed approximately 3 days after admission. SPECT was also repeated 3 months later. We found a significant correlation between BNP and both the peak CK-MB concentrations (r = 0.40, p = 0.001) and the perfusion defect size at SPECT (r = 0.38, p = 0.002). BNP was weakly related to LV ejection fraction (LVEF) assessed both early and 3 months after AMI (r = -0.29, p = 0.02; and r = -0.27, p = 0.04, respectively). The sensitivity and specificity of BNP for predicting survival of patients over 1 year of follow-up was 100% and 43%, respectively, with a negative predictive value of 100%. The positive predictive power of BNP was very modest (12%). Considering our results, the measurement of BNP did not look nearly as promising when tested in the setting of our cardiological intensive care.     

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.     

Measurement of troponin I 48 h after admission as a tool to rule out impaired left ventricular function in patients with a first myocardial infarction.

Few studies have evaluated cardiac troponin I (cTnI) as a marker for infarct size and left ventricular (LV) dysfunction. Here we investigated the ability of a single-point cTnI, measured with a second-generation assay (Access AccuTnI), to estimate infarct size and assess LV function in patients with a first myocardial infarction (AMI). cTnI measurements were performed 12 and 48 h after admission in 63 consecutive AMI patients. LV function was evaluated by gated single-photon emission computed tomography (SPECT) and infarct size was estimated by CK-MB peak and SPECT myocardial perfusion. LV function and infarct size were evaluated by SPECT before hospital discharge. SPECT was also repeated 3 months later. Significant correlations (p<0.001) were found between cTnI at 12 and 48 h and both the peak CK-MB (r=0.61 and r=0.82, respectively) and the perfusion defect size at SPECT (r=0.55 and r=0.61, respectively). cTnI at 12 and 48 h were inversely related (p<0.001) to LV ejection fraction (LVEF) assessed both early (r=-0.45 and r=-0.57, respectively) and 3 months after AMI (r=-0.51 and r=-0.69, respectively). cTnI >14.8 microg/L at 48 h predicted an LVEF <40% at 3 months with a sensitivity of 100% [95% confidence interval (CI) 73.5-100%], specificity of 65% (CI 49-79%), and a negative predictive value of 100%. Our findings demonstrate that a single cTnI measurement 48 h after admission is useful for ruling out impaired LV function in a routine clinical setting.     

Changes in serum CK-MB mass after coronary artery bypass surgery

We assessed the release of creatine kinase MB as both mass and activity during the postoperative period following cardiac surgery. CK-MB mass was determined by enzyme immunoassay using reagents obtained from Hybritech. CK-MB activity was determined both by agarose electrophoresis and by an immunochemical method. Fifty-five patients who underwent coronary artery bypass surgery and 52 control subjects who had orthopedic surgery were selected for study. Serial serum samples were collected following surgery and total LD, CK, AST, LD-1, CK-MB mass, and CK-MB activity determined. Results were compared to each other and to surgical parameters. All patients exhibited significant CK-MB mass and activity after surgery and peak serum levels were 6-94 micrograms/L and 12-84 U/L, respectively. CK-MB mass correlated with CK-MB activity on paired samples (r = 0.94). Total AST and CK activities correlated with CK-MB mass (r = 0.60, and 0.63, respectively). Peak levels of CK-MB mass correlated significantly with peak MB activity (r = 0.88), peak LD-1 (r = 0.62), peak AST (r = 0.71), and time on pump (r = 0.54). Similar correlations were also seen between peak CK-MB activity and these parameters. No relationship could be identified between extent of CK-MB mass release and number of grafts, degree of hypothermia, or minimum PaO2. The time course of CK-MB mass release exhibited 85% concordance with CK-MB activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

促红细胞生成素用于急性心肌梗死的临床观察

目的 探讨重组型促红细胞生成素(rh-EPO)对改善急性心肌梗死(AMI)患者心功能的作用.方法48例符合诊断标准、接受静脉溶栓治疗且溶检成功的首次AMI患者随机分为两组,治疗组在溶栓后即给予rh-EPO 2000 U/次,每周3次,共治疗4周.期间测定肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)峰值浓度,采用Hindmen修正的12导联QRs积分系统估算梗死面积(S),第4周末测定左心室舒张末内径(LVEDd)和左心室射血分数(LVEF),并与对照组比较,同时观察rh-EPO治疗期间不良反应的发生情况.结果治疗组反映梗死严重程度的CK、CK-MB和梗死面积均较对照组明显减轻,差异有统计学意义(均P<0.05);在rh-EPO治疗4周后,反映心功能的LVEDd和LVEF在治疗组也有改善趋势,但两组差异无统计学意义.结论 rh-EPO治疗AMI能有效保护缺血和梗死心肌,明显减轻梗死程度,并可在一定程度上改善心功能.     

Diagnostic use of CK-MM and CK-MB isoforms for detecting myocardial infarction

Following acute myocardial infarction, total CK and CK-MB levels begin to rise 5 to 6 hours after the onset of chest pain. The serial profile of the rise and fall of both activities is nearly always indicative of AMI. The recent increase in the use of thrombolytic agents in an attempt to attain reperfusion of occluded coronary arteries alters the enzyme profiles observed in blood after AMI. After successful reperfusion a washout phenomenon occurs in which early restoration of blood flow to damaged myocardium causes an early rise in total CK and MB levels above the normal range 2 to 4 hours after AMI, with earlier and higher peak enzyme values. Recently reports have appeared describing numerous serum and plasma CK-MM and CK-MB isoform patterns after AMI. Following release from injured myocardium CK-MM3 and CK-MB2 (designated the tissue isoforms) are converted in the circulation to post-translation products (MM2, MM1, MB1, respectively). Studies have now shown that CK-MM isoform patterns provide a unique means of assessing the time of onset of necrosis and a monitor of the duration of enzyme release from the site of injury. Following AMI, MM3, the MM3/MM1 ratio, or both rises and peaks earlier than either total CK or CK-MB levels. During successful reperfusion, the rate of rise of CK-MM3 is more rapid and the MM3/MM1 ratio peaks earlier than without reperfusion. However, any concomitant release of CK-MM3 from skeletal muscle would decrease the clinical utility of MM isoforms in detecting myocardial damage. Recent advances in technology have shown that CK-MB2 rise parallels the CK-MM increase and also rises earlier than total CK and total MB levels and provides increased specificity for the myocardium. The full potential of the diagnostic utility of MM and MB isoforms will not be realized until a reliable, sensitive, simple, and rapid quantitative assay becomes available.     

CK-MB mass test in ischemic myocardial injury. Comparison of two tests: BioMerieux Vidas and sanofi access immunoassays

The analytical and clinical performances of the new fluorescent immunoassay (CK-MB mass Vidas-BioMerieux) were examined and compared to the chemiluminescent test (CK-MB mass Access-Sanofi-Pasteur). Assay precisions of the CK-MB Vidas test within-assay or between-assay were less than 5.4 and 5.3%, respectively. Linearity was tested up to 214 microg/L. The CK-MB Vidas test was free of interference with CK-BB, CK-MM, and macro-CK. One hundred nineteen blood samples from patients with ischemic myocardial injury (IMI): acute myocardial infarction (AMI), suspected myocardial contusion (SMC), and unstable angina pectoris (UA), were tested using both immunoassays. In AMI, a good correlation was found (Y [CK-MB Access] = 1.1372 x [CK-MB Vidas] - 6.3902; r(2) = 0.96). In UA and SMC, low values were observed and both methods were well correlated (Y [CK-MB Access] = 1.3662 x [CK-MB Vidas] + 0.0671; r(2) = 0.97). Clinical data were in good agreement with both immunoassays. ROC analysis performed in AMI demonstrated that the clinical performances of the two assays were similar.     

急性心肌梗死患者白细胞计数与梗死范围的相关性研究

目的 :探索白细胞计数与急性心肌梗死梗死范围的关系。方法 :3 5 8例急性心肌梗死患者 ,按白细胞计数水平分为 6组 ,分别统计并比较各组肌酸磷酸激酶同工酶MB(CK MB)值 ,并确定其与不同白细胞计数水平间的相关关系。结果 :各组间CK MB水平差别显著 (P <0 .0 5 ) ,各组不同的CK MB水平与其白细胞计数水平呈显著正相关关系 (r=0 .89,P =0 .0 18)。结论 :心肌梗死急性期白细胞计数与梗死范围呈正相关