AMI患者早期CK同工酶亚型的高压电泳图谱分析

目的探讨CK同工酶亚型在AMI胸痛发作后24h内的变化规律,为AMI患者的早期诊断提供依据。方法采用REP全自动高压电泳仪检测AMI胸痛发作后不同时间以及对照组的CK-MM1、CK-MM2、CK-MM3、CK-MB1、CK-MB2等指标并进行荧光扫描,同时在Olympus2700全自动生化分析仪上测定CK、CK-MB的总活性,对所得数据进行恰当的统计分析。结果在AMI患者胸痛发作24h内,CK同工酶亚型有一特殊的变化规律:4~6h内,CK-MB2、CK-MM3开始升高,8~12h达高峰,92%的病人CK-MB2/CK-MB1>1.5,同时91%的病人CK-MM3/CK-MM1>0.5。结论CK同工酶亚型CK-MM3/CK-MM1、CK-MB2/CK-MB1的检测可作为AMI早期诊断的指标。     

Adenylate kinase mimics creatine kinase-MM isoenzyme in a CK isoenzyme electrophoresis assay

Adenylate kinase activity (AK) originating from erythrocytes, present in hemolyzed serum behaves like creatine kinase MM isoenzyme (CK-MM) in some CK electrophoresis assays that employ, in their visualization reagent kits, adenosine monophosphate (AMP) as the sole inhibitor of AK, rather than a combination of AMP and a more potent inhibitor of erythrocyte AK, diadenosine pentaphosphate (Ap5A), to inhibit all contaminating-AK activities in serum and quantify only the CK isoenzyme activities in serum following electrophoretic fractionation on agarose gel. This can spuriously overestimate the CK-MM fraction and thereby result in underestimation of CK-MM or CK-BB isoenzymes if present. A hemolyzed serum sample obtained from an elderly patient was erroneously reported as containing low CK-MB due to such overestimation of CK-MM fraction in the sample. Supplementing the AMP already present in the visualization reagent formulation, used to estimate CK isoenzyme concentration in serum, with Ap5A can eliminate or effectively minimize AK interference, especially that caused by hemolysis, and thereby prevent reporting false-negative CK-MB result obtained with CK isoenzyme electrophoresis assays. © 1994 Wiley-Liss, Inc.     

体外循环心内直视手术患者血清心肌肌钙蛋白Ⅰ检测的临床意义

目的观察体外循环心内直视手术患者血清心肌肌钙蛋白Ⅰ（cTnⅠ）的动态变化,探讨血清cTnⅠ对体外循环心内直视手术心肌损伤的诊断价值。方法采用双抗体夹心光化学法检测34例行体外循环心内直视手术患者（观察组）术前,术后6、12、24、48、72h和32例开胸非心脏手术患者（对照组）术前,术后12h的血清cTnⅠ水平,同时采用免疫抑制酶动力学法检测血清肌酸激酶同工酶MB（CK—MB）的活性。结果观察组术前血清cTnⅠ水平和CK—MB活性与对照组比较差异均无统计学意义（均P〉0．05）,术后12h血清cTnⅠ水平和CK—MB活性与对照组比较差异均有统计学意义（P〈0．01或P〈0．05）。观察组血清CK—MB活性术后6h开始升高,术后12～24h达高峰,术后48～72h基本恢复至术前水平;血清cTnⅠ水平术后6h开始升高,术后12h达高峰,术后72h有所降低,但仍高于术前水平。对照组术后12h血清cTnI水平与术前比较差异无统计学意义（P〉0．05）,血清CK—MB活性较术前显著升高（P〈0．01）。结论体外循环心内直视手术可引起心肌损伤。血清cTnⅠ水平检测优于血清CK—MB活性。血清cTnⅠ对体外循环心内直视手术心肌损伤有重要的诊断价值。     

83例窒息新生儿血清肌钙蛋白Ⅰ及肌酸激酶同工酶检测分析

目的 探讨窒息新生儿血清肌钙蛋白Ⅰ(cTnⅠ)、肌酸激酶同工酶(CK-MB)的变化及临床意义.方法 对83例窒息新生儿(其中轻度窒息48例、重度窒息35例)与30例健康新生儿(对照组),采用微粒子化学发光法和干化学分析法,进行血清cTnⅠ和CK-MB水平检测.结果 对照组cTnⅠ和CK-MB平均水平分别为(0.03±0.02)ng/mL、(37.0±12.3)U/L;轻度窒息组cTnⅠ和CK-MB平均水平分别为(0.12±0.05)ng/mL、(71.0±19.3)U/L;重度窒息组cTnⅠ和CK-MB平均水平分别为(0.19±0.14)ng/mL、(92.0±25.4)U/L.结论 新生儿窒息后血清cTnⅠ和CK-MB水平可明显升高,通过检测血清cTnⅠ和CK-MB水平不仅可用来判断窒息对患儿心肌损害的程度,亦可间接反映患儿窒息程度,有助于早期诊断及治疗.     

国产尿激酶经静脉溶栓治疗急性心肌梗死血管再通的评价

观察了51例急性心肌梗死病人静脉应用尿激酶治疗后，冠状动脉再通组及未通组心电图ST段以及血清肌酸激酶（CK）和肌酸激酶同功酶（CK－MB）的变化规律，并对血管再通组及未通组的临床疗效进行了分析。结果表明：急性心肌梗死病人经静脉溶栓治疗后，冠脉再通组的心电图ST段在用药后30min开始下降，90min下降达53．1％，与未通组心电图ST段具有显著差异；冠脉再通组血清CK及CK－MB在胸痛后14h达到高峰，而未通组在胸病后20h达到高峰；冠脉再通率为67％，再通组心力衰竭、心律失常及病死率明显低于未通组。AMI病人早期经静脉应用溶栓剂治疗，可改善急性期预后，应积极推广。     

免疫抑制法检测肌酸激酶同工酶活性高于肌酸激酶的临床价值分析

目的探讨免疫抑制法检测肌酸激酶同工酶(CK-MB)结果高于肌酸激酶(CK)活性的临床价值。方法回顾分析4例免疫抑制法检测CK-MB结果高于CK活性的病例,并比较心内科与脑外科心肌酶谱检测结果CK-MB/CK比值。结果结果4例病例中3例为颅脑损伤,1例为结肠癌术后,4例病例均无心肌损伤;脑外科CK-MB/CK比值明显高于心内科(P<0.05)。结论免疫抑制法检测CK-MB活性假性高于CK活性,或CK-MB/CK比值上高有重要的脑损伤警示价值。     

肌酸激酶同工酶质量判定肌病心肌损害的局限性

目的 通过对比小儿心肌炎、肌病时血清中肌酸激酶同工酶(CK-MB)质量与肌钙蛋白I(cTnI)和肌红蛋白(Mb)的动态变化,观察CK-MB质量在判定心肌损伤中的意义.方法 测定40例心肌炎患儿(其中有20例为暴发性心肌炎)和38例肌病患儿的肌酸激酶(CK)、CK-MB活性、CK-MB质量、cTnI、Mb、心电图以及脉冲多普勒超声心动图;肌病组同时进行肌电图、遗传代谢病筛查以及基因检测.以同期本院发育儿科门诊除外甲状腺功能减低症的10例身矮待查儿童为对照.结果 ①健康对照组儿童CK(U/L)为95.0±27.0,CK-MB活性(U/L)为22.6±1.3,CK-MB质量(μg/L)为2.4±0.3,cTnI(μg/L)为0.012±0.001.②心肌炎组患儿治疗前CK(1 033.0±408.0)、CK-MB活性(101.2±31.5)、CK-MB质量(38.2±13.2)、cTnI(5.544±1.554)均较健康对照组明显升高(均P＜0.01);随着治疗时间延长,各项指标逐渐下降;治疗2周后CK(59.3±25.1)、CK-MB活性(24.6±13.2)、CK-MB质量(3.3±2.9)、cTnI(0.125±0.128)均恢复至正常水平(均P＞0.05).治疗1周后CK、CK-MB质量增高率即较治疗前明显下降[CK:5.9％(1/17)比56.4％(22/39);CK-MB质量:8.3％(1/12)比61.1％(22/36),均P＜0.01],CK-MB质量恢复先于cTnI,增高率出现明显差异[8.3％(1/12)比73.7％(14/19),P＜0.05].③肌病组治疗前CK(10 193.0±1 447.0)、CK-MB活性(311.7±44.4)以及CK-MB质量(229.2±47.9)均较健康对照组明显升高(均P＜0.01),但cTnI不高(0.021±0.002);治疗2周后CK(5 735.6±6 187.8)、CK-MB活性(170.7±143.0)、CK-MB质量(207.4±136.6)仍维持在高水平,cTnI(0.230±0.150)则维持在正常水平;各项指标的增高率与治疗前均无显著差异[CK:85.7％(6/7)比97.4％(37/38); CK-MB活性:85.7％(6/7)比97.4％(37/38);CK-MB质量:100.0％(2/2)比94.1％(32/34);cTnI:0(0/1)比6.4％(2/31),均P＞0.05].结论 ①在心肌炎时,CK-MB质量与cTnI一致,急性期升高,恢复期降至正常,但CK-MB质量观察窗短于cTnI.②在肌病时,CK-MB质量与cTnI 分离,前者治疗前后均升高,后者正常,故用测定CK-MB质量来判定肌病患儿是否有心肌损害意义有限.     

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。     

Development and performance of an enzyme immunoassay to detect creatine kinase isoenzyme MB activity using anti-mitochondrial creatine kinase monoclonal antibodies

Abstract

Objective: The MB fraction of creatine kinase (CK-MB) has long been used as a cardiac marker. It is known that the CK-MB immunoinhibition method lacks selectivity and accuracy, because the appearance of macro CK type 2, corresponding to mitochondrial creatine kinase (MtCK) in some patient serum may render CK-MB activity measured by conventional method abnormally high. Thus, to improve the specificity and accuracy of the CK-MB assay, we developed two types of monoclonal anti-MtCK antibodies against sarcomeric MtCK and ubiquitous MtCK, and present herein the performance of a new method using these antibodies. Material and methods: The performance of our test for detecting CK-MB activity was compared with other methods, and the range of CK-MB activities in normal human serum was investigated. Results: The two types of monoclonal antibodies developed by us were isoenzyme-specific to sMtCK or uMtCK. The correlation coefficients of our method and conventional method to electrophoresis were 0.973 and 0.873, respectively. The mean CK-MB activity in normal human serum by our method and the conventional method was 2.4 and 11.7 U/L, respectively. Thus, our data indicated that about 80% of CK-MB activity, determined using the conventional method, seems to correspond to the MtCK activity. Conclusion: Our method is novel in offering higher accuracy of measuring true CK-MB contents in human serum as compared to the conventional method. The possibility of accurately estimating CK-MB activity by our method which can inhibit MtCKs in healthy person and patient serum is likely to bring a break-through in clinical diagnostics.     

免疫抑制法检测肌酸激酶同工酶MB临床应用评价

目的 对选定的肌酸激酶同工酶MB(CK-MB)检测试剂盒进行性能验证及对异常CK-MB结果的临床标本进行回顾性分析.方法 对CK-MB检测试剂盒的正确度、精密度、线性范围、最大稀释比以及参考区间进行验证;随机选取50例表观健康体检者作为健康人对照组,50例临床确诊心血管疾病患者作为心血管疾病组并用于临床应用的验证;收集...     

A Km mutant of arylsulfatase A

Semi-micro techniques are presented for the genotyping of galactokinase and galactose-1-phosphate uridyltransferase. Radioactive assays are used to quantitate the levels of enzyme activity, while agarose gel electrophoresis is used to type the variants of galactose-1-phosphate uridyltransferase. All three methods can be performed on 1 ml whole blood, making the procedures ideal for use in confirmation of galactosemia or galactokinase deficiency in newborn screening programs.     

重组人肌酸激酶MM同工酶的酶动力学研究

目的:对纯化后重组肌酸激酶MM同工酶(CK-MM)的米氏常数(Km)进行研究,为其作为参考品或校准品应用于临床奠定基础。方法:将重组酶置于自制类人血清基质中,按IFCC参考方法配制试剂,采用HITACHI全自动生化分析仪测定重组酶与天然酶[底物分别是磷酸肌酸(PCr)和腺苷二磷酸(ADP)]的Km常数。结果:重组酶KmPCr值高于天然酶1.4倍,Km ADP重组酶与天然酶近似。结论:重组CK-MM的酶动力学常数基本符合参考方法的测定要求,初步具备作为基因工程人源酶校准品的基本特点。     

Clinical role of recurrently elevated macro creatine kinase type 1

The typical creatine kinase (CK) isoenzymes include CK-BB, CK-MB, and CK-MM. Macro CK type 1, one of the atypical CK enzymes, has been identified in human serum, but the clinical significance still remains uncertain. In our laboratory, 105 patients who expressed serum macro CK isoenzyme type 1 were identified from March 2004 to March 2007. We found that macro CK type 1 recurred after at least one month in 16 patients. Clinical diagnoses were myopathy in 14 patients, sepsis in one, and acute coronary syndrome in one. The averages of serum total CK and macro CK type 1 were 9,132 and 1,925 (U/L), respectively. The linear regression analysis between recurrent macro CK type 1 and total CK revealed a good correlation (y=3.5054x+2381.3, R(2)=0.7822, P<0.001). Three patients had critical illness, including one respiratory failure and two mortalities. Good linear correlation is documented between total CK and recurrent macro CK type 1. In conclusion, the macro CK type I isoenzyme recurred primarily in patients with myopathy.     

血清CK、CK-MB、磷的测定对绞窄性肠梗阻的临床诊断价值

目的探讨血清中肌酸激酶（CK）、肌酸激酶同工酶（CK—MB）、血清磷的测定对绞窄性肠梗阻的临床诊断价值。方法所有病例均于入院当时及以后每4小时抽取静脉血5ml送检,直至手术前2h,将手术中证实为肠绞窄的42例、没有绞窄的28例和保守治疗成功出院的31例肠梗阻患者分别确定为绞窄组、单纯组、对照组,取绞窄组和单纯组术前2h、6h、10h的血清CK、CK—MB、磷值和对照组的血清CK、CK—MB、磷平均值,观察三组间的差异。结果绞窄组CK、CK—MB和血清磷值术前2h为383．15&#177;128．12、38．69&#177;11-32、1．45&#177;0．42．6h为368．67&#177;120．28、31．89&#177;10．12、1．41&#177;0．38,10h为312．18&#177;128．72、27．32&#177;12．51、1．26&#177;0．39,而单纯组和对照组基本正常。绞窄组CK、CK—MB和血磷值和单纯组比较差异有统计学意义,分别为2h（t分别：12．01、4．72、3．91,P均〈0．05）、6h（t分别=15．10、10．16、6．20,P均〈0．05）、10h（t分别=12．01、4．72、3．91,P均〈0．05）;单纯组CK、CK—MB、血清磷值与对照组相比差异无统计学意义（t分别=0．02、0．39、0．11,P均〉0．05）;试验测得绞窄组CK、CK—MB及血清磷的敏感度分别为71．41％、73．80％和14．20％．而CK、CK—MB和血清磷的特异度为93_33％、90．91％和100．00％。结论血清CK及CK—MB升高提示肠梗阻患者出现肠绞窄可能性大．特异度高,但血清CK、CK—MB、血清磷阴性不能排除绞窄性肠梗阻的可能;血清磷升高提示肠管有不可逆坏死,但对早期肠绞窄的诊断敏感性差：血清CK、CK—MB和血清磷可以作为判断肠梗阻病人是否发生早期肠绞窄或肠坏死的辅助诊断依据。     

Measuring creatine kinase MB isoenzyme in a maintenance hemodialysis population: chemiluminometric immunoassay and electrophoresis compared

In an effort to clarify the issue of potentially false increases in creatine kinase (EC 2.7.3.2) MB isoenzyme (CK-MB) in uremia, we evaluated the CK profile of 84 persons undergoing chronic maintenance hemodialysis. We compared the performance of a new commercial two-site chemiluminometric immunoassay of CK-MB (Magic Lite; Ciba Corning Diagnostics) with that of electrophoresis on agarose gel (Cardio Trak-CK; Corning Medical). Results of the new chemiluminometric immunoassay for samples from hemodialysis patients correlated well with those of the electrophoretic method (r = 0.86, P less than 0.001), showing that neither substances in the serum of uremic patients nor CK-MM isoenzyme give false-positive increases in CK-MB isoenzyme. Our evidence suggests that the chemiluminometric method may be more specific than is electrophoresis in establishing absolute CK-MB values in the diagnosis of suspected myocardial injury in this population.     

Direct measurement of creatine kinase-MB activity in serum after extraction with a monoclonal antibody specific to the MB isoenzyme

Fusion of splenocytes from A/J mice immunized by creatine kinase (EC 2.7.3.2)-MB isoenzyme (CK-MB) with SP2/0-Ag14 myeloma cell line generated hybridomas producing monoclonal antibodies specific to CK-MB. One of these monoclonal antibodies ("Conan-MB") was used to develop a direct assay for CK-MB activity. In the assay, serum is incubated for 30 min at room temperature with "Conan-MB" immobilized on latex beads. The beads are then washed, and CK-MB activity bound to the antibody is measured after incubation with CK enzyme reagent for 30 min at 37 degrees C. Results with the assay correlated well (r = 0.997) with those for CK-MB concentration as measured by a two-site immunoassay. Neither CK-MM, CK-BB, mitochondrial CK, nor a hemolysate of erythrocytes interfered. Use of this unique monoclonal antibody allows rapid, precise, and direct determination of CK-MB activity.     

Monoclonal antibody inhibiting creatine kinase MM3 but not isoform MM1

Monoclonal antibody CKM-G01 inhibited greater than 99% of the activity of porcine and human creatine kinase(CK)-MM isoenzyme purified from muscle. However, it inhibited only 54% of CK-MM in human serum. Chromatofocusing of serum CK-MM showed that CKM-G01 inhibited 100% of MM3 but not isoform MM1. CKM-G01 inhibited CK-MM2 by 57%. CKM-G01 specifically inhibited only the original CK-M subunit and not the subunit modified by removal of C-terminal lysine by carboxypeptidase N. CKM-G01 can be used for assay of CK isoforms. We devised a new diagnostic reagent involving it, which requires no analytical separation of isoforms, based on the immunoinhibition method, and applied it to early diagnosis of acute myocardial infarction. The "inhibition index," (inhibited CK activity/total CK activity) x 100, increased more rapidly than did total CK and CK-MB. Evidently this diagnostic reagent can be used for easy, early diagnosis of acute myocardial infarction.     

不稳定型心绞痛患者血清cTnI、CK-MB、CRP水平变化及与心肌微循环状态的关系

目的探讨不稳定型心绞痛(UA)患者血清心肌肌钙蛋白I(cTnI)、肌酸激酶同工酶MB(CKMB)、C反应蛋白(CRP)水平变化及与心肌微循环状态的关系。方法选取2019年2月至2020年7月于南京中医药大学附属盐城市中医院和江苏省苏州市相城人民医院就诊住院的109例心绞痛患者和54例同期体检健康者为研究对象,根据WHO分级标准分为稳定型心绞痛(SA)组44例、UA组65例、健康组54例,采用夹心酶联免疫吸附法、免疫抑制法、乳胶增强免疫透射比浊法分别检测3组研究对象血清cTnI、CK-MB、CRP水平,并记录其阳性检出率。UA组行冠状动脉造影(CAG),根据入院时的Braunwald分级标准另分为Ⅰ级低危险组20例、Ⅱ级中危险组23例、Ⅲ级高危险组22例,对比各危险组患者血清cTnI、CK-MB、CRP水平及阳性检出率,并分析UA组患者血清cTnI、CK-MB、CRP水平与心肌微循环状态关系。结果 UA组、SA组与健康组的血清cTnI、CK-MB、CRP水平及其阳性检出率由高到低均呈UA组>SA组>健康组变化(P<0.05)。高危险组、中危险组与低危险组的cTnI、CK-MB、CRP水平及其阳性检出率、病变血管支数组间两两比较,差异均无统计学意义(P>0.05);高危险组、中危险组与低危险组CTFC值由高到低呈高危险组>中危险组>低危险组变化(P<0.05)。UA组中cTnI、CK-MB、CRP检测结果为阳性者发生血管病变的比例均明显高于结果为阴性者(P<0.05)。结论 UA患者血清CK-MB、CRP水平较SA患者及健康人群高,其血清水平上调可能预测心肌微循环状态不良,临床监测上述指标对其具有重要诊断及鉴别价值。     

肌酸激酶及其同工酶试剂对三酰甘油自动分析的影响

目的研究对三酰甘油(TG)自动分析产生交叉污染的项目及避免交叉污染的方法。方法将疑似对TG测定有交叉污染的项目的试剂加入混合血清中作为实验管测定TG,并与加入同比例生理盐水的对照管相比较,初筛出对TG测定结果存在交叉污染的项目;先测定初筛实验中对TG测定存在交叉污染的项目CK和CK-M B,再连续测定TG 9次,观察自动分析顺序对TG测定结果的影响,同时观察CK和CK-M B试剂对TG测定结果影响的持续程度。结果CK和CK-M B试剂对TG测定结果存在明显的交叉污染;先测CK和CK-M B后测TG的分析顺序对TG的测定结果有明显影响,CK及CK-M B试剂对TG测定结果的影响均持续到第2管。结论CK和CK-M B试剂对TG测定结果存在明显的交叉污染。生化自动分析中应注意分析顺序对实验结果的影响。     

Clinical importance of elevated CK-MB and troponin I levels in congestive heart failure

Myocyte necrosis has been considered to play a fundamental role in the pathophysiology of congestive heart failure (CHF), which has usually evolved as a consequence of depletion of compensatory mechanisms and contractile reserve of myocardium. Elevated levels of creatine kinase MB (CK-MB) and troponin I (Tn-I) have been regarded as biochemical markers of myocyte necrosis. This study was planned to investigate the specificity and sensitivity of Tn-I and CK-MB in CHF and to examine the correlation of these markers with disease severity. A total of 104 patients (38 female, 66 male; mean age, 66 y [range, 36–89]) with symptoms and signs of heart failure on admission and with a reduced left ventricular ejection fraction (EF; by transthoracic echocardiography) were labeled “the patient group”, and 58 patients (40 female,18 male; mean age, 61 y [range, 34–77]) with no signs or symptoms of CHF and with a normal EF detected by transthoracic echocardiography were included in the study as “the control group.” Left ventricular EFs, end-diastolic diameters, and end-systolic diameters of patients in both groups were measured. Blood samples were drawn from all patients in both groups on admission, so that levels of CK-MB and Tn-I could be measured. All patients in both groups also underwent coronary angiography. Conditions leading to elevation of CK-MB or Tn-I were considered exclusion criteria. The 2 groups failed to show any significant differences in terms of mean age and the presence of coronary artery disease, hypertension, or diabetes mellitus (P > .05). Mean EF in the patient group was lower than that in the control group (P < .05). Mean CK-MB and Tn-I in the patient group were significantly higher than in the control group (P < .05). In the patient group, hypertensive patients were found to have significantly higher mean values of CK-MB than were seen in normotensive patients in the same group (P < .05). In the patient group, 52 cases were considered to be class I-II (New York Heart Association [NYHA]) (group 1), and 52 were considered to be class III-IV (group 2). Group 1, group 2, and the control group did not differ significantly from one another with regard to the presence of coronary artery disease, hypertension, and diabetes mellitus (P > .05).The mean EF in group 2 was significantly lower than that in group 1 and in the control group (P < .05); the mean EF in group 1 was significantly lower than that in the control group (P < .05). Group 1 values did not differ significantly from those of group 2 or the control group in terms of enzymatic markers (P > .05), but group 2 had significantly higher mean values of CK-MB and Tn-I than were noted in the control group (P < .05). The uphill course of CK-MB and Tn-I values from the control group to group 2 (NYHA class III-IV) was statistically significant (P< .05). Serum concentrations of CK-MB and Tn-I may become elevated in severely symptomatic patients with CHF (particularly NYHA class III-IV), demonstrating a relationship between clinical severity of the disease and elevation of myocardial enzymes (CK-MB and Tn-I).