Creatine Kinase Band Research Articles

Chronic Metformin Treatment is Associated with Reduced Myocardial Infarct Size in Diabetic Patients with ST-segment Elevation Myocardial Infarction

Increased myocardial infarct (MI) size is associated with higher risk of developing left ventricular dysfunction, heart failure and mortality. Experimental studies have suggested that metformin treatment reduces MI size after induced ischaemia but human data is lacking. We aimed to investigate the effect of metformin on MI size in patients presenting with an acute MI. All consecutive patients (n = 3,288) presenting to our hospital with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI between January 2004 and December 2010 were included in this retrospective analysis. Patients with diabetes were divided according to metformin versus non-metformin based pharmacotherapy. MI size was estimated using peak values of serum creatine kinase (CK), myocardial band of CK (CK-MB), and troponin-T. We identified 677 (20.6%) patients with diabetes, of whom 189 (27.9%) were treated with metformin. Chronic metformin treatment was associated with lower peak levels of CK (1,101 vs. 1,422 U/L, P = 0.005), CK-MB (152 vs. 182 U/L, P = 0.018) and troponin-T (2.5 vs. 4.0ng/L, P = 0.021) compared to non-metformin using diabetics. After adjustment for age, sex, TIMI flow post PCI, and previous MI, the use of metformin treatment remained an independent predictor of smaller MI size. Patient with diabetes treated with metformin had even smaller MI size than patients without diabetes. Chronic metformin treatment is associated with reduced MI size compared to non-metformin based strategies in diabetic patients presenting with STEMI. Metformin might have additional beneficial effects beyond glucose lowering efficacy.

Effect of High-Dose Intracoronary Adenosine Administration During Primary Percutaneous Coronary Intervention in Acute Myocardial Infarction: A Randomized Controlled Trial

Effect of High-Dose Intracoronary Adenosine Administration During Primary Percutaneous Coronary Intervention in Acute Myocardial Infarction: A Randomized Controlled Trial

Propofol with N-Acetylcysteine Reduces Global Myocardial Ischemic Reperfusion Injury More than Ketamine in a Rat Model

Objective: We examined the cardioprotective effects of propofol and ketamine with and without N-acetylcysteine (NAC). Methods: 60 rats were divided into six groups of 10 rats each. Anesthesia induction was produced with an intraperitonal injection of ketamine in Groups 1–3 and propofol in Groups 4–6. NAC (200 mg kg− 1) was given intraperitonally during anesthesia induction in Groups 3 and 6. Groups 2, 3, 5, and 6 were subjected to 90 s of myocardial ischemia by clamping the ascending aorta, and then reperfusion was begun by unclamping the ascending aorta. After 60 min of reperfusion, blood samples were taken from the ascending aorta for biochemical analyses, and heart tissue samples were taken for biochemical and histopathological analyses. Results: Creatine kinase (CK), myocardial band of creatine kinase (CK-MB), and troponin-I (Tn-I) levels were significantly higher in the ischemia–reperfusion groups (2, 3, 5, 6) compared to the nonischemic groups (1, 4). CK, CK-MB, and Tn-I levels did not differ significantly between the ketamine groups (1–3) and the propofol groups (4–6) p >. 05). Malondialdehyde levels were significantly higher in Groups 2 and 3 than in Group 1 and were significantly lower in Groups 4 and 6 than in Group 5 (p <. 05). Malondialdehyde levels in the propofol groups (4–6) were significantly lower than in the ketamine groups (1–3; p <. 05). Catalase levels in propofol groups were higher than ketamine groups. Superoxide dismutase levels were significantly higher in Group 6 than in Group 3 (p <. 05). Conclusions: In this rat model of global cardiac ischemia, propofol with NAC attenuates myocardial injury more than ketamine (with or without NAC).

Discordant Cardiac Biomarkers: Frequency and Outcomes in Emergency Department Patients With Chest Pain

We evaluate associations between pairs of discordant cardiac biomarkers (positive MB band of creatine kinase [CKMB] with negative creatine kinase, positive CKMB with negative cardiac troponin, and positive troponin with negative CKMB) and the presence of acute coronary syndromes in emergency department (ED) chest pain patients. This was a secondary analysis of a prospective registry. Data were obtained from the multicenter Internet Tracking Registry of Acute Coronary Syndromes, which included 17,713 ED visits for possible acute coronary syndrome between June 1999 and August 2001. First visits and first ED cardiac biomarker results from the 9 sites, 8 in the United States and 1 in Singapore, were included. Subjects were excluded for incomplete information or an initial ECG consistent with ST-segment elevation myocardial infarction. Acute coronary syndrome was defined by diagnosis-related group code indicating myocardial infarction, positive invasive or noninvasive diagnostic testing, revascularization, or death during hospitalization or within 30 days. Of 8,769 eligible patients, 1,614 (18.4%) had acute coronary syndrome. The CKMB and cardiac troponin results were discordant in 7% of patients (CKMB+/cardiac troponin-, 4.9%, CKMB-/cardiac troponin+ 2.1%), whereas increased CKMB with normal creatine kinase levels occurred in 239 (3.1%) patients. The unadjusted odds ratios with 95% confidence intervals for acute coronary syndrome in patients with and without discordant markers were: CKMB+/CK- 5.7 (4.4-7.4), CKMB+/CK+ 4.4 (3.6-5.2), CKMB-/cTn+ 4.8 (3.4-6.8), CKMB+/cTn- 2.2 (1.7-2.8), CKMB+/cTn+ 26.6 (18.0-39.3). For the group with cardiac troponin, the reference category was negative troponin and negative CKMB; for the group with creatine kinase, the reference category was negative CKMB but either a positive or negative creatine kinase. Among the spectrum of ED patients with chest pain, an increased CKMB level with a normal creatine kinase level identifies patients at increased risk for acute coronary syndrome. Similarly, an increased troponin level regardless of CKMB level and an increased CKMB level regardless of troponin level identify patients at higher risk for acute coronary syndrome than those with uniformly normal cardiac biomarker levels. Our data suggest that discordant cardiac biomarkers may identify patients at increased risk for acute coronary syndrome.

Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function.

Previous animal studies have demonstrated that the transmural extent of acute myocardial infarction defined by contrast-enhanced MRI (ceMRI) relates to early restoration of flow and future improvements in contractile function. We tested the hypothesis that ceMRI would have similar predictive value in humans. Twenty-four patients who presented with their first myocardial infarction and were successfully revascularized underwent cine and ceMRI of their heart within 7 days (scan 1) of the peak MB band of creatine kinase. Cine MRI was repeated 8 to 12 weeks later (scan 2). The transmural extent of infarction on scan 1 and wall thickening on both scans were determined using a 72-segment model. A total of 524 of 1571 segments (33%) were dysfunctional on scan 1. Improvement in segmental contractile function on scan 2 was inversely related to the transmural extent of infarction on scan 1 (P=0.001). Improvement in global contractile function, as assessed by ejection fraction and mean wall thickening score, was not predicted by peak creatine kinase-MB (P=0.66) or by total infarct size, as defined by MRI (P=0.70). The best predictor of global improvement was the extent of dysfunctional myocardium that was not infarcted or had infarction comprising <25% of left ventricular wall thickness (P<0.005 for ejection fraction, P<0.001 for mean wall thickening score). In patients with acute myocardial infarction, the transmural extent of infarction defined by ceMRI predicts improvement in contractile function.

Muscle damage induced by experimental hypoglycemia

To determine organ damage due to hypoglycemia, we studied the effects of insulin dose and hypoglycemia duration on serum enzyme activity in rabbits. Thirty rabbits were randomly divided into five groups according to hypoglycemia duration and insulin dose: A 2, hypoglycemia for 30 minutes with 2 U/kg insulin; A 10, hypoglycemia for 30 minutes with 10 U/kg insulin; B 2, hypoglycemia for 60 minutes with 2 U/kg insulin; B 10, hypoglycemia for 60 minutes with 10 U/kg insulin; and C, no hypoglycemia with 10 U/kg insulin and 50% glucose. Insulin-induced hypoglycemia was reversed by intravenous injection of glucose. Alterations in serum enzyme activity and creatine kinase (CK) isoenzyme distribution were determined before and after insulin injection. Serum CK activity increased significantly in all hypoglycemic groups compared with preinjection values, and tended to remain high for 24 hours in both groups A 10 and B 10. Serum activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) increased only in group B 10. In addition, the level of band 4 of serum CK isoenzymes, which exists predominantly in skeletal muscle and myocardium, increased significantly in group B 10. These results suggest that the increase in both serum enzyme and CK band 4 isoenzyme activities during hypoglycemia is primarily due to damage in muscle rather than liver, and that the hypoglycemia duration and insulin dosage may influence the extent of organ damage.

クレアチンキナーゼアイソザイム電気泳動分析により検出されたアルコール脱水素酵素

We found the fluorescent band revealed to cathodal position than mitochondria creatine kinase (CK) using the method of fluorescent staining (TAITAN N-CK, Helena) on CK electrophoresis, when we examined the serum of a patient with aplastic anemia who have been in serious liver damage (because of appearing graft versus host disease after bone marrow transplantation). However, it is widely noted that the alcohol dehydrogenase (ADH) band is believed to more cathodal position than lactate dehydrogenase (LDH) 5 on LDH electrophoresis. In this study, the fluorescent band revealed to cathodal position than mitochondria CK was also shown without substrate and addition of ethanol enhanced fluorescent strength. From these observations, these results suggest that this abnormal CK band will be ADH.

Elevated Atypical Creatine Kinases

To the Editor.— We read with interest the CASE REPORT by Gibson and Schnur 1 concerning an atypical creatine kinase (CK) in a patient with adenocarcinoma of the lung. The CK profile was unusual in that there was a persistent intermediately migrating electrophoretic band that was initially confused with CK-MB and accounted for the majority of the CK activity. We wish to offer two possible explanations for the atypical CK observed by Gibson and Schnur that coincide with our experimental observations. Macro CK type 1 is a term used to designate some atypical electrophoretic CK bands occasionally found migrating between CK-MM and CK-MB. Macro CK type 1 is composed of a CK isoenzyme, usually CK-BB or possibly CK-MM, complexed to another serum protein. The isoenzyme is usually complexed with IgG, but IgA and β-lipoprotein complexes have also been identified. We have found that the addition of antiserum to CK-BB to

Serum creatine kinase isoenzymes in patients with advanced malignant disease.

Serum creatine kinase (CK) B subunit (CK-B) activity, as estimated by the enzymatic anti-M immunoinhibition method, and the CK isoenzyme pattern after agarose gel electrophoresis, were studied in 28 patients with advanced, untreated malignant disease. CK-B was above the decision limit, i.e. the discrimination limit used in the diagnosis of acute myocardial infarction (AMI), in 14 patients (50%). Electrophoresis demonstrated, besides CK-MM, an atypical, cathodically migrating CK band in 10 of these patients. This band may represent mitochondrial CK. The CK-BB isoenzyme was detected in 9 and CK-MB in 3 subjects. Histopathologic findings indicated that the occurrence of these isoenzymes was related to tumour burden and the overall severity of the disease. Survival among patients with CK-B elevation was shorter than among other patients. The present findings are relevant to the enzyme diagnosis of AMI and of potential significance for the evaluation of patients with known or suspected malignant tumours.

Peripheral source of MB band of creatine kinase in alcoholic rhabdomyolysis. Nonspecificity of MB isoenzyme for myocardial injury in undiluted serum samples

Peripheral source of MB band of creatine kinase in alcoholic rhabdomyolysis. Nonspecificity of MB isoenzyme for myocardial injury in undiluted serum samples

Peripheral Source of MB Band of Creatine Kinase in Alcoholic Rhabdomyolysis

The MG isoenzyme of creatine kinase (CK MB) was strongly positive in the serum of a patient with alcoholic rhabdomyolysis, and it remained detectable by a standard qualitative assay over a two-year period without clinical or laboratory evidence of myocardial disease. MB isoenzyme was also demonstrated in a homogenate of skeletal muscle. Isoenzyme determinations in serum and tissue were repeated after dilution of toal CK activity to the range optimal for the assay (300 IU/L). Such dilution before isoenzyme separation rendered these samples negative for CK MB. The MB isoenzyme may be detectable in serum from peripheral sources in the presence of high total CK concentrations.

Genetic basis of creatine kinase isozymes in skeletal muscle of salmonid fishes.

The genetic basis of isozyme phenotypes of creatine kinase (CK) from extracts of skeletal muscle of salmonids has been resolved through breeding data including double heterozygous crosses and backcrosses of rainbow trout (Salmo gairdneri), and backcrosses of coho salmon (Oncorhynchus kisutch). The two-three-, or four-banded phenotypes of homozygous individuals and all heterozygous and hybrid phenotypes of ten salmonid species are readily explained by the following model: (1) there are no detectable heterodimers either between allelic products at a single locus or between loci: (2) each allele is represented electrophoretically by two bands, presumably a reflection of stable posttranslational modification of a single polypeptide unit; (3) CK of salmonid muscle is encoded by two loci--CK-1 and CK-2. The distance separating the paired bands reflecting each allele provides a basis for two groupings--a broad-spaced group (including all species of Oncorhynchus tested excepting O. masou) and a narrow-spaced group (including all species of Salmo tested and O. masou). The relationships among species suggested by the relative mobilities and spacings of these CK bands are consistent with taxonomic schemes inferred from morphological, cytogenetic, and other isozymic data.

A Study of the Sarcoplasmic Proteins of Porcine Muscle by Starch Gel Electrophoresis

SUMMARY– Extensive investigations were conducted on numerous variables in order to establish the most ideal conditions for the starch gel electrophoresis of the proteins of porcine skeletal muscle sarcoplasm. This technique was used to evaluate the characteristics of the sarcoplasm extracted from (a) muscles at various times post‐mortem, (b) muscles which ultimately remained normal in color and gross morphology as well as muscles which became extremely PSE and (c) muscles which had altered color and gross morphology due to post mortem treatment (i.e., normal color and gross morphology due to surface treatment with L‐N2 and PSE characteristics due to post‐mortem incubation at 37°C for 4 hr).There were no discernible differences between the starch gel electrophoretograms of sarcoplasmic proteins extracted from pre‐ and post‐rigor muscle. Likewise, there were no visually detectable differences between the starch gel electrophoretograms of sarcoplasmic proteins extracted from naturally occurring normal and PSE muscles. Furthermore, the preservation of normal color and gross morphology through L‐N, treatment did not give rise to electrophoretic differences when compared with either naturally occurring normal or PSE muscle.Although sarcoplasmic protein solubility diminished in naturally occurring PSE muscle, this loss in soluble protein did not necessarily manifest itself in the preferential denaturation of a specific sarcoplasmic protein. However when muscles were incubated at 37°C for 4 hr to induce the PSE condition they yielded sarcoplasmic extracts with marked electrophoretic reductions in creatine kinase, phosphoglucomutase, triosephosphate isomerase and F‐protein (Scopes, 1965). Although there were no apparent differences in creatine kinase isozymes between samples of muscle which ultimately remained normal or became PSE, the minor (fastest moving) creatine kinase band, as well as the phosphoglucomutase bands, appeared more labile during incubation at 37°C than the major (slowest moving) creatine kinase band.