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Markers creatine kinase

Biochemical markers (creatine kinase [CK], CK-MB fraction, troponin I and troponin T) are elevated in Ml (ST-segment elevation Ml and non-ST-segment elevation Ml), but normal in chronic stable angina and unstable angina. [Pg.68]

NSTEMI differs from UA in that ischemia is severe enough to produce myocardial necrosis, resulting in release of detectable amounts of biochemical markers, primarily troponin I or T and creatine kinase myocardial band (CK-MB) from the necrotic myocytes into the bloodstream. [Pg.56]

FIGURE 5-2. Biochemical markers in suspected acute coronary syndrome. (AMI, acute myocardial infarction CK-MB, creatine kinase myocardial band Ml, myocardial infarction.)... [Pg.59]

The enzyme responsible for this topping-up ATP in active muscle is CK. CK is found in high concentration in muscle cells, both free within the sarcoplasm and also associated with membranes of mitochondria and the sarcoplasmic reticulum. Structurally, creatine kinase is a dimeric enzyme of B and/or M subunits, each of about 40 kDa. Three quaternary structure isoenzyme forms arise CK-MM, CK-BB and CK-MB. The predominant form in all muscles is CK-MM, but cardiac muscle also contains a significant amount of CK-MB and this isoenzyme can be used as a specific marker of myocardial damage (see Case Notes at the end of this chapter). [Pg.247]

Z. Li, H. Qiao, C. Lebherz, S. R. Choi, X. Zhou, G. Gao, H. F. Kung, D. J. Rader, J. M. Wilson, J. D. Glickson and R. Zhou, Creatine kinase, a magnetic resonance-detectable marker gene for quantification of liver-directed gene transfer. Hum. Gene Ther., 2005,16,1429-1438. [Pg.158]

Creatine kinase (CK) occurs in high concentrations in the brain, cardiac and skeletal muscle and is elevated in the blood with muscle damage. A rise in CK is seen in acute myocardial infarction but also in other conditions. A more specific marker is creatine kinase MB (CK-MB), which is an isoenzyme of creatine kinase that is more specific for cardiac muscle damage. CK or CK-MB will rise approximately 4 hours after an acute cardiac event and will reach a peak after approximately 24 hours and will remain raised for 3-4 days. [Pg.45]

Chemical markers are released into the bloodstream following injury of the cardiac muscle. Three types of troponin, as well as elevated creatine kinase-MB (CK-MB) levels, are indicators of cardiac tissue damage (Apak et al., 2005 Q Brien, 2008). [Pg.496]

The procedure was continued with a propofol infusion. No treatment for malignant hyperpyrexia was undertaken and no other markers for malignant hyperpyrexia were observed. She made a normal recovery from anesthesia. Creatine kinase activities were raised at 2370 U/1 intraoperatively and 18 046 U/1 at 20 hours postoperatively. [Pg.1495]

Creatinine results from the irreversible, nonenzymatic dehydration and loss of phosphate from phosphocreatine (Fig. 1). Creatinine is used as an indicator of skeletal muscle mass because it is a by-product of the creatine kinase reaction and it is one of the most widely used clinical markers to assess renal function. Urine levels of creatinine are good indicators of the glomerular filtration rate of the kidneys (i.e., the amount of fluid filtered per unit time). [Pg.465]

The myocardium contains bundles of striated muscle fibers, each of which is typically 10 to 15 pm in diameter and 30 to 60 pm in length. Work of the heart is generated by the alternating of the contraction and relaxation of these fibers. The fibers are composed of cardiac-specific contractile proteins actin and myosin, and regulatory proteins caEed troponins. They also contain a variety of enzymes that are vital for energy use, such as myoglobin, creatine kinase (CK), and lactate dehydrogenase (LD), some of which can be used as markers of cardiac injury. [Pg.1621]

Figure 44-15 Serial serum creatine kinase-2 (CK-MB), cardiac troponin I (cTni), and cardiac troponin T (cTnT) profiles after AMI. Cardiac markers are plotted as multiples of the upper reference limit. Figure 44-15 Serial serum creatine kinase-2 (CK-MB), cardiac troponin I (cTni), and cardiac troponin T (cTnT) profiles after AMI. Cardiac markers are plotted as multiples of the upper reference limit.
Patients with ischemic chest discomfort and suspected ACS are risk-stratified based on a 12-lead electrocardiogram (ECG), past medical history, and results of creatine kinase (CK) MB and troponin biochemical marker tests. [Pg.291]

A positive biochemical marker for infarction is a value of troponin I, troponin T, or creatine kinase MB of greater than the Ml detection limit. [Pg.296]

Creatine kinase a marker of muscle damage and acute Ml. [Pg.110]

Several urinary enzymes are useful in the assessment of nephrotoxicity, and these are discussed separately in Chapter 4. Although there is some application of cholinesterases in studying hepatotoxicity, these enzymes are important markers in pesticide-induced toxicities and are discussed in Chapter 11. Creatine kinase (CK) remains a useful marker for myotoxicity, but it is rapidly losing its place to troponins in the detection of cardiotoxicity (see Chapter 7). Amylase and lipase remain the enzyme markers of pancreatic toxicity. [Pg.31]


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See also in sourсe #XX -- [ Pg.756 ]




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