Authors Wu AH, Feng YJ, Contois JH, Pervaiz S
Troponin I Sensitivity in Acute MI
Institution Department of Pathology and Laboratory Medicine, Hartford Hospital, CT 06102, USA.
Comparison of myoglobin, creatine kinase-MB, and cardiac troponin I for diagnosis of acute myocardial infarction.
Annals of Clinical & Laboratory Science. 26(4):291-300, 1996 Jul-Aug
Abstract Serial plasma concentrations of myoglobin, creatine kinase MB (CK-MB) isoenzyme, and cardiac troponin I (cTnI) were measured in 25 patients with a confirmed diagnosis of acute myocardial infarction (AMI), and 74 patients who were suspected of AMI but were subsequently ruled out for this diagnosis. The cutoff concentration for the cTnI assay was optimally determined to be 2.5 ng/mL. Of the three markers, myoglobin had the highest clinical sensitivity (50 percent) when blood was collected between 0 to 6 h after the onset of chest pain. Assays for all serum markers used had high clinical sensitivity (> 93 percent) 6 to 24 h after onset. The CK-MB remained highly sensitive for 48 h, while cTnI was sensitive for up to 72 h. Between 72 and 150 h, cTnI had a clinical sensitivity of 70 percent as compared to 21 percent and 18 percent for myoglobin and CK-MB, respectively. The clinical specificity of cTnI for non-AMI patients was equivalent to CK-MB and significantly higher than for myoglobin. The clinical efficiency of cTnI for all samples was better than either CK-MB or myoglobin, owing mainly to the wider diagnostic window. The specificity of cTnI for 59 patients with chronic renal failure, skeletal muscle trauma and disease was better than all of these markers including cardiac troponin T (cTnT). Results of this study show that cTnI is an effective marker for the retrospective diagnosis of AMI, and consideration should be given to its use in place of CK-MB.
CARDIAC TROPONIN-I - A HIGHLY SPECIFIC BIOCHEMICAL MARKER FOR MYOCARDIAL-INFARCTION
JOURNAL OF CLINICAL IMMUNOASSAY
Creatine kinase MB isoenzyme (CK-MB) has become the biochemical marker of choice for diagnosing myocardial infarction (MI). However, limitations of CK-MB measurement such as delayed response and short duration of elevation following an MI as well as lack of specificity necessitate the finding of a more suitable diagnostic marker. Cardiac troponin I (cTnI), a heart tissue-specific regulatory protein, has received much attention recently as a potential choice to replace CK-MB. Monoclonal antibody based immunoassays have shown that cTnI is undetectable in sera of healthy blood donors. cTnI concentration is <3.1 ng/mL in sera of 95% of hospitalized patients who have no heart disease. Following an MI, cTnI becomes elevated approximately 6 hours after the onset of chest pain and its concentration peaks around 12 hours. In contrast to the short duration of elevation of CK-MB, cTnI remains diagnostic for at least a week after MI. cTnI appears to be extremely cardiac-specific. No cTnI has been found in patients who had rhabdomyolysis but no cardiac muscle injury even when CK reached >70,000 U/L and CK-MB >270 ng/mL. cTnI was 100% sensitive and 100% specific in detecting MI in patients with acute (n = 39) and chronic (n = 10) skeletal muscle injury, chronic renal failure (n = 159), or in marathon runners (n = 10).
BODOR GS, VANDERBILT UNIV,MED CTR,SCH MED,DEPT PATHOL,4605 TVC,NASHVILLE,TN 37232
CLINICAL LIGAND ASSAY SOC, 3139 S WAYNE RD, WAYNE, MI 48184