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| A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # |
TROPONIN I (HS)
Test CodeTROPONIN I (HS)
Preferred Specimen
PST
Minimum Volume
1mL
Instructions
Only plasma tubes containing dried lithium heparin have been validated for use with this assay.
Transport Temperature
Room temperature (15 to 30°C)
Specimen Stability
8 Hours
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
· heat-inactivated specimens
· pooled specimens
· grossly hemolyzed specimens
· specimens with obvious microbial contamination
· specimens with fungal growth
· frozen specimens
Methodology
chemiluminescent microparticle immunoassay (CMIA)
Setup Schedule
Daily
Report Available
Stat-45 minutes
Routine-8 hours
Routine-8 hours
Limitations
· Results should be used in conjunction with other data; e.g., symptoms, results of other tests, and clinical impressions.
· Specimens may be stored on the red blood cells or separator gel for up to 8 hours at room temperature (15 to 30°C).
· The Alinity i STAT High Sensitivity Troponin-I assay is susceptible to interference effects from total protein > 8.8 g/dL. Total protein from 9.0 to 12.0 g/dL decreased troponin values at 500 ng/L by up to -16.3%.
· Specimens from individuals with elevated levels of fibrinogen may demonstrate falsely elevated values.
· Specimens from patients who have received preparations of mouse monoclonal antibodies for diagnosis or therapy may contain human anti-mouse antibodies (HAMA). Such specimens may show either falsely elevated or depressed values when tested with assay kits such as Alinity i STAT High Sensitivity Troponin-I that employ mouse monoclonal antibodies. Additional information may be required for diagnosis.
· Heterophilic antibodies in human serum can react with reagent immunoglobulins, interfering with in vitro immunoassays. Patients routinely exposed to animals or to animal serum products can be prone to this interference, and anomalous values may be observed. Additional information may be required for diagnosis.
· The Alinity i STAT High Sensitivity Troponin-I assay is susceptible to interference effects from HAMA > 150 ng/mL. HAMA at 225 ng/mL decreased troponin values up to -11.0%.
· Rheumatoid factor (RF) in human serum can react with reagent immunoglobulins, interfering with in vitro immunoassays.27
· The Alinity i STAT High Sensitivity Troponin-I assay is susceptible to interference effects from RF > 1200 IU/mL. RF at 1495 IU/mL decreased troponin values up to -18.9%.
· Although the Alinity i STAT High Sensitivity Troponin-I assay is specifically designed to minimize the effects of HAMA, heterophilic antibodies, and RF, assay results may be impacted by these proteins.
· Using the established overall 99th percentile (27 ng/L), the lower bound of the 95% confidence interval (CI) for positive predictive value (PPV) for female subjects was as low as 29.19%, and for male subjects was as low as 23.92% in the clinical validation study. Up to 70.81% and 76.08% of positive troponin results could come from females and males, respectively, without an MI. Using the established sex-specific 99th percentiles in the same study (female 14 ng/L, male 35 ng/L), the lower bound of the 95% CI for PPV for female subjects was as low as 21.45% and for male subjects was as low as 27.88%. Up to 78.55% and 72.12% of positive troponin results could come from females and males, respectively, without an MI.
Reference Range
| Gender | Reference High | Units |
| Male | <35 (99th percentile) | ng/L |
| Female | <14 (99th percentile) | ng/L |
Critical High 200 ng/L (Delta check 15). |
Clinical Significance
Cardiac troponin I is a regulatory subunit of the troponin complex associated with the actin thin filament within cardiac muscle cells.1 Troponin I, in conjunction with troponin C and troponin T, plays an integral role in the regulation of muscle contraction. Three distinct tissue-specific isoforms of troponin I have been identified from skeletal and cardiac muscles. The cardiac isoform exhibits only 60% similarity with the skeletal muscle isoform and contains additional amino acids at the N-terminus; cTnI has a molecular weight of approximately 24,000 daltons.2, 3
High sensitivity troponin assays have been defined as those which can achieve less than or equal to 10 %CV at the 99th percentile of a healthy population and are capable of detecting troponin in greater than 50% of both men and women individually.4, 5 Clinical studies have demonstrated the release of cTnI into the blood stream within hours following MI or ischemic injury. High sensitivity assays can detect elevated levels of cTnI (above the 99th percentile of an apparently healthy reference population) within 3 hours after the onset of chest pain.6 Cardiac troponin I reaches peak concentrations in approximately 8 to 28 hours and remains elevated for 3 to 10 days following MI.2, 7 Cardiac troponin is the preferred biomarker for the detection of myocardial infarction based on improved sensitivity and superior tissue-specificity compared to other available biomarkers of necrosis, including CK-MB, myoglobin, lactate dehydrogenase, and others.8, 9, 10 The high tissue specificity of cTnI measurements is beneficial for identifying myocardial infarction in clinical conditions involving skeletal muscle injury resulting from surgery, trauma, extensive exercise, or muscular disease.11, 12, 13, 14 High tissue specificity of cTnI, however, should not be confused with the specificity for the mechanism of injury (e.g., MI versus myocarditis). When an increased value for cTnI is encountered (e.g., exceeding the 99th percentile of a reference control population) in the absence of evidence of myocardial ischemia, other etiologies for cardiac damage should be considered.8 Elevated troponin levels may be indicative of myocardial injury associated with heart failure, renal failure, chronic renal disease, myocarditis, arrhythmias, pulmonary embolism, or other clinical conditions.15, 16
Per the fourth universal definition of MI,17 the term myocardial injury should be used when there is evidence of elevated cardiac troponin (cTn) values with at least one value above the 99th percentile upper reference limit (URL). The myocardial injury is considered acute if there is a rise and/or fall of cTn values. The term acute myocardial infarction should be used in specific situations when there is acute myocardial injury with clinical evidence of acute myocardial ischemia and with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following: symptoms of myocardial ischemia, new ischemic electrocardiogram (ECG) changes, development of pathological Q waves, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology, identification of a coronary thrombus by angiography.
A sex difference in 99th percentiles has been reported.18
High sensitivity troponin assays have been defined as those which can achieve less than or equal to 10 %CV at the 99th percentile of a healthy population and are capable of detecting troponin in greater than 50% of both men and women individually.4, 5 Clinical studies have demonstrated the release of cTnI into the blood stream within hours following MI or ischemic injury. High sensitivity assays can detect elevated levels of cTnI (above the 99th percentile of an apparently healthy reference population) within 3 hours after the onset of chest pain.6 Cardiac troponin I reaches peak concentrations in approximately 8 to 28 hours and remains elevated for 3 to 10 days following MI.2, 7 Cardiac troponin is the preferred biomarker for the detection of myocardial infarction based on improved sensitivity and superior tissue-specificity compared to other available biomarkers of necrosis, including CK-MB, myoglobin, lactate dehydrogenase, and others.8, 9, 10 The high tissue specificity of cTnI measurements is beneficial for identifying myocardial infarction in clinical conditions involving skeletal muscle injury resulting from surgery, trauma, extensive exercise, or muscular disease.11, 12, 13, 14 High tissue specificity of cTnI, however, should not be confused with the specificity for the mechanism of injury (e.g., MI versus myocarditis). When an increased value for cTnI is encountered (e.g., exceeding the 99th percentile of a reference control population) in the absence of evidence of myocardial ischemia, other etiologies for cardiac damage should be considered.8 Elevated troponin levels may be indicative of myocardial injury associated with heart failure, renal failure, chronic renal disease, myocarditis, arrhythmias, pulmonary embolism, or other clinical conditions.15, 16
Per the fourth universal definition of MI,17 the term myocardial injury should be used when there is evidence of elevated cardiac troponin (cTn) values with at least one value above the 99th percentile upper reference limit (URL). The myocardial injury is considered acute if there is a rise and/or fall of cTn values. The term acute myocardial infarction should be used in specific situations when there is acute myocardial injury with clinical evidence of acute myocardial ischemia and with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following: symptoms of myocardial ischemia, new ischemic electrocardiogram (ECG) changes, development of pathological Q waves, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology, identification of a coronary thrombus by angiography.
A sex difference in 99th percentiles has been reported.18
Performing Laboratory
Test performed at West Roxbury Chemistry Lab
Contact: Jonathan Dryjowicz-Burek 857-203-5418
Last Updated: December 23, 2024
