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 # |
ROMI Panel
Test CodeCPT Codes
83874; 84484
Preferred Specimen
Serum (gold top tube), collected at onset, 3 hours post onset, 6 hours post onset, and 12 hours post onset
Minimum Volume
Other Acceptable Specimens
Instructions
Collect 4 samples: The first specimen is considered the "Onset" specimen, followed by specimens collected 3 hours later, 6 hours later, and 12 hours later.
Transport Container
Serum (gold top) tubes or Lithium Heparin Plasma (green top) tubes
Transport Temperature
Specimen Stability
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Methodology
Chemiluminescence
Setup Schedule
Daily upon receipt
Report Available
Limitations
Reference Range
Reference Range: <0.034 ng/mL
Interpretative Data:
0.034 ng/mL or less: Negative; repeat testing as clinically indicated.
0.034 - 0.12 ng/mL: Suspicious for myocardial injury. Serial measurements may be necessary to confirm or exclude the diagnosis of acute coronary syndrome.
0.12 ng/ml: Consistent with myocardial injury.
*Changes in results should be interpreted based on method.
Clinical Significance
Troponin I (TnI) is a protein normally found in muscle tissue that, in conjunction with Troponin T and Troponin C, regulates the calcium dependent interaction of actin and myosin. Three isotypes of TnI have been identified: one associated with fast-twitch skeletal muscle, one with slow-twitch skeletal muscle and one with cardiac muscle. The cardiac form has an additional 31 amino acid residues at the N terminus and is the only troponin isoform present in the myocardium. Clinical studies have demonstrated that cardiac Troponin I (cTnI) is detectable in the bloodstream 4–6 hours after an acute myocardial infarct (AMI) and remains elevated for several days thereafter. Thus, cTnI elevation covers the diagnostic windows of both creatine kinase-MB (CK-MB) and lactate dehydrogenase. Further studies have indicated that cTnI has a higher clinical specificity for myocardial injury than does CK-MB. Other conditions resulting in myocardial cell damage can contribute to elevated cTnI levels. Published studies have documented that these conditions include, but are not limited to, sepsis, congestive heart failure, hypertension with left ventricular hypertrophy, hemodynamic compromise, myocarditis, mechanical injury including cardiac surgery, defibrillation and cardiac toxins such as anthracyclines. Factors such as these should be considered when interpreting results from any cTnI test method. Because of its cardiac specificity and sensitivity, cTnI has been used as a reliable marker in evaluating patients with unstable angina and non-ST segment elevation acute coronary syndrome (ACS). Previous clinical studies of patients with ACS have shown that minor increases in cTnI values provide important prognostic information about the short and long term risk of death. Ultimately, the assessment of the prognosis can be useful in identifying patients most likely to benefit from specific therapeutic interventions. |