No special patient preparations are necessary.

Mix anticoagulant with specimen adequately. Specimens should be centrifuged at minimum 2500 RPM for minimum 5 minutes. Remove plasma promptly from cells to an appropriately labeled tube, unless using PST tube.

Centrifuge and remove plasma from the cells with 2 hours of collection.

Storage:

   Room temperature for 4 hours  

   Refrigerator temperature for 48 hours

   Freezer temperature for 72 hours  

Chemistry.
Daily, routine and STAT.

Access hsTnI is a paramagnetic particle, chemiluminescent immunoassay for the quantitative determination of cardiac troponin I (cTnI) levels in human plasma using the Access 2 Immunoassay Systems to aid in the diagnosis of myocardial infarction (MI).
The troponins (I, C, and T) are members of a complex of proteins that modulate the calcium‐mediated interaction between actin and myosin within muscle cells. The nomenclature of these distinct proteins of the troponin complex is derived from their respective function in muscle contraction. Troponin T anchors the troponin complex to tropomyosin of the thin filament, whereas troponin I inhibits actomyosin ATPase, and troponin C is a calcium‐binding subunit. Three isoforms of troponin I (TnI) have been identified: one associated with fast–twitch skeletal muscle, one with slow–twitch skeletal muscle, and one with cardiac muscle. The slow and fast–twitch isoforms have a similar molecular weight of approximately 20,000 dalton (Da) each. The cardiac–specific TnI isoform has a molecular weight of approximately 24,000 Da and contains a post–translational tail of 31 amino acids on the N–terminus of the molecule. This sequence and the 42% and 45% dissimilarity with the sequences of the other two isoforms have made possible the generation of highly specific monoclonal antibodies without cross–reactivity with other non–cardiac TnI forms.
As a result of its high tissue specificity cTnI is a cardio–specific, highly sensitive marker for myocardial injury. The Access hsTnI assay uses monoclonal antibodies specifically directed against human cTnI.
In myocardial infarction, cTnI levels rise in the hours after the onset of cardiac symptoms, reaching a peak at 12–16 hours and can remain elevated for 4–9 days post MI.  Numerous pathologies can potentially cause troponin elevations without overt ischemic heart disease. These pathologies include, but are not limited to, congestive heart failure, acute and chronic trauma, electrical cardioversion, hypertension, hypotension, arrhythmias, pulmonary embolism, severe asthma, sepsis, critical illness, myocarditis, stroke, non–cardiac surgery, extreme exercise, drug toxicity (adriamycin, 5–fluorouracil, herceptin, snake venoms), end stage renal disease, and rhabdomyolysis with cardiac injury. Importantly, these other etiologies rarely demonstrate the classic rising and falling pattern experienced with a MI, which highlights the importance of serial monitoring when the clinical scenario is unclear.
In 2012, a Task Force of the Joint European Society of Cardiology (ESC), American College of Cardiology Foundation (ACCF), American Heart Association (AHA), and World Heart Federation (WHF) published an updated redefinition of MI in which cardiac troponin (cTn) plays a central role.



The 2012 Third Universal Definition of Myocardial Infarction document states that in patients presenting to the Emergency Department with chest pain, or other ischemic symptoms, the criteria for diagnosis of MI are:
Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin] with at least one value above the 99th percentile of the upper reference limit (URL) and with at least one of the following:
• Symptoms of ischemia;
• New or presumed new ST-segment-T wave (ST-T) changes or new left bundle branch block (LBBB);
• Development of pathological Q waves in the ECG;
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality;
• Identification of an intracoronary thrombus by angiography or autopsy.
Additionally, the Third Universal Definition of Myocardial Infarction document recommends an optimal imprecision level (coefficient of variation, or CV) for troponin assays ≤ 10% at the 99th percentile URL of a healthy population.
Cardiac troponin should be measured upon admission, and then serially at regular intervals to demonstrate a rise and/or fall in cTn values. When an increased cTn value does not support the diagnosis of acute myocardial ischemia, a careful search for other possible etiologies of myocardial injury should be undertaken.
The International Federation of Clinical Chemistry (IFCC) has issued guidance on high sensitivity troponin assays. In order to be classified as a high sensitivity assay, two performance requirements must be met:
• The assay must have analytical imprecision ≤ 10% CV at the 99th percentile URL of a healthy population.
• The assay must be able to measure cTn above the Limit of Detection (LOD) in ≥ 50% of a healthy population.
Compared to contemporary troponin assays, high sensitivity assays demonstrate significantly improved precision at and below the 99th percentile URL, allowing better discrimination of small differences in cTn values between serial measurements.  More precise determination of the 99th percentile URL has also led to an ability to report distinct reference ranges for male and female subjects.
The Access hsTnI assay is a two–site immunoenzymatic (“sandwich”) assay. Monoclonal anti–cTnI antibody conjugated to alkaline phosphatase is added to a reaction vessel along with a surfactant–containing buffer and sample. After a short incubation, paramagnetic particles coated with monoclonal anti–cTnI antibody are added. The human cTnI binds to the anti–cTnI antibody on the solid phase, while the anti–cTnI antibody–alkaline phosphatase conjugate reacts with different antigenic sites on the cTnI molecules. After incubation in a reaction vessel, materials bound to the solid phase are held in a magnetic field while unbound materials are washed away. Then, the chemiluminescent substrate is added to the vessel and light generated by the reaction is measured with a luminometer. The light production is directly proportional to the concentration of cTnI in the sample. The amount of analyte in the sample is determined from a stored, multi–point calibration curve.

Elevations of Troponin-I may be seen in congestive heart failure, pulmonary embolism, hypertension, myocarditis/pericarditis, renal failure, cocaine abuse, and hypothyroidism.
The assay should not be used to evaluate patients younger than 21 years of age (e.g., children, teens, etc.).  These patients will typically present with elevated but unchanging troponin values over time.

The validated 99th percentile cutoff was established as 15 ng/L for women and 20 ng/L for men with the following specificity (plasma Lithium heparin specimens):
(i) initial evaluation: 91% for women and 87% for male
(ii) 1-3 h after ED admission: 92% for women and 88% for male
(iii) 3-6 h after ED admission:  92% for women and 88% for male
(iv) 6-9h after ED admission: 88% for women and 81% for male.

Chemistry.
Daily, routine and STAT.

Results same day.

Normal
99^th Percentile 
Male       < 20 ng/L                  
Female   < 12 ng/L

Flag high
Male     > 20 ng/L but < 50 ng/L
Female > 15 ng/L but < 50 ng/L
“Elevated value indicating possible myocardial injury. See Hyperlink (EPIC) for management algorithms. Elevated troponin values may be seen in congestive heart failure, pulmonary embolism, hypertension, myocarditis/pericarditis, and renal failure” 




Flag High
Elevated and Actionable
Male     > 50 ng/L
            Female > 50 ng/L      
“Actionable value indicating myocardial injury. See Hyperlink (EPIC) for management algorithms. Elevated troponin values may be seen in congestive heart failure, pulmonary embolism, hypertension, myocarditis/pericarditis, and renal failure”

Delta
Flag High
Male     > 7 ng/L
Female > 7 ng/L
“The Delta Value represents the absolute change in the Troponin value from the most recent previous value (within 7 hours). A Delta value increase of >7 ng/L for initial Troponin values Flagged High but < 50 ng/L indicates ongoing myocardial injury.”

Critical Value:   Males:      > 375 ng/L
Females:  > 350 ng/L
Delta:       >25 (If the first troponin and second troponin are elevated non-critical)
                        (If the first troponin is critical, don't call the delta regardless)
“Value consistent with myocardial infarction. Elevated troponin values may be seen in congestive heart failure, pulmonary embolism, hypertension, myocarditis/pericarditis, and renal failure”

The hsTROP order battery consists of three reportable values:  PTROP (previously reported troponin collected less than seven hours prior to current collection), HSCTN (currently measured troponin), and DELTA (calculated difference between PTROP and HSCTN (i.e., HSCTN minus PTROP).

If no prior troponin value is available or available within the last seven hours, the PTROP will be reported as NOPREV (no previous result) and the DELTA will be reported as NODELT (not calculated).  If the PTROP value is higher that the HSCTN value, the DELTA will be resulted as TRPDEL.

The Delta Value represents the absolute change in the Troponin value from the most recent previous value (within 7 hours). A Delta value increase of >7 ng/L for initial Troponin values flagged high but <50 ng/L indicates ongoing myocardial injury.