Lab dx of MI and HF week 2 Flashcards
differences btwn cTnT and cTnI
There are several differences between the cTnT and cTnI markers. CTnT is patented and thus available from only one vendor. In contrast, cTnI is available from multiple sources so different assays may perform differently, despite efforts to standardize performance.
Relative to cTnT, cTnI is more cardio specific and levels are not as elevated in renal failure. (In one study of chronic kidney disease patients, cTnT was elevated above the 99% reference limit in 43% of patients versus cTnI which was elevated in 18% of patients (Abbas NA, et al. Clinical Chemistry 51:2059-2066, 2005.)
The sensitivity and specificity of cTnI exceeds 99%; cTnT performs similarly in non-renal failure patients.
Both markers are normally undetectable in serum and are released into the bloodstream when myocardial damage occurs. Studies have demonstrated that both markers are useful for assessing reperfusion following thrombolytic therapy.
Conditions (OTHER THAN AMI) where troponin may be elevated
What may cause FP results?
Acute pulmonary embolus
Acute pericarditis
Myocarditis
Sepsis / shock
Renal Failure
Severe Heart failure
False positive result due to assay interference from heterophile antibodies
Values of cTnI that are diagnosistic
clincal uses of troponin
The reference range for cTnI at NYUMC is less than or equal to 0.4 ng/mL. Values above this cutoff represent evidence of cardiac injury. However, 99% of apparently healthy subjects typically have a value less than 0.1 ng/mL. Values between 0.1 and 0.4 are considered indeterminate and likely represent minor myocardial damage. These patients appear to be at increased risk. Whether these patients should be classified as AMI or unstable angina will become clearer as vendors improve assay performance at low concentration and perform additional clinical studies.
To summarize, clinical uses of troponin are:
- Exclusion / confirmation of AMI
- Diagnosis of peri-operative myocardial damage
- Monitoring the outcome of thrombolytic therapy
- Risk stratification of patients with unstable angina and diagnosis of micro
3 main locations of CK
3 isoenzymes of CK
How CK-MB is diagnositc of MI
other instances where it may be elevated
what age group can it not be used as indicator of myocardial injury?
The CK in normal adult serum is comprised of the MM fraction. Though a small amount of CK - MB may be present, it represents less than 3% of the total serum CK. Therefore, the presence of CK- MB is an excellent indicator of an acute myocardial infarct. In the laboratory, CK-MB is measured by immunoassay. In some clinical instances when the total CK is high, the CK-MB may also be elevated without cardiac muscle damage, thus it is not cardiospecific. CK-MB is present in small amounts in skeletal muscle and may be elevated in Duchenne’s muscular dystrophy, intense exercise, or skeletal muscle injury. However, it accounts for less than 5% of total serum CK. CK-MB is found in relatively large amounts in the serum of neonates; it cannot be used as an indicator of myocardial injury in this age group.
first marker to rise in AMI
myoglobin-rises 2 hours post MI (although not used very much clinically)
more valuable when its a neg result rather than pos (bc can have myoglobin release in any type of muscle damage)-sensitive but not specific!
AMI can only be excluded on the basis of what lab tests performed after how many hours after onset of symptoms?
AMI can be excluded only on the basis of troponin determinations performed 8-12 hours after the onset of symptoms and CK-MB determinations performed 12-24 hours post onset.
What stimulates BNP release?
What heart function parameter has been shown to correlate with BNP levels?
How do BNP levels correlate with adverse outcomes? In what diseases?
LV wall stretch and volume overload
BNP measurements can be used to monitor the impact of therapy and progression of disease. The plasma level of BNP has been shown to correlate with Left Ventricular Ejection Fraction (LVEF) and New York Heart Association Functional Class, with BNP levels increasing as LVEF decreases and NYHA Class increases. Rising levels suggest decreasing LVEF and a worsening of disease.
Several studies have shown that BNP is a predictor of adverse outcomes after episodes of CHF and after myocardial infarction, with higher levels predictive of re-admission and death in CHF and recurrent MI or death after myocardial infarction.
