CV labs Flashcards
CPK
transfers high energy phosphate between creatine and ADP. Fraction MM from muscle and BB from brain, yet myocardial infarct = increased MB fraction, ie. CPK-MB.
Troponin
Calcium causes a conformational change in tropomysin that allows the reaction between actin and myosin to proceed. A free fraction in cytoplasm allows early leakage during an MI, resulting in a rise with the CPK. The troponin stays elevated for 5-10 days whereas the CPK usually hits normal at 3 days. Higher sensitivity test for troponin are now available.
Reinfarction after 3 days could be diagnosed with
a CK-MB elevation
different types of troponin
Troponin consists of three single chain polypeptides which regulate muscle contraction: troponin C (binds Ca2+), troponin I (binds actin-inhibiting actin–myosin interaction), and troponin T (binds tropomyosin and facilitates contraction). Cardiac muscle contains specific cTnI and cTnT isoforms. Most cTn is bound, but a small amount is free in the cytosol. The initial rise of cTn after myocyte damage is thought to be release of the unbound cytosolic cTn. This is followed by more prolonged appearance of troponin from damage to the myofilament structures.*
what causes changes in troponin?
AMI = elevated or falling troponin I or T* on the basis of ischemia in the presence of appropriate clinical information, EKG changes or new wall motion abnormality.
Elevation may be due to an acute injury (ie, pericarditis, myocardititis, pulmonary embolism, sepsis), or a chronic process (ie LVH, CHF, CKD, or DM); rather than an infarction which is based on ischemia.
Troponins can be used to diagnose cardiac injury after PCI (5 fold increase) or CABG (must have 10 fold increase).
The diagnosis of an acute myocardial infarction depends on
observation of a rise and/or fall of blood biomarkers with at least one value above the 99th percentile. Cardiac troponins are preferred to CK-MB measurements for diagnostic and prognostic purposes. A change in troponin levels is needed to diagnose myocardial infarction because troponin elevation can also be seen in a variety of other diseases, such as sepsis, hypovolemia, atrial fibrillation, heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure.
**Thus, an increased or falling troponin must be accompanied with symptomatic, electrocardiographic, nuclear, or echocardiographic evidence of myocardial ischemia in order to diagnose a myocardial infarction!. **
A 45 y/o male presents with substernal chest pain of three hours duration. A highly sensitive troponin I assay is elevated. EKG is as shown. What should be done next?
Repeat the troponin in 2 hours
MI/hs-cTnT When are they sensitive enough to detect an MI?
High sensitivity troponins* (hs-cTnT) are now able to confirm MI in 2 hours.
Some patients who present 2 hours or more after onset of chest pain, with a TIMI of 0 or 1, and with a negative one hour hs-cTNT (no changes in an hour) can be sent home.
what does cTnT of more than 14 ng/L indicate?
In patients with stable ischemic heart disease, a highly sensitive troponin (cTnT) of > 14 ng/L indicates an increased risk of MI, stroke, CHF, or CV death.
hsCRP
Released by hepatocytes under influence of cytokines IL6 and TNF alpha.
May bind to oxidized LDL particles for macrophage ingestion.
Useful in “stable” CHD in that a level > 3 mg/L = worse prognosis.
Useful in ACS where a level > 10 mg/L = worse prognosis.
hsCRP is decreased by statins and thiozolinediones.
Best level of hsCRP is
Lipids lab testing
Total cholesterol, triglycerides and HDL-C (done fasting due to triglycerides).
LDL-C = total-C – [VLDL-C (1/5 trig) + HDL-C]. This only works for triglycerides
Non-HDL-C
= total C – HDL-C = cholesterol in LDL, lipoprotein (a), IDL and VLDL. Better measurement of risk than LDL-C
LDL-C
level does not reveal the number of LDL particles, ie one may have a relatively normal LDL-C with level of 100 mg/dL and yet have many more small dense and dangerous particles than someone else with an LDL-C level of 100*.
*LDL-P (a core of lipid surrounded by phospholipid) measured by NMR
spectroscopy is a better assessment of lipid status than LDL-C or
Apo-B.
Which of the following lab test is best for supporting the
diagnosis of cardiovascular disease?
hs CRP Myeloperoxidase Homocysteine Cholesterol Fibrinogen
Cholesterol
BNP*
Brain naturetic peptide – mainly from cardiac ventricles (ANP mainly from atria) and activates G-protein coupled receptors.
BNP inhibits RAAS, endothelin secretion and sympathetic activity (norepinephrine), and increases renal blood flow and sodium excretion.
Useful in accessing severity in ACS, stable angina, mitral regurgitation, and aortic stenosis, but not to be used to guide treatment.
***Aberrantly low in obesity.
Uses:
Evaluation of dyspnea: 100 – 400 pg/mL = No value. Greater than 400 pg/mL = possible CHF. Less than 100 pg/mL = no CHF.***
Monitoring of established HF (fair) and prognosis in CHF (better).
May be of use in heart failure therapy, ie nesiritide
N-terminal Pro-BNP*
NT proBNP useful to suggest CHF in in patients with dyspnea less than 50 , 50-75 and > 75 yoa at levels of 450pg/mL, 900 pg/mL and 1800 pg/mL respectively.
Age > 70, NT proBNP less than 400 pg/ml excludes CHF, and NT proBNP > 2000 pg/ml suggest CHF when diagnosis is uncertain.
Acute heart failure can be ruled out with normal levels of
BNP and NTproBNP
Serum Sodium
A marker for a poor prognosis in CHF.
Na below 135 meq/L indicates that a CHF patient has an increased chance of falls as well as more likely reoccurrence of CHF episodes.
Related to excess vasopressin (ADH)
Which of the following would be the best marker for the severity of CHF?
Serum sodium BNP NT Pro-BNP Uric acid Fibrinogen
Serum sodium
Which of the following cardiac markers is useful in excluding congestive heart failure?
hsCRP myeloperoxidase homocysteine Cholesterol NT-pro BNP
NT-pro BNP
Other Lab Methods of Risk Assessment
TC/HDL-C Non-HDL-C Apolipoprotein B Apolipoprotein (a) Small dense LDL-C LDL-P
High Cholesterol with High LDL-C
High cholesterol with high LDL-C (Fredrickson type 2A) is a lab presentation that includes Familial and Polygenic Hypercholesterolemia*.
All relate to high LDL-C (with essentially normal triglycerides) because of a **defective LDL receptor or problems with LDL-C attachment **(defective apo B ligand) to the receptor or various combinations thereof.
Patients have corneal arcus, xanthelasma and tendinous xanthomata, premature CAD, and aortic stenosis.
Type IIa Hyperlipidemia
Familial or Polygenic Hyperlipidemia
Mutation in LDL receptors or defective Apo B 100 ligand (90% Type II a ). LDL - C usually > 250 mg/dl. Tendon xanthomas, arcus, premature CAD, PVD, strong family history.
High Cholesterol with High Triglycerides
High Cholesterol with High Triglycerides = Fredrickson Types 2B or Familial Combined Hyperlipidemia (most common primary hyperlipidemia, though usually no skin findings).
