cadiac enzyme

موضوع: cadiac enzyme الثلاثاء مارس 08, 2011 12:39 pm

cadiac enzyme

The substances monitored for indication of cardiac damage or disease include

Creatine
kinase (CK) has a 98% sensitivity for AMI 72 hours after infarction. CK
is a catalyst for energy production and is found in brain, myocardium,
and skeletal muscle. CK is sensitive but not specific for myocardial
injury

CK isoenzymes are more
specific than CK. Three CK isoenzymes have been identified: CK-MM,
CK-MB, and CK-BB, with only CK-MB related to the heart. The specificity
of CK-MB is greater than 85% and in some cases as high as 100%, but
false positives do occur. Two types of CK-MB assays (CK-MB mass and
CK-MB activity) are presently used. CK-MB mass assays are found to be
more sensitive than CK-MB activity assays; CK-MB mass increases about 3
hours after onset of chest pain, whereas CK-MB activity requires
another 1 hour to elevate. CK-MB index is the ratio of CK-MB to the
total CK, and is considered abnormal when it exceeds 3% to 5%

Eventually,
electrophoresis further breaks down CK-MB into its isoforms or subforms
(CK-MB1 and CK-MB2). Normally, the ratio of CK-MB2 to CK-MB1 is 1:1. In
myocardial injury, the CK-MB2/MB1 ratio increases to greater than 1.5
within 1 to 1آ½ hours. CK-MB isoforms have 56% sensitivity for patients
presenting within 4 hours of the onset of symptoms

The
troponin complex is located on the thin filament of the contractile
apparatus of striated and skeletal muscle and consists of three
subunits: troponin C (TnC), troponin T (TnT), and troponin I (TnI). In
the presence of myocardial damage, the troponin complex on the
myofibril breaks down and the subunits of troponin are slowly released
into the bloodstream. TnC is not sensitive or specific for myocardial
injury. TnT has a sensitivity of approximately 50% within 4 hours of
the onset of chest pain, but increases to approximately 75% sensitivity
after 6 hours of onset and approximately 100% sensitivity in 12 hours.
However, its specificity for myocardial injury is lower. TnI has been
found to be the most sensitive and specific for myocardial injury. It
has little sensitivity within 4 hours of the onset of chest pain, but
increases to 96% sensitivity after 6 hours of the onset of symptoms

Myoglobin is a small, oxygen-binding protein found in cardiac and
skeletal muscles and is rapidly released into the bloodstream.
Myoglobin is sensitive very early after injury, but has poor
sensitivity over time and can generate many false-positive results.
When myoglobin levels are assessed with CK-MB results, sensitivity
increases (as high as 96%), but specificity can drop to as low as 81%.
Myoglobin is directly related to muscle mass and is affected by age
(levels increase with age), race (blacks have higher levels), gender
(women have higher levels), and physical activity. Myoglobins can be
elevated in the presence of reinfarction, skeletal muscle or
neuromuscular disorders, trauma, severe burns, electrical shock,
alcohol withdrawal delirium, metabolic disorders, systemic lupus
erythematosus, strenuous exercise, renal failure, I.M. injections,
cardiac bypass surgery, seizures, and heart failure

Homocysteine
is a toxic by-product of the metabolism of the amino acid methionine
into cysteine. Homocysteine exerts a direct cytotoxic effect on the
endothelium of blood vessels by blocking the production of nitrous
oxide, resulting in decreased pliability of vessels and the development
of atherosclerotic plaque. Increased homocysteine levels ultimately
result in atherosclerosis, CAD, MI, stroke, thromboembolism, and
peripheral vascular disease. Hyperhomocystinemia (increased
homocysteine levels) are related to gender (male), advanced age,
smoking, hypertension, elevated cholesterol, decreased folate,
decreased vitamin B6 and B12, and lack of exercise. Homocysteine can
also be elevated in the presence of other diseases, drug use, and
caffeine intake

B-type natriuretic peptide (BNP) is synthesized in the ventricular
myocardium and released as a response to increased wall stress. BNP is
used for diagnosis and prognosis of suspected heart failure. Plasma
levels of BNP increase in the presence of left ventricular systolic and
diastolic dysfunction, particularly in the presence of decompensating
heart failure. An increased BNP level identifies patients at the
highest risk of developing sudden cardiac death and those who are in
need of heart transplant. It is also associated with heart failure
readmissions. BNP is considered a useful marker of myocardial function
and is used to guide therapy

C-reactive protein (CRP) is an inflammatory marker that may be an
important risk factor for atherosclerosis and ischemic heart disease.
CRP is an inflammatory marker produced by the liver in response to
systemic cytokinases. Elevated CRP is associated with AMI, stroke, and
the progression of peripheral vascular disease. However, it can also be
elevated with any inflammatory process. In addition to revealing events
associated with CAD, CRP can also be used to identify patients at risk
for developing CAD.

Lipoprotein(a)
is a molecule that is similar to low-density lipoprotein cholesterol
(LDL-C). It increases cholesterol deposits in the arterial wall,
enhances oxidation of LDL-C, and inhibits fibrinolysis, resulting in
the formation of atherosclerotic plaque and thrombosis. Treatment of
elevated lipoprotein(a) is suggested only for patients with a history
of premature vascular disease without other risk factors.
Factor I, or fibrinogen, is directly linked to increased cardiovascular
risk. It is involved in the coagulation cascade (converting fibrinogen
to fibrin by thrombin), stimulates smooth-muscle cell migration and
proliferation, and promotes platelet aggregation, which increases blood
viscosity