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inflammation and infection, so it can be used as a very rough proxy
for heart disease risk. Since many things can cause elevated CRP,
this is not a very specific prognostic indicator.Nevertheless, a level
above 2.4 mg/l has been associated with a doubled risk of a
coronary event compared to levels below 1 mg/l;Recent research
suggests that patients with elevated basal levels of CRP are at an
increased risk of diabetes,hypertension and cardiovascular
disease.A study of over 700 nurses showed that those in the
highest quartile of trans fat consumption had blood levels of CRP
that were 73% higher than those in the lowest quartile.Although
one group of researchers indicated that CRP may only be a
moderate risk factor for cardiovascular disease[15].
In an attempt to improve global cardiovascular risk prediction,
considerable interest has focused on C-reactive protein (CRP), a
marker of inflammation that has been shown in multiple
prospective epidemiological studies to predict incident
myocardial infarction, stroke, peripheral arterial disease, and
sudden cardiac death. CRP levels have also been shown to predict
risk of both recurrent ischemia and death among those with stable
and unstable angina, those undergoing percutaneous angioplasty,
and those presenting to emergency rooms with acute coronary
syndromes. These highly consistent clinical data are supported by
abundant laboratory and experimental evidence that demonstrate
that atherothrombosis, in addition to being a disease of lipid
accumulation, also represents a chronic inflammatory process. In
terms of clinical application, CRP seems to be a stronger predictor
of cardiovascular events than LDL cholesterol, and it adds
prognostic information at all levels of calculated Framingham Risk
and at all levels of the metabolic syndrome[16]. Using widely
available high-sensitivity assays, CRP levels of <1, 1 to 3, and >3
mg/L correspond to low-, moderate-, and high-risk groups for
future cardiovascular events. Individuals with LDL cholesterol
below 130 mg/dL who have CRP levels >3 mg/L represent a high-
risk group often missed in clinical practice. The addition of CRP to
standard cholesterol evaluation may thus provide a simple and
inexpensive method to improve global risk prediction and
compliance with preventive approaches.
11. CK-MB
CK-MB is relatively specific when skeletal muscle damage is not
present. CK-MB resides in the cytosol and facilitates high-energy
phosphates into and out of mitochondria. It is distributed in a large
number of tissues even in the skeletal muscle. Since it has a short
duration, it cannot be used for late diagnosis of acute MI but can be
used to suggest infarct extension if levels rise again. This is usually
back to normal within 2-3 Days+
Creatine kinase is an enzyme responsible for transferring a
phosphate group from ATP to creatine. It is composed of M and/or
B subunits that form CK-MM, CKMB, and CK-BB isoenzymes. Total
CK (the activity of the MM, MB, and BB isoenzymes) is not
myocardial-specific. However, the MB isoenzyme (also called CK-
2) comprises about 40% of the CK activity in cardiac muscle and
2% or less of the activity in most muscle groups and other tissues.
In the proper clinical setting, MB is both a sensitive and specific
marker for myocardial infarction. MB usually becomes abnormal
three to four hours after an MI, peaks in 10-24 hours, and returns to
normal within 72 hours. However, an elevated serum MB may occur
in people with severe skeletal muscle damage (such as in muscular
dystrophy or a crush injury) and renal failure. In such cases, the CK
index (MB divided by total CK) is very helpful. If the index is under
4%, a nonmyocardial cause of a high MB should be suspected. CK-
MB is considered the benchmark for cardiac markers of myocardial
injury. Measurement of CK-MB may be performed via
electrophoresis or immunoassays; the latter demonstrates better
analytical sensitivity and better precision[17] .
12.Conclusion
Cholesterol has been singled out as the primary factor in the
development of atherosclerosis. HDL is regarded as one of the most
important protective factors against arteriosclerosis. HDL's
protective function has been attributed to its active participation in
the reverse transport of cholesterol. Numerous cohort studies and
clinical trials have confirmed the association between a low HDL
and an increased risk of coronary heart disease. The concentration
of LDL correlates positively whereas HDL correlates inversely to the
development of coronary heart disease. Smokers have significantly
higher serum cholesterol, triglyceride, and LDL levels, but HDL is
lower in smokers than in non-smokers. Evidence suggests that
oxidatively modified LDL contribute to the pathogenesis of
atherosclerosis. Increased oxidative stress and the generation of the
free oxygen radicals can result in modification of LDL to oxidized
LDL that could lead to atherosclerotic lesions. CK and more
particularly its isoenzyme CK-MB still have a formal place in
defining myocardial infarction. These enzymes normally exist in
cellular compartment and leak out into the plasma during
myocardial injury due to disintegration of contractile elements and
sarcoplasmic reticulum. Cardiovascular disease (CVD) is ranked as
the number one cause of mortality and is a major cause of morbidity
worldwide. Reducing high blood cholesterol, which is a risk factor
for CVD events, is an important goal of medical treatment. Available
for almost 2 decades, the 3-hydroxy-3-methylglutaryl coenzyme A
reductase inhibitors, or statins, have emerged at the forefront of
preventive drugs for cardiovascular disease because of a substantial
clinical trial database demonstrating that statins reduce the risk for
coronary artery disease morbidity and death across a broad range of
at-risk patient cohorts.
In the present administration of 10 mg of simvastatin was found
to be most effective in reducing the level of triglycerides.The
administration of statin did not contribute to a significant increase
in HDL levels.Simvastatin also considerably reduced the LDL level in
hyperlipidaemic patients.Apolipoprotein B level was considerably
reduced by the administration of simvastatin and Apolipoprotein A-
1 was reduced by intake of atrovastatin.
Atrovastatin also markedly reduced the level of CK and CK-MB
isoenzymes which are regarded as efficient markers of
cardiovascular diseases.Atrovastatin had a profound effect on the
liver function test markers where it lead to an increase in total
protein and albumin level and SGPT and SGOT was markedly
reduced.