Smoking
cigarettes has been proven to be deleterious to one’s health in numerous ways.
One harmful side effect of smoking is the increased risk of having a heart
attack. A recent paper published in the International Journal of Basic and
Applied Physiology sought to answer why chronic cigarette smokers have a
threefold higher risk of heart attacks than non-smokers. The researchers
discovered two key indicators of increased heart attack prevalence in smokers,
which were elevated levels of C-reactive protein and increased platelet
aggregability in smokers compared to non-smokers.
The
researchers determined that C-reactive protein (CRP) levels were a good predictor
of coronary artery disease, which is narrowing of the arteries. The levels CRP directly
correlate with inflammation, and levels are typically high after events like
surgery, injury, or infection. CRP is a protein that can easily be detected by
a routine blood analysis test. When macrophages secrete a specific signaling
molecule, CRP is produced in the liver and released into the blood. From there
its role is to function in an immune response by binding to damaged cells,
which promotes phagocytosis and apoptosis of the injured cells. Inflammation
and damaged epithelium in the bronchioles due to smoking increases the level of
CRP. 78% of smokers in the study had increased CRP levels in their blood
compared to just 8% of non-smokers.
In
addition, researchers found that smoking increases the ability for platelets in
the blood to aggregate. With increased platelet aggregability, there is a
greater chance for a thrombotic episode, which is a blood clot in an artery or
vein. Normally we want our platelets to function by aggregating and binding
fibrinogen and Von Willebrand factor to form a clot when bleeding occurs.
However, when this platelet aggregation pathway is improperly triggered, it can
result in potentially deadly blood clots like coronary thrombosis, a pulmonary
embolism, or deep vein thrombosis. While the researchers did not determine the
exact mechanism how chronic cigarette smoking leads to platelet aggregation,
they did find that smoking increased platelet aggregability 4 times as compared
to non-smokers.
Overall,
the study found that people who have smoked 5 or more cigarettes per day for 3
years, are three times more likely to have a heart attack than non-smokers. The
researchers concluded that this increased risk of heart attacks in smokers is
partially due to elevated CRP levels and increased ability for platelets to
aggregate and form clots.
Sources
http://ijbap.weebly.com/uploads/1/3/1/4/13145127/21final_ijbap_2013_-_copy_.pdf
http://www.nlm.nih.gov/medlineplus/ency/article/003356.htm
This is very interesting since some of my relatives smoke a lot. I wonder what the levels of the CRP protein would be in obese individuals since they also have a high incidence of coronary artery disease. I guess the study has been done: 10.1371/journal.pone.0036062. It showed a higher prevalence of the CRP protein in obese individuals. Is CRP just reactive within blood vessels or does it aggregate in other parts of the body? It would also be interesting to see if the same results from this study were found in women with the same exclusion/inclusion criteria.
ReplyDeleteHi Charlie, the research that I have looked through says that CRP is produced in the liver in response to inflammatory signals and released into the systemic blood circulation there. The only research that I have been able to find indicates that CRP and aggregation of CRP is found exclusively in arteries and veins, but the levels of CRP are associated with a variety of diseases and illnesses from schizophrenia to urological cancers.
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