Atherosclerosis is a condition often associated with age
that involves a narrowing of the lumen of the arteries usually associated with
age (see image below). This condition
often leads to coronary heart disease.
Traditionally there are a number of risk factors that are generally associated
with this syndrome – high blood pressure (hypertension), high cholesterol, heredity,
life style, diet etc. However, a
significant percentage of those individuals that show evidence of
atherosclerosis have no known risk factors.
Research done by Dr. Siddhartha Jaiswal and his colleagues that has been
published in the New England Journal of Medicine (July, 2017) sheds significant
light on the possible etiology of this perplexing reality.
Within the bone marrow, reside stem cells that are so-called,
pluripotent cells; they are responsible for the production of the body’s
complement of immune-competent cells such as red blood cells, white blood cells
including lymphocytes, neutrophils etc.
It has been well documented that over the lifetime of the individual these
stem cell undergo mutations that can lead to blood – hematopoietic – cancers such
as leukemia.
According to Jaiswal, “Clonal hematopoiesis of indeterminate
potential (CHIP), which is defined as the presence of an expanded somatic
blood-cell clone in persons without other hematologic abnormalities, is common
among older persons and is associated with an increased risk of hematologic
cancer.”
Jaiswal and his associates now have evidence that CHIP may
be the underlying cause of atherosclerotic cardiovascular disease of no known
etiology. The results of their studies
indicate that the presence of CHIP in the cell population of circulating blood was
associated with a near doubling of the incidence of atherosclerotic
cardiovascular disease. Furthermore, the
common mutations that were present in CHIP were found to be in the genes
DNMT3A, TET2 AND ASXL1. These genetic
mutations have also been shown to be associated myelodysplastic syndrome (MDS)
and acute myeloid leukemia (AML). These
clones seem to be more prevalent with age – more that 10% of persons older than
70 years carry such a mutation.
This finding is significant in that it shed further light
upon the etiology of atherosclerosis.
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