CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 2, March/April 2010
AFRICA
107
contains response elements for inflammatory factors such as
IL-6.
63
Ramharack
et al
. reported that Lp(a) and apo(a) mRNA
levels in primary monkey hepatocyte culture were responsive to
cytokines.
64
During inflammation, the lipid changes that are observed are
not only quantitative but also qualitative, with changes in the
composition of lipoproteins. Therefore, the proportion of triglyc-
erides, phospholipids and cholesterol is increased in VLDL, IDL
and LDL particles, whereas the proportion of cholesterol and
triglycerides decreases in HDL particles.
65
TNF-
α
administration
in rodents led to an increase in HMG CoA reductase mRNA
levels.
66
In addition to the changes in LDL-C levels observed,
a change in LDL size and susceptibility to oxidation of these
particles was also observed.
TNF-
α
levels in humans correlated negatively with particle
peak size.
67
Infection and inflammation was associated not only
with a decrease in HDL cholesterol levels but also with a change
in the composition. HDLs that circulated during infection and
inflammation were depleted in cholesterol esters but enriched
in free cholesterol, triglyceride and sphingolipids.
68
In addition,
HDL-associated Apo-AI1 and paraoxonase, lecithin:cholesterol
acyl transferase (LCAT), cholesterol ester transport protein
(CETP), hepatic lipase (HL), and phospholipid transfer protein
(PLTP) levels decreased but Apo-B and serum amyloid A levels
increased.
69,70
Because of these changes in HDL metabolism, it
is postulated that the main function of HDL, namely its role in
protecting LDL against oxidation and reverse cholesterol trans-
port, may be decreased in APR.
The present study highlights significantly higher levels of
inflammatory mediators such as CRP and TNF-
α
in the North
Indian male patients with acute myocardial infarction, compared
with control subjects, and a highly significant positive correla-
tion between Lp(a) and TNF-
α
levels in male patients in the
atherosclerosis-prone Indian population, clearly pointing to a
role in the interplay of inflammation and dyslipidaemia in the
pathogenesis of CAD in the atherosclerosis-prone North Indian
population.
The strength of this work lies in the fact that the CAD-prone
North Indian population constituted the study population and
there was a large sample size involved. However, the present
study has a few limitations, which include the lack of follow-up
data due to patients’ incompliance and administrative constraints,
which could have provided precious information about the role of
these mediators as markers for risk stratification and prognosis.
Accumulating data indicate that information gained from the
link between inflammation, dyslipidaemia and atherosclerosis
can yield predictive and prognostic information of considerable
clinical utility. New insights into the interplay between dysli-
pidaemia and inflammation in atherosclerosis may aid in iden-
tifying innovative therapeutic strategies to improve outcomes
of individuals at risk for or affected by this scourge growing
worldwide. We therefore stand on the threshold of clinical appli-
cation of the interplay between dyslipidaemia and inflammation
in atherosclerosis, which could fundamentally alter the way in
which we practice preventive medicine, and prove immeasurably
beneficial to the public as well.
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