January 12, 2005
Boston, MA- Statins
lower the low-density lipoprotein (LDL) cholesterol and
C-reactive protein (CRP). In a study published by Paul Ridker,
M.D., et al, in the January 6, 2005 issue of The New England
Journal of Medicine in Boston, the relationship between the LDL
cholesterol and CRP levels achieved after treatment with 80 mg
of atorvastatin or 40 mg of pravastatin was evaluated. Their
data indicated that among patients with acute coronary
syndromes, who are treated with a statin, achieving a target
level of CRP of less than 2 mg per liter is associated with a
significant improvement in event-free survival.
In a study population derived from the Pravastatin or
Atorvastatin Evaluation and Infection Therapy-Thrombolysis in
Myocardial Infarction 22 (PROVE IT-TIMI 22) study, plasma
samples of LDL and CRP were obtained as part of protocol. The
relationship between LDL and CRP levels achieved after treatment
with 80 mg of atorvastatin or 40 mg of pravastatin per day and
the risk of recurrent myocardial infarction or death from
coronary causes among 3,745 patients with acute coronary
syndromes was evaluated.
There was a linear relationship between the levels of LDL
cholesterol achieved after statin therapy and the risk of
recurrent myocardial infarction or death from coronary causes.
Patients in whom statin therapy resulted in LDL cholesterol
levels of less than 70 mg per deciliter had lower event rates
than those with higher levels (2.7 vs. 4.0 events per 100
person-years, P=0.008). An identical difference was observed
between those who had CRP levels of less than 2 mg per liter
after statin therapy and those who had higher levels (2.8 vs.
3.9 events per 100 person-years, P=0.006). This effect was
present at all LDL levels.
Evaluation of the effectiveness of the two statins was also
obtained. With regard to CRP, the median levels were similar in
the atorvastatin and pravastatin groups at randomization (12.2
and 11.9 mg per liter, respectively; P=0.60). They were
significantly lower in the atorvastatin group than in the
pravastatin group at 30 days (1.6 vs. 2.3 mg per liter, P<0.001)
and at the end of the study (1.3 vs. 2.1 mg per liter, P<0.001).
Despite the greater ability of atorvastatin than pravastatin to
reduce LDL and CRP levels, there was little evidence that either
agent led to better clinical outcomes.
suggest clinical relevance for several reasons. First of all,
strategies that aggressively lower cardiovascular risk by means
of statin therapy should monitor inflammation as well as
cholesterol. Next, the change in CRP and LDL levels were
independent predictors of plaque regression after statin
therapy. Thirdly, reducing inflammation, and thus the level of
CRP, may alter the atherothrombotic process.
In summary, this study demonstrates that the use of statin
therapy to achieve target levels of both LDL cholesterol and CRP
decreases the risk of recurrent myocardial infarction or death
from coronary causes in patients with acute coronary syndromes.
Thus, therapies designed to reduce inflammation may improve
Co-authors: Christopher P. Cannon, M.D., David Morrow, M.D.,
Nader Rifai, Ph.D., Lynda M.Rose, M.S., Carolyn H. McCabe, B.S.,
Marc Pfeffer, M.D., Ph.D, and Eugene Braunwald, M.D.