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Amanda Jekowsky , American College of
Cardiology, 202-375-6645, ajekowsk@acc.org
March
23, 2009
Combination of Very Low LDL Cholesterol
and Normal Systolic Blood Pressure Attenuate Coronary Artery
Disease
Moderately good control of LDL-C and systolic
BP is not enough; optimal control of both is best to halt
or even reverse coronary plaque progression
New data published in the March 31, 2009, issue of the Journal
of the American College of Cardiology show that patients
with coronary artery disease (CAD) who achieve very low levels
of low-density lipoprotein (LDL) cholesterol along with normal
systolic blood pressure have the slowest progression of CAD.
The results suggest that patients with CAD should be treated
to the most stringent target levels so that they can achieve
optimal results from their lipid lowering and antihypertensive
therapies.
“This paper has a simple but important message regarding
dual targets for prevention of coronary artery disease,”
says Adnan K. Chhatriwalla, M.D., interventional cardiology
fellow at the Cleveland Clinic, Cleveland, Ohio, and lead
author of the study. “It is the first study to demonstrate
that normal blood pressure and very low LDL cholesterol in
combination are associated with attenuation of the progression
of coronary disease in humans. Even though patients may have
reasonable control of blood pressure and cholesterol, getting
them to optimal treatment goals is best in terms of slowing
plaque progression.”
Dr. Chhatriwalla and his colleagues studied changes in atheroma
burden as monitored by intravascular ultrasound (IVUS) in
3,437 patients with CAD. The patients were stratified based
on LDL cholesterol greater or less than 70 mg/dL and systolic
blood pressure greater or less than 120 mmHg. Four different
measures of plaque progression were studied: Percent atheroma
volume, total atheroma volume, percent of patients with significant
plaque progression, and percent of patients with significant
plaque regression.
For all of those variables, there was less progression of
disease in patients who achieved LDL-cholesterol = 70 mg/dL
and systolic blood pressure = 120 mmHg in combination.
“The finding that patients who were able to get their
LDL below 70 mg/dL and their systolic blood pressure below
120 mmHg had the slowest progression of heart disease supports
the growing concept that more than one risk factor is driving
the disease,” says Stephen J. Nicholls, assistant professor
of molecular medicine at the Cleveland Clinic, and co-author
of the study. “The thought really needs to be that the
greatest bang for your buck in terms of preventing heart disease
is going to be by trying to have aggressive control of all
the risk factors.”
Chhatriwalla et al. “provide an interesting commentary
on the need for more aggressive treatment guidelines for ‘pre-hypertension,’
i.e, blood pressure of 120 to 139/80 to 89 mm Hg in patients
with established coronary artery disease,” comment Jonathan
Tobis, M.D. and Alice Perlowski, M.D., from the David Geffen
School of Medicine at UCLA, Los Angeles, California, in an
accompanying editorial.
However, they caution that IVUS, although a robust clinical
and research tool, is subject to limitations. “Although
we may use plaque progression/regression on IVUS to deduce
that we are producing positive results for our patients, the
true determination of the impact of our therapy depends on
clinical and mortality end points, which can only be obtained
from large-scale randomized clinical trials.”
Dr. Chhatriwalla maintains his study sends an important message.
“This study suggests that when it comes to cholesterol
and blood pressure targets, ‘close’ is not good
enough. We need to stress that patients with the best risk
factor control have the best clinical results. This is the
take-home message.”
Dr. Chhatriwalla reports no conflict of interest. Dr. Nicholls
reports honoraria from Pfizer, AstraZeneca, Takeda, and Merck
Schering-Plough; consulting fees from AstraZeneca, Roche,
Merck Schering-Plough, Takeda, Pfizer, and Anthera Pharmaceuticals,
and research support from AstraZeneca and LipidSciences.
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reports of clinical studies published in the Journal of
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