It seems there's a reason other than the obvious lack
of alliteration that LDL-cholesterol never made it into
the folk saying, "Close only counts in horseshoes and
hand grenades." In a large cohort study of post myocardial
infarction (MI) patients with hypercholesterolemia, "only
optimal treatment reduced the rate of death or myocardial
infarction," claims Dr Heribert Schunkert, Director of
the Medizinische Klinik II at the University of Luebeck,
Germany, referring to the results of the study he and
his colleagues from the University of Regensburg and the
Medical College of Wisconsin published in the May 25 issue
of International Journal of Cardiology. "Patients
treated "suboptimally," ... who received statins but displayed
LDL levels > 3.0mmol/L, had the same event rate as
untreated subjects," cautions Dr Schunkert.
The researchers used a German family
registry to enroll 2,045 patients under 60 years of
age who had had an MI between six months and five years
prior to entry, had remained event-free during this
interval and showed no cardiac specific symptoms for
more than six months after. All of these individuals
should have received a statin according to current guidelines.
However, in this population-based setting only 1,396
had been treated with statins since their MI, while
649 had never received any statin treatment. To effectively
compare doses of the various statins used, a 10mg dosage
of atorvastatin was defined as an LDL lowering equivalent
dose of 1.00 and all other statin equivalent doses were
approximated according to the relative LDL lowering
effects obtained in the 1998 comparative dose efficacy
study of atorvastatin versus simvastatin, pravastatin,
lovastatin, and fluvastatin in patients with hypercholesterolemia
(CURVES).
100
OR BUST
Despite using the conservative LDL target of 3.0mmol/L
for optimal treatment recommended by the Joint European
Societies on Coronary Prevention, the researchers found
only 16.1% of the study subjects met this goal —
and less than 3% achieved the more stringent 2.6mmol/L
target used by the American Heart Association and the
National Cholesterol Education Program.
After completing a comprehensive
health questionnaire, physical exam and serum lipid
analysis, the patients were followed for 30 months by
telephone interview, with more than 95% completing the
epidemiological survey. The 173 MI patients who developed
a cardiac event (nonfatal myocardial infarction, coronary
death or coronary artery bypass) were compared to 346
matched controls (MI patients who had no cardiac complications).
SUBOPTIMAL
PROTECTION
Failure to control LDL levels turned out to be very
costly. Suboptimally treated patients had a two-fold
greater relative risk of future non-fatal MI and coronary
death while untreated patients had a three-fold greater
risk.
But monitoring LDL-C levels is
only one part of the clinical picture, according to
Dr Paul Ridker and other members of the pravastatin
or atorvastatin evaluation and infection trial (PROVE-IT)
and thrombolysis in MI (TIMI)-22 trial undertaken at
the Department of Medicine, Brigham and Women's Hospital
in Boston. Initial PROVE-IT/TIMI results showed that
acute coronary syndrome patients with lower C-reactive
protein (CRP) levels after statin therapy have better
clinical outcomes than those with higher CRP levels
— regardless of LDL-C level.
CRP,
THE NEW LDL?
In more recent data, patients who achieved both an LDL-C
level < 1.8mmol/L and CRP level < 2mg/dl had a
28% lower risk of recurring MI or vascular death. According
to the latest PROVE-IT/TIMI results, achieving LDL and
CRP control is more important than the specific choice
of therapy. These results are published in the May 17
issue of the Journal of the American College of Cardiology.
"Best clinical care following statin
therapy may require measuring and monitoring CRP in
the same way that we currently measure and monitor LDL
cholesterol," contends Dr Ridker. "These data strongly
support the fact that both cholesterol and inflammation
are important in cardiovascular disease and that the
statin drugs are 'two-for-one' agents in that they both
lower cholesterol and CRP."
For more on statins see "Fibrates
raise HDL-C if levels plummet in response to statins"
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