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(Circulation. 1999;99:3215-3217.)
© 1999 American Heart Association, Inc.
Editorial |
From the Cardiology Division, Departments of Medicine, San Francisco General Hospital and the University of California, San Francisco.
Correspondence to David Waters, MD, Cardiology Division, Room 5G1, San Francisco General Hospital, 1001 Potrero Ave, San Francisco, CA 94110. E-mail dwaters@medsfgh.ucsf.edu
Key Words: Editorials cholesterol
Some of the treatments we use in cardiology must be applied urgently, such as cardiopulmonary resuscitation or thrombolytic therapy for myocardial infarction. The urgency is driven by pathophysiological imperatives, such as the need to prevent cerebral anoxia or to limit the extent of myocardial necrosis. Most other therapies can be instituted in a more leisurely way. Cholesterol lowering is often the last thing that we do, the treatment that we are slowest to initiate.
One of the reasons is that cholesterol levels are depressed for several weeks after the onset of an acute coronary event,1 and some of us wait to obtain measurements. Some of us withhold drug therapy in coronary patients to see whether diet alone will be effective, even though most coronary patients will not meet the LDL cholesterol goal of 100 mg/dL with diet alone.2 Also, we have understood that cholesterol lowering appears to reduce coronary events only after a delay. The outcome curves of the secondary prevention trials do not separate appreciably until 1 to 2 years after initiation of treatment.
Several pieces of accumulating evidence, including the article by
Dupuis et al3 in this issue of Circulation,
indicate that we may have to reassess our approach. These investigators
have demonstrated in patients with unstable angina that
cholesterol lowering with pravastatin improved
endothelial function within 6 weeks. If
cholesterol lowering has relatively immediate consequences
that may favorably affect coronary events, the benefits of
cholesterol lowering could be extended to acute
coronary conditions, and the speed
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