Abstract & Commentary
Synopsis: Cerivastatin therapy resulted in decreased progression of coronary calcifications.
Source: Achenbach S, et al. Circulation. 2002;106:1077-1081.
Several studies have clearly demonstrated that the quantity of coronary artery calcification measured by electronic beam computed tomography (EBCT) normally increases at a variable rate over time1-6 reaching as high as 24% annually.2 Retrospective analyses have revealed that lipid-lowering therapy slows the rate of coronary artery calcium deposition3,4 but thus far, no prospective investigation that demonstrates the effects of lipid-lowering drug treatment on the rate of progression or regression of coronary calcification has been published.
Achenbach and colleagues conducted a cohort study that prospectively compared the rate of change in the amount of coronary calcification before and after lipid-lowering therapy with the cholesterol synthesis enzyme inhibitor cerivastatin. EBCT studies were performed in 66 patients before treatment with cerivastatin and repeated 14 months later after which treatment with cerivastatin (0.3 mg/d) was initiated. A third EBCT study was completed 12 months after treatment initiation and all coronary calcifications were quantified using a volumetric score. Cerivastatin therapy lowered the mean LDL cholesterol level from 164 mg/dL to 107 mg/dL. The median annual relative increase in coronary calcium score was 25% during the untreated period vs. 8.8% 1 year after the lipid-lowering therapy was administered. Equally important, in 32 patients who demonstrated LDL cholesterol levels < 100 mg/dL during drug treatment, the median relative increase in the coronary calcium score was 27% during the control period vs. -3.4% during the treatment period.
Comment by Harold L. Karpman, MD, FACC, FACP
The measurement of coronary artery calcification with EBCT is rapidly earning respect as a powerful early marker of the atherosclerotic burden in the coronary arteries. Although there has been some variability previously reported in coronary calcification scores obtained by EBCT studies, Achenbach et al attempted to control interscan variability by using a standard ECG triggering mechanism and by measuring progression over 2 consecutive time periods in the same individual rather than comparing 2 simultaneous groups over the same time period. Although there were no significant changes in objective measurements (ie, body weight) in the subjects, one must recognize that some of the patients may have modified their lifestyle after being made aware of an abnormality in their coronary artery calcium score early in the study. Of note is the interesting fact that regression of the coronary calcium score was observed in only 7 patients during the control period compared with 24 patients who were receiving the lipid-lowering therapy.
Although this prospective study has many limitations (ie, lack of medication control, interscan variability, etc), it would appear that quantification of coronary artery calcification by EBCT or ultrafast CT will prove to be a promising tool for the assessment of coronary artery calcification progression and/or regression. How this translates into prediction of outcomes or in the evaluation of changes in the coronary atherosclerotic plaque burden and composition remains to be determined. Although many physicians are disturbed by the intense commercialization of CT and coronary artery calcification scoring, it would appear to be important to remember that one should be cautious about throwing out the baby with the bathwater—properly used, the value of these techniques in contemporary clinical practice may prove to be invaluable. For the time being, even though there are many limitations to the Achenbach study, there seems to be little question that lipid-lowering agents may have significant value in diminishing the progression or even possibly contributing to the regression of the coronary atherosclerotic burden.
Dr. Karpman, Clinical Professor of Medicine, UCLA School of Medicine, is Associate Editor of Internal Medicine Alert.
References
1. Shemesh J, et al. Radiology. 2000;217:461-465.
2. Maher JE, et al. Mayo Clinic Proc. 1999;74:337-355.
3. Callister TQ, et al. N Engl J Med. 1998;339:1972-1978.
4. Budoff MJ, et al. Am J Cardiol. 2000;86:8-11.
5. Schmermund A, et al. Arterioscler Thromb Vasc Biol. 2001;21:421-426.
6. Sutton-Tyrrell K, et al. Am J Cardiol. 2001;87:560-564.
7. Bielak L, et al. Radiology. 2001;218:224-229.
Readers are Invited. . .
Readers are invited to submit questions or comments on material seen in or relevant to Internal Medicine Alert. Send your questions to: Robert Kimball, Internal Medicine Alert, c/o American Health Consultants, P.O. Box 740059, Atlanta, GA 30374. For subscription information, you can reach the editors and customer service personnel for Internal Medicine Alert via the internet by sending e-mail to [email protected].
This cohort study prospectively compared the rate of change in the amount of coronary calcification before and after lipid-lowering therapy with the cholesterol synthesis enzyme inhibitor cerivastatin.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content