Letter by Schmermund and Erbel Regarding Article, “Coronary Artery Calcium: Should We Rely on This Surrogate Marker?”
To the Editor:
We read with interest the editorial by Dr Redberg1 published with our article on the progression of coronary artery calcification (CAC) in patients treated with 10 or 80 mg atorvastatin.2 We respectfully disagree, however, with Dr Redberg’s suggestion that “as of now, the weight of the evidence suggests that CAC scores are not reliable predictors of cardiac events” (p 337). A number of lines of evidence support a link between CAC and cardiovascular events. First, CAC closely relates to extent of coronary atherosclerosis, which is a well-established predictor of cardiovascular risk.3 The association between CAC and the extent of atherosclerosis holds true whether severity is expressed as maximum stenosis severity, number of significant stenoses, or number of significant and nonsignificant stenoses (<50%) in the coronary tree. Second, recent studies in unselected populations with no suggestion of selection bias consistently report that CAC quantification adds prognostic information over and above cardiovascular risk factors assessed with up-to-date methodology.4,5 Finally, emerging data suggest that an increased rate of CAC progression is associated with a significantly increased rate of cardiovascular hard events.4
We need to differentiate between (1) the well-documented ability of CAC scanning to identify high-risk patients, and (2) the question of whether serial CAC scanning is a good tool for tracking the progression of coronary atherosclerosis over 12 months to document the effects of a specific therapy. The “negative” finding in our study2 needs to be interpreted with the knowledge that in both randomized treatment groups, effective lipid-lowering therapy was given. Intensive statin therapy can reduce cardiovascular events (vascular risk). The process of vascular calcification (vascular aging) is, however, not attenuated. The mineralization process may be influenced in a different manner than the overall activity of atherosclerotic disease once appropriate treatment has been initiated. We believe the current findings should stimulate further research into the mechanisms of CAC progression and into new treatment opportunities to stop or attenuate this process. Clearly, with the advent and widespread use of multidetector computed tomography scanners, such research will be increasingly important.6 Fortunately, large epidemiological studies are underway in the United States (the Multi-Ethnic Study of Atherosclerosis) and Germany (the Heinz Nixdorf Recall Study) that will provide important data in this respect.
Sources of Funding
Drs Erbel and Schmermund have received research grants or other research support from Pfizer Germany.
Drs Erbel and Schmermund have received speakers’ honoraria from Pfizer Germany.
Redberg RF. Coronary artery calcium: should we rely on this surrogate marker? Circulation. 2006; 113: 427–437.
Schmermund A, Achenbach S, Budde T, Buziashvili Y, Forster A, Friedrich G, Henein M, Kerkhoff G, Knollmann F, Kukharchuk V, Lahiri A, Leischik R, Moshage W, Schartl M, Siffert W, Steinhagen-Thiessen E, Sinitsyn V, Vogt A, Wiedeking B, Erbel R. Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter, randomized, double-blind trial. Circulation. 2006; 113: 336–337.
Vliegenthart R, Oudkerk M, Hofman A, Oei HH, van Dijck W, van Rooij FJ, Witteman JC. Coronary calcification improves cardiovascular risk prediction in the elderly. Circulation. 2005; 112: 572–577.