We thank Dr. Friedlander for his letter regarding our systematic review of calcified carotid artery atheromas (CCAA) and stroke, and also for introducing his latest retrospective cohort study1 on the prediction of adverse vascular events based on CCAA seen on panoramic radiographs.
Our study2 showed that the literature lacked the evidence to demonstrate a strong association between the presence of CCAA on a panoramic radiograph and the increase in stroke compared with a control population without CCAA. Dr. Friedlander claims that this study addressed many of our objections, but we do not agree.
The Friedlander and Cohen study retrospectively reviewed charts for CCAA and risk-matched a control group for follow-up on the incidence of "adverse, nonfatal vascular events." Our study evaluated stroke, not vascular events, as the endpoint.
Drs. Friedlander and Cohen have blurred the definition of stroke by including vascular events. The risk stratification of coronary vessels is very different from that of carotid vessels. They should be separated from one another, as the predisposition of the vessels to the formation of plaques varies significantly based on the lumen width, flow and other associated factors.
Even though the putative results of their subanalysis for stroke/cardiovascular accident (Table 2 of their study) supports our conclusion, we are not convinced of the reliability of their results. Our doubt arises from the inappropriate and inadequate control group used in their study, which consisted of patients with no panoramic radiographs. Hence, the CCAA status in the control group was unknown. This significant methodological error nullifies their results and undermines any conclusions or recommendations based upon the results. This one flaw overshadows any remaining concerns we have with their study.
Although Drs. Friedlander and Cohen’s study was published after we conducted our literature search, even if we had been aware of this study, it would not have met the criteria used in our systematic review.
Recently, studies have focused on determining independent risk factors for stroke and transient ischemic attacks (TIA). A good example is the Framingham study by Salaycik and colleagues.3 They demonstrated that depression is an independent and powerful risk factor for the incidence of stroke or TIA in individuals who are younger than 65 years. Their controls and study groups were followed for up to eight years prospectively. We are in dire need of such studies in order to reach a conclusion regarding the status of the CCAA.
It is essential in this age of evidence-based medicine to review the current literature on this topic. There is mounting evidence in the literature regarding the role of calcium within the atheromas with regard to the vulnerability of the plaques. We discussed this in our JADA article and, since then, more studies have appeared in the medical literature. It has been shown that, in general, calcification appears to be a marker of stability within the atheromas,4 and the degree of carotid calcification does not independently predict the future stroke risk.5
As clinicians, we must be able to critically examine the current literature to provide the best advice to our patients. At this point, the association of radiographically detectable CCAA with the incidence of stroke remains incomplete and inconclusive.
TOP
REFERENCES
