Neutralizing the Adverse Prognosis of Coronary Artery Calcium Salman K. Bhatti, MD; James J. DiNicolantonio, PharmD; Becky K. Captain, APN; Carl J. Lavie, MD; Ales Tomek, MD; and James H. O’Keefe, MD Abstract Objectives: To report and compare the outcomes and survival of patients with abnormal computed tomographyederived coronary artery calcium (CT-CAC) scores undergoing aggressive medical treatment at a cardiac prevention clinic. Patients and Methods: We conducted a retrospective analysis of 849 patients with intermediate risk based on the Framingham risk score and an abnormal CT-CAC score who were aggressively treated in a preventive cardiology risk factor modification program from June 23, 2000, to September 1, 2012. The primary outcome was a composite end point of myocardial infarction, resuscitated cardiac arrest, revas- cularization, and cardiovascular death. The effect of the CT-CAC subgroup on major adverse coronary heart disease events (MACEs) was evaluated by calculating hazard ratios with Cox proportional hazards regression modeling. The Centers for Disease Control and Prevention Wonder database was used to identify age- and sex-matched controls from the general population of Kansas and Missouri. Results: The mean age of the study patients was 65.4 years (58.4% men [496]). The median follow-up was 58 months, and the mean CT-CAC score was 336 Agatston units. Thirty-four patients (4.0%) reached the primary end point, including 4 deaths. The adjusted 10-year mortality rates were similar in the study group and control group (9.3 vs 10.6; P¼.80). After adjustment, a CT-CAC score greater than 400 Agatston units correlated with a higher risk of MACEs (hazard ratio, 3.55; P¼.01). Conclusion: These results suggest that intermediate-risk patients with abnormal CT-CAC scores when treated with intensive risk factor reduction have lower rates of MACEs than predicted by the Framingham risk score and the presence of coronary artery calcium. ª 2013 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2013;88(8):806-812 T he age-adjusted mortality rate for coro- nary heart disease (CHD) has decreased steadily during the past 4 decades in the United States. 1 Factors that contribute to this decrease include improved treatment mo- dalities and better screening for and treatment of CHD risk factors. Still, currently one Amer- ican dies of CHD every minute, 2 and traditional risk factors predict CHD events only moder- ately well. Thus, efforts to explore other meth- ods to identify patients who would benefit most from intensive CHD prevention efforts have gained momentum. A considerable pro- portion of patients classified as intermediate risk using standard risk prediction models can be reclassified into higher- or lower-risk categories using newer risk markers. Multiple studies have consistently reported that the computed tomographyederived coronary ar- tery calcium (CT-CAC) score is a strong and independent predictor of incident CHD and provides predictive information beyond that provided by standard risk prediction models. 3,4 Results from recent studies have, in fact, indi- cated that among all the different CHD risk markers, including the Framingham risk score (FRS) and novel cardiac risk markers, CT- CAC score is superior for CHD risk prediction and risk reclassification. 5,6 A considerable pro- portion of patients categorized as intermediate risk by FRS have high CT-CAC scores, putting them at increased risk of having CHD events and underscoring the need for aggressive man- agement of their risk factors. Disappointingly, risk factor modification does not lower CT- CAC scores, which generally increase with age, particularly in individuals who remain un- treated. Thus, many patients are discouraged af- ter learning that a high CT-CAC score places them at considerably increased risk of future CHD events and that coronary artery calcifica- tion is irreversible. This knowledge may also From the Saint Luke’s Mid America Heart Institute (S.K.B., J.J.D., B.K.C., J.H.O.) and the Department of In- ternal Medicine, University of MissourieKansas City School of Medicine (S.K.B., J.H.O.), Kansas City; John Ochsner Heart and Vascular Institute, Ochsner Clinical SchooleThe University of Queensland School of Medicine, New Orleans, LA (C.J.L.); Depart- ment of Preventive Medicine, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge (C.J.L.); and Department of Neurology, Second Faculty of Medicine, Charles University, Prague, and University Hospital, Motol, Czech Republic (A.T.). 806 Mayo Clin Proc. n August 2013;88(8):806-812 n http://dx.doi.org/10.1016/j.mayocp.2013.05.019 www.mayoclinicproceedings.org n ª 2013 Mayo Foundation for Medical Education and Research ORIGINAL ARTICLE