Author + information
- Harvey S. Hecht, MD∗ ()
- ↵∗Icahn School of Medicine at Mount Sinai, Saint Luke’s Mount Sinai Medical Center, 1111 Amsterdam Avenue, New York, New York 10025
Dr. Conti’s letter is greatly appreciated because it so clearly illustrates the educational gap and misconceptions that have contributed to the slow acceptance of coronary artery calcium (CAC). His major concern is that “no risk score is useful clinically if there is no intervention that might alter the clinical outcome.”
Let us examine Dr. Conti’s 3 clinical scenarios:
1. “Early detection of coronary atherosclerosis by calcium…because there is nothing to treat.” In fact, this patient has atherosclerosis to treat, and, depending on the degree of CAC, will be at higher risk than implied by the absence of risk factors. In 542,008 patients presenting with a first myocardial infarction, 48.5% had ≤1 risk factor (1) and would not have qualified for statin treatment unless CAC had been detected, as is the case in 95% of acute events (1). If there is high risk by CAC, the patient will benefit from statin therapy irrespective of low-density lipoprotein.
2. “The patient is a 55-year-old asymptomatic man who has mildly elevated…but I think most cardiologists (including me) would be fairly aggressive…whether or not coronary artery calcium is present.” In reality, the extent of CAC determines whether the risk is increased, decreased, or remains the same. The outcome based net reclassification indexes of the Framingham Risk Score by CAC from 3 major trials (MESA , Heinz-Nixdorf , and Rotterdam ), ranged from 52% to 65.6% in the intermediate-risk group. The clinician’s ability to accurately assess risk in this group is worse than a flip of the coin, and CAC avoids the mistakes inherent in extrapolating risk classification from large population groups to the individual. Thus, high-risk CAC will mandate aggressive lipid treatment and 0 CAC may obviate the need for statin therapy because there are no data that statins can lower the risk below the 1.0% 10-year event rate of the 0 CAC group (1). Simply because most cardiologists would be fairly aggressive in this case does not mean that they are correct, assuming that treatment should be data driven.
3. “I have no idea whether there is calcium in my coronary arteries,…and if I did know, I am not sure what I would do about it…” That depends on the CAC results and what you are already doing. If you had extensive CAC, more aggressive lipid lowering than you may have already achieved would be appropriate if you believe lower low-density lipoprotein is better, assuming you are on a statin; if you are not, then you should be. If you were statin intolerant and had a 0 or low score, the statin could be stopped.
Thus, in an era of increasing concern over the benefit versus harm of any therapy, including statins, the use of CAC will routinely alter treatment by tailoring it to the patient’s accurately determined risk rather than guessing on the basis of inaccurate risk factor–based paradigms.
Please note: Dr. Hecht is a consultant for Philips Medical Systems and HeartFlow.
- American College of Cardiology Foundation