Coronary artery calcification: More than meets the eye

Excerpt

As the clinical world moves closer toward personalized medicine, we learn once again that the devil is in the details. If we take a one-fits-all perspective, we can perhaps miss nuances that can explain why all the pieces of the puzzle do not fit perfectly for every patient. In this issue of the journal, Hsu et al1 use computed tomographic (CT) and ¹⁸F-NaF positron emission tomographic (PET) imaging to unravel the mystery of why athletes have a high burden of coronary artery calcium (CAC), a strong predictor of cardiovascular morbidity and mortality, but have better survival than more sedentary persons. In their study, they found that “active” Apolipoprotein E deficient mice (Apo E^−/−) have similar burdens of aortic CAC on microCT after 9 weeks of consuming a Western diet despite varying levels of activity, suggesting that exercise training did not alter plaque structure and may not modify risk. Taking their analysis a step further, however, they used ¹⁸F-NaF PET imaging to examine the micro-architecture of the calcified plaque of “active” compared to “sedentary” mice. Interestingly, the mice randomized to exercise had a lower ¹⁸F-NaF signal density, defined as ¹⁸F uptake normalized to injected dose per deposit volume, and each individual calcium deposit in the aorta had decreased mineral surface area index, calculated as the perimeter divided by the cross-sectional area by histology. Taken together, these findings suggest that exercise reduces the amount of exposed surface area per unit bone volume, a measure that has been associated with plaque vulnerability. Based on the findings of Hsu et al1¹⁸F-NaF PET imaging may be a promising technology to better risk stratify patients and serially monitor the effectiveness of lifestyle modifications, such as exercise, or new pharmacological therapy designed to stabilize plaque. …