Author + information
- Hiroyoshi Mori, MD,
- Renu Virmani, MD and
- Aloke V. Finn, MD∗ ()
- ↵∗CVPath Institute Inc., 19 Firstfield Road, Gaithersburg, MD 20878
We read with interest the comment by Drs. Budoff and Tayek on our paper, “Coronary Artery Calcification and Its Progression: What Does It Really Mean?” (1). Drs. Budoff and Tayek are concerned about our lack of citation of studies pertaining to coronary artery calcium (CAC) progression and subsequent cardiovascular events. References 2 and 3 in our paper highlight the role of CAC detection and risk of future events on a population basis. We certainly acknowledge that there are copious data showing an important association between CAC progression and subsequent cardiac events, as referenced by Dr. Budoff and colleagues. Although CAC and its progression can predict generic risk of cardiovascular events, it cannot yet be used prospectively to identify a culprit lesion. Moreover, our review is meant to highlight the complexities of this subject while demonstrating the discrepancy between what is known pathologically and how CAC is currently used in the clinic. Reference 3 in our paper highlights this by showing that whereas CAC volume is positively associated with cardiovascular disease events, at any levels of CAC volume CAC density is inversely and significantly associated with cardiovascular disease events (2). We demonstrate through pathology that patterns of calcification such as sheet calcification correlate more with plaque stability, whereas microcalcification and fragmented calcification correlate with thin cap fibroatheroma and plaque rupture. From a pathological point of view, just looking at CAC score (Agatston score) is not enough to understand fully the complex relationship between vascular calcification and plaque stability or instability. Although it is very practical clinically, it fails to tell when the event will take place or which lesion will cause an event. Based on our current pathological understanding of the subject, we believe the presence of calcium (small, fragmented, spotty) is a better predictor of unstable plaque; however, heavy calcium (diffuse, fibrocalcific plaques, sheet of calcium) is a better predictor of stable plaque. If this type of analysis were to be added to current CAC scoring, perhaps on the basis of higher-resolution computed tomography imaging than is currently available, it could allow us to distinguish better which specific patients are at risk of future events. Identification of patients harboring high-risk plaques may allow for more intensive medical therapy, lowering their risk of future events.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation