Coronary Atherosclerosis

Corresponding Author

We agree that, as a group, those with CACþ are at higher risk of an ASCVD event than those with CAC 0.
But CAC is a late manifestation of plaque evolution.
Accordingly, the difference is between the risk of a group, all of whom have the disease and, therefore, all of whom may suffer the consequences of the disease and another group, only some of whom have the disease, and only these can suffer the consequences of the disease.We also agree that risk is an imperfect tool to identify those who could benefit from statin therapy to reduce ASCVD risk. 2 However, when risk is sufficiently high as it was in this cohort-an average of 14.7%-statin therapy is undoubtedly cost-effective and indicated.It is clear from such clinical trials as the PROSPER (Prospective Study of Pravastatin in the Elderly at Risk) study 3 and the HPS (Heart Protection Study) 4 as well as meta-analyses 5,6 that statin therapy reduces ASCVD events in patients 65 years of age and older in both the primary and secondary prevention settings.Given that age is the most significant driver of ASCVD risk, coronary imaging in most cases is not necessary to identify individuals likely to benefit from lipid-lowering therapy.
In our view, the most striking finding in this report was that just under half of all subjects who were CAC 0 at baseline became CACþ after less than an average of 3.5 years of follow up.This is an extraordinary conversion rate in a short period of time.That the incidence of CACþ rises sharply with age has been known for some time.However, these subjects were on average 70.3 years of age at baseline and, therefore, represent the group who had remained the  10 This will also require further study.As these authors have shown us, it is time to focus on the wall of arteries, not just on the concentration of atherogenic agents within the lumen of arteries.We have only begun to understand the complex relations between the causes of atherosclerosis and their complications within the arterial wall as affected by the passage of time.
Toth and Sniderman

FUNDING SUPPORT AND AUTHOR DISCLOSURES
Dr Toth has served on the Speakers Bureau for Amgen; and has been a consultant to Novartis.Dr Sniderman has reported that he has no relationships relevant to the contents of this paper to disclose.
demonstrate that almost half of 815 individuals enrolled in the MESA (Multi-Ethnic Study of Atherosclerosis) (average age 70.2 years initially) became positive for coronary artery calcification (CACþ) with a median time to conversion of 4.3 years.The main emphasis in their analysis was on which "nontraditional risk factors" were predictors of this conversion.Although albuminuria, carotid artery plaque, and thoracic aortic calcification did not improve discrimination of incident CAC when added to traditional risk factors, individually they were significant predictors.By contrast, apolipoprotein B (apoB), lipoprotein(a), high-sensitivity troponin T, and N-terminal probrain natriuretic peptide were not significant predictors, even individually.Thus, evidence of noncoronary atherosclerosis and nephropathy help to identify older asymptomatic patients who might benefit from CAC screening.The authors cite data demonstrating atherosclerotic cardiovascular disease (ASCVD) risk is higher in CACþ vs CAC 0 individuals and suggest these positive markers are useful in identifying those at high risk for conversion and, therefore, constitute a subgroup who should receive intensive preventive therapy.We congratulate them on an analysis that has been carefully considered and meticulously done.Although we differ significantly in the conclusions we draw, we acknowledge that different interpretations of the same data are reasonable.Where you wind up often depends on where you are coming from.
atherosclerotic disease with age, is due to the interplay of cause and consequence over time.
8SSN 2772-963X https://doi.org/10.1016/j.jacadv.2023.100756*Editorialspublished in JACC: Advances reflect the views of the authors and do not necessarily represent the views of JACC: Advances or the American College of Cardiology.From the a Department of Preventive Cardiology, CGH Medical Center, Sterling, Illinois, USA; b Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; and the c Department of Medicine, Mike and Valeria Rosenbloom Centre for Cardiovascular Prevention, McGill University Health Centre, Montreal, Quebec, Canada.The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors' institutions and Food and Drug Administration guidelines, including patient consent where appropriate.For more information, visit the Author Center.apoBlipoproteinswithinplasma is the primary, but not exclusive, determinant of the number of apoB particles that will be trapped over time.8Calcification is a histologic hallmark of advanced atherosclerotic disease.Thus, apoB causes atherosclerosis and CAC is a consequence of atherosclerosis.The declining HR of apoB with age, notwithstanding the ever increasing incidence of