Recently published guidelines de-emphasize use of coronary calcium to predict cvd risk. However, some studies underlying these recommendations show higher event rates for intermediate FRS and zero CACS than studies not considered in developing the guidelines. This may partly be due to Greenland using 6mm slices and, perhaps missing some calcium and wrongly assigning patients to the 0 CACS category. Conversely, the guidelines emphasize the more modest increase in risk with CACS above 300 compared to the highest FRS category. However, this could be seen as a straw man argument. What about CACS >1000? This is highly predictive of vastly increased CVD risk. Perhaps CACS screening on a one time or repeat basis should be routine.
CACS zero in asymptomatic low-to-intermediate risk patients is related to an extremely low rate of events of aproximately 0.10 % per year, and provides a safe 5-year window. On the other hand, CACS zero in symptomatic patients should lead to a cautious interpretation, particularly due to a number of factors.
To begin with, aproximately 30 % of acute coronary thromboses, particularly in young women and smokers, are attributed to plaque erosions, a type of plaque that has no lipid core or calcifications and is therefore so far undetectable to any invasive and non-invasive technique. Furthermore, spiculated calcifications sometimes cannot be detected by the 3 mm slices of CAC.
Regarding the longitudinal use of CAC, with the available evidence, I still think of CAC as a one-time screening tool. This belief is based on the paradox that although CAC progression leads to a significant increment in the risk of events, patients treated with statins (one of the most effective prevention strategies in selected populations) showed a null effect or even persistent CAC progression. This is probably driven by the effect of statins on plaque composition, towards a more stable phenotype.
dear Richard,
Traditional cardiovascular risk factors seem to play a significant role, with good discrimination and calibration, in the prediction of CAC progression in those at low 10-year CHD risk. Individual or combinations of novel markers (including CIMT and CRP) only minimally improved this prediction. efforts should aimed at identifying those at risk for disease development and progression should be focused on these well-known traditional risk factors, rather than the novel markers.
A positive CAC remains a very strong predictor of CVD events even in the low risk categories presented in the new guidelines.
The one time issue is tricky: the question might be what is a reasonable interval between CAC evaluations if the first study is negative: 5 years?10 years?
That is a good question Joseph. Accumulation of CACS at a rate greater than 15% per year implies a poor prognosis. Perhaps one test, then repeat in 3 years, than no more.
That way, you know the overall burden, and you know the rate of accumulation.
I am not sure about that. Given that the interscan variability of CAC averages a 10 %, the fact that very popular drugs such as statins and ACE inhibitors have a plaque stabilization effect (therefore incresing calcium score), and the physiological progressive calcification of lesions, I am quite certain that (unfortunately) there are many confounders and we have not reached a clear threshold,
Good point Gaston. At a minimum, CACS may lose its usefulness once the patient begins statin. However, a low score, of say 80, might be an indication for a repeat CACS at some point, rather than pharmacologic treatment.
Richard good question. observational data suggest that calcium scoring in certain populations has a better NRI (net reclassification index) than risk factor based models and. There are also data in JUPITER type trial patients that the benefit of statins are confined to patients with elevated calcium scores. If CT scanning had no deleterious effect of ionising radiation then it would seem attractive to use it as a screening tool at the age of 50 to guide statin treatment in patients with intermediate risk. There is evidence that statin treatment may increase calcium scores this might be because the plaques mature and stabilise and calcification is part of the natural history of coronary atherosclerosis. We know that risk models overstate CV risk and plenty of patients that have statins recommended do not need them. If you talk to individual patients and explain that a CT scan can tailor their individual risk rather than a population estimate many are happy to accept the exposure to ionising radiation on a one off basis to make a statin decision. CCTA gives information over and above CAC and in well prepared patients images can be obtained with an xray dose of 1-2mSv
These are all very helpful answers. It might be useful to add to Tom's answer that the x-ray dose described is not particularly high. Many women get a .4 mSv breast x ray every year, and no excess in non breast tumors has been demonstrated in those women.
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