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CAC scoring, biomarkers may help CVD risk prediction
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BOSTON — Coronary artery calcium scoring and biomarker assessment appear to improve prediction of CVD risk, according to two presentations at the Cardiometabolic Health Congress.
When added to traditional risk factors, CAC scoring and biomarker analysis improve individualization of risk prediction and can be part of an integrated management plan, the experts said.
Virtues of imaging
Matthew J. Budoff, MD, FACC, FAHA, endowed chair of preventive cardiology, professor of medicine and director of cardiac CT at Harbor-UCLA Medical Center, said the 2013 American College of Cardiology/American Heart Association cholesterol guidelines call for considering CAC scoring if traditional risk assessment shows a patient to be intermediate risk and does not provide a clear treatment pathway.
However, using the Pooled Cohort Equation from the cholesterol guidelines can overestimate risk by as much as four times in adults aged 40 to 75 years without diabetes, he said.
“What that will lead to is a dramatic overtreatment of patients because you are dramatically overestimating their risk,” he said. “Forty percent of our patients end up in this intermediate category, and we need better risk stratification.”
Budoff said a 2011 study in the Journal of the American College of Cardiology indicated that CAC scoring can improve outcomes; compared with patients who did not have a scan, patients who did have one had greater reductions in LDL and BP, were more likely to exercise and were more likely to get new prescriptions for lipid-lowering, BP-lowering and antiplatelet medications.
The group that had a scan also had reduced procedure and medication costs, he said.
A 2015 study in PLOS ONE concluded that CAC scoring accurately stratified intermediate-risk patients into risk levels identifying who can benefit from more aggressive therapy, which is a cost-effective strategy, he said.
In the intermediate-risk population, approximately 50% will have a CAC score of 0 and thus will not need statin therapy, whereas those who do have CAC will be able to see it, and visual confirmation of disease tends to improve medication adherence, according to Budoff.
“A picture is worth 1,000 words,” he said.
He concluded that imaging has at least three virtues. “It individualizes risk assessment beyond use of age, which is a less reliable surrogate for atherosclerosis burden. It provides an integrated assessment of the lifetime exposure to risk factors. It identifies individuals who are susceptible to developing atherosclerosis beyond established risk factors,” Budoff said.
Virtues of biomarkers
Risk prediction goes beyond atherosclerotic CVD and needs to be extended to conditions such as HF and atrial fibrillation, James A. de Lemos, MD, professor of medicine and the Sweetheart Ball-Kern Wildenthal, MD, PhD Distinguished Chair in Cardiology at UT Southwestern Medical Center, said during his presentation.
“We need to consider disrupting the traditional ‘silo’ approach to augmenting risk prediction,” he said. “We need to evaluate biomarker combinations that cross testing modalities.”
One study showed that adding C-reactive protein and N-terminal pro-B-type natriuretic peptide biomarker findings to traditional risk factors improved prediction of CVD events and CVD death in men aged 60 to 79 years, he said.
Another biomarker test proving to be important is change in high-sensitivity troponin T, which has been associated with CVD death and HF among people without cardiac symptoms, according to de Lemos.
He said his team has tested whether a comprehensive assessment that includes a clinical evaluation, a 12-lead ECG, CT for coronary calcium and biomarker tests for high-sensitivity troponin T, high-sensitivity CRP and NT-proBNP can improve risk prediction in the Dallas Heart Study and MESA cohorts.
“What we found was that each of the tests, except for CRP in the Dallas Heart Study, provided independent information with regard to global cardiovascular disease outcomes, including heart failure and atrial fibrillation,” de Lemos said. “This information was independent of all the traditional risk factors in the Pooled Cohort Equation, as well as all the information in the other four tests. We think that most clinicians will want to use this in a simple fashion, with defined abnormal values. We are trying to characterize individuals who are not at low risk. We’ve created a simple integer score, counting up the number of these abnormal tests. Those with no abnormal tests had an extremely low incidence of any adverse cardiac event over a 10-year period. That increases 30- to 35-fold for individuals who had three or more abnormal tests. If we want to move the needle in regard to discrimination and risk reclassification, we are going to have to have tests or combinations of tests that identify a large spread in risk.” – by Erik Swain
References:
Budoff MJ.
de Lemos JA. Risk assessment for global cardiovascular disease: Imaging and biomarkers. Both presented at: Cardiometabolic Health Congress; Oct. 24-27, 2018; Boston.
deFilippi CR, et al. JAMA. 2010;doi:10.1001/jama.2010.1708.
de Lemos JA, et al. Circulation. 2017;doi:10.1161/CIRCULATIONAHA.117.027272.
Roberts ET, et al. PLoS One. 2015;doi:10.1371/journal.pone.0116377.
Rozanski A, et al. J Am Coll Cardiol. 2011;doi:10.1016/j.jacc.2011.01.019.
Wannamethee SG, et al. J Am Coll Cardiol. 2011;doi:10.1016/j.jacc.2011.02.041.
Disclosures: Budoff reports he receives grant support from General Electric. De Lemos reports he receives grant support from Abbott Diagnostics and Roche Diagnostics and consultant fees from Abbott Diagnostics, Ortho Clinical Medicine and Roche Diagnostics, serves on endpoint committees for Radiometer and Siemens Health Care Diagnostics and serves on a steering committee for Amgen.