JACC: What is the true value of coronary artery calcium progression?
Recent studies have validated the prognostic nature of coronary artery calcium (CAC) scoring, on its own or in conjunction with the Framingham risk score. But, there is no current standardization of how CAC progression should be assessed and exactly what meaningful progression constitutes, according to a study in the Nov. 9 issue of the Journal of the American College of Cardiology.
John W. McEvoy, MD, from Johns Hopkins Ciccarone Center for the Prevention of Heart Disease in Baltimore, and colleagues reviewed the published literature to better understand the importance of CAC progression as a clinical measurement.
They found that annual rates of CAC progression range from 20 to 30 percent in patients at average Framingham risk score and also confirmed that increased CAC progression correlates with worsening atherosclerosis and may facilitate prediction of future cardiac events.
While statin therapy might inhibit CAC progression, no randomized controlled data support this hypothesis. Consequently, "routine quantification of CAC progression cannot currently be recommended in clinical practice," the authors concluded.
To get closer to that end game, researchers called for the development of standards for quantifying CAC progression and assessment, as well analyzing other cardiac therapies on CAC progression and cardiac outcomes.
McEvoy and colleagues categorized three subgroups to better define CAC progression and the response of CAC to treatment:
Another problem with CAC measurement is the interscan variation. The original unit of measurement, the Agatston score, tends to not accurately capture changes in coronary calcium. The newer method—calcium volume or mass score—is more reliable and tends to reduce variability between scans. Researchers recommended reporting with calcium volume scores, with or without Agatston scores, to facilitate universal comparisons of CAC progression in future clinical trials.
The study reported that baseline CAC score by cardiac CT is "one of the most consistent predictors of future CAC progression." Carotid intima-media thickness by ultrasound has become an important surrogate for atherosclerosis, and baseline thoracic aortic calcium is correlated with CAC progression. However, aortic calcium is measured with CT at the time that CAC is quantified.
Studies have shown that statins might decrease the risk of cardiac events by helping to calcify soft plaque. Consequently, some studies have noted an increase in CAC progression related to statin use. "It is possible that statins need more time to affect the downstream process of calcium deposition," they wrote.
Lastly, studies have shown that certain hypertension therapies have more pronounced effect on CAC progression. In addition, studies have shown lack of CAC progression in dialysis patients taking sevelamer compared with those taking calcium-based phosphate binders.
The researchers wrote that serial CAC quantification "has considerable potential as a noninvasive measure of the progression of atherosclerosis and might have ongoing applicability to the study of interventions targeted at reducing this progression."
However, they stressed that randomized trials need to be conducted comparing baseline CAC with serial scanning.
John W. McEvoy, MD, from Johns Hopkins Ciccarone Center for the Prevention of Heart Disease in Baltimore, and colleagues reviewed the published literature to better understand the importance of CAC progression as a clinical measurement.
They found that annual rates of CAC progression range from 20 to 30 percent in patients at average Framingham risk score and also confirmed that increased CAC progression correlates with worsening atherosclerosis and may facilitate prediction of future cardiac events.
While statin therapy might inhibit CAC progression, no randomized controlled data support this hypothesis. Consequently, "routine quantification of CAC progression cannot currently be recommended in clinical practice," the authors concluded.
To get closer to that end game, researchers called for the development of standards for quantifying CAC progression and assessment, as well analyzing other cardiac therapies on CAC progression and cardiac outcomes.
McEvoy and colleagues categorized three subgroups to better define CAC progression and the response of CAC to treatment:
- Incident CAC: defined as detectable CAC at the follow-up examination in a participant initially free of CAC;
- Calcified nonprogressor: defined as an unchanged or reduced CAC score in participants with detectable CAC at baseline; and
- Calcified progressor: defined as an increase in CAC score in participants with detectable CAC at the initial examination.
Another problem with CAC measurement is the interscan variation. The original unit of measurement, the Agatston score, tends to not accurately capture changes in coronary calcium. The newer method—calcium volume or mass score—is more reliable and tends to reduce variability between scans. Researchers recommended reporting with calcium volume scores, with or without Agatston scores, to facilitate universal comparisons of CAC progression in future clinical trials.
The study reported that baseline CAC score by cardiac CT is "one of the most consistent predictors of future CAC progression." Carotid intima-media thickness by ultrasound has become an important surrogate for atherosclerosis, and baseline thoracic aortic calcium is correlated with CAC progression. However, aortic calcium is measured with CT at the time that CAC is quantified.
Studies have shown that statins might decrease the risk of cardiac events by helping to calcify soft plaque. Consequently, some studies have noted an increase in CAC progression related to statin use. "It is possible that statins need more time to affect the downstream process of calcium deposition," they wrote.
Lastly, studies have shown that certain hypertension therapies have more pronounced effect on CAC progression. In addition, studies have shown lack of CAC progression in dialysis patients taking sevelamer compared with those taking calcium-based phosphate binders.
The researchers wrote that serial CAC quantification "has considerable potential as a noninvasive measure of the progression of atherosclerosis and might have ongoing applicability to the study of interventions targeted at reducing this progression."
However, they stressed that randomized trials need to be conducted comparing baseline CAC with serial scanning.