How Much, How Tight? Plaque Burden Sharpens CT Angiography Stenosis-Based Risk Prediction

Adding computed tomographic angiography (CTA) findings on coronary plaque extent to those on plaque presence and severity can greatly improve CAD risk evaluations, suggests a retrospective cohort study [1]

In it, whether or not coronary disease seen at CTA was deemed obstructive-that is, included a stenosis of at least 50% severity-adding data on CAD extent (number of diseased coronary segments) further stratified risk of CV death or nonfatal MI over several years, according to a report published online February 18, 2014 in Circulation: Cardiovascular Imaging.

The analysis, with first author Dr Marcio Sommer Bittencourt (Harvard Medical School, Boston, MA), covered patients without a prior CAD history undergoing clinically indicated coronary CTA.

Traditionally, CTA studies have categorized patients with CAD as having obstructive lesions <50% vs >50% luminal-stenosis severity, with less attention paid to plaque extent or volume, observed senior author Dr Ron Blankstein (Brigham and Women’s Hospital, Boston, MA).

“Those initial studies showed that patients who have a >50% lesion are the ones at the highest risk. We now have identified a subgroup of those with [stenoses of] <50% who have as high a risk as some patients who have a >50% lesion,” Blankstein told heart wire .

Most referrals to coronary CTA are due to symptoms suggestive of CAD, and in practice, most referred patients will not have obstructive disease, he elaborated. In the current series, 40% of patients had “normal” CTA findings, while 38% had nonobstructive disease (<50% stenoses) and 22% had obstructive disease. Typically, it would be only the 22% with obstructive disease who would be referred for further invasive or noninvasive testing.

“However, if we now know that [some] patients with nonobstructive disease have a higher risk of future myocardial infarction or cardiovascular death, that tells us that we need to be treating these patients more aggressively.”

In an email to heart wire , Dr Matthew Budoff (Los Angeles Biomedical Research Institute, CA) said, “The findings are unique, in that regardless of whether obstructive or nonobstructive disease is present, the extent of plaque detected by coronary CTA enhances risk assessment.” Therefore, according to Budoff, who is not connected with the study, “it is not how tight the stenosis is, but how much atherosclerosis one has that predicts events.”

In the analysis, all CTA scans were performed using 64-row or newer systems on 3242 consecutive patients without prior CAD referred to two experienced centers, who were then followed for the primary outcome of CV death or nonfatal MI for at least two years (median 3.6 years). Such events occurred in 2.8% of patients.

In multivariate analyses, the risk of the primary outcome was significantly elevated in patients with extensive CAD (involvement in more than four coronary segments) that was either nonobstructive (p=0.002) or obstructive (p<0.001), and in nonextensive CAD (involvement in four or fewer segments) that was obstructive (p=0.009). The risk was not elevated for CAD that was both nonextensive and nonobstructive.

Importantly, Blankstein pointed out, patients with nonobstructive CAD and extensive disease had as high an event rate as those with obstructive CAD and nonextensive disease. Yet such patients with nonobstructive, extensive disease would be among those declared negative for CAD at any traditional form of stress testing, because they would not show a presence of flow-limiting lesions. But, he said, “Those tests are not designed to identify plaque.”

Plaques that are not flow-limiting can certainly be high risk for rupture, underscoring that in some cases more plaque can equate with higher risk.

“This actually explains, I think, as a side note, why some patients can still have events even after a normal stress test.”

Neither Blankstein nor the other authors had disclosures. Budoff recently disclosed receiving research/grant support from HeartFlow and study funding from Wakunaga of America and GE Healthcare and having served as a consultant and speaker for GE Healthcare.

By Steve Stiles

 

 

http://www.medscape.com/viewarticle/821190?src=rss