Nonobstructive Coronary Disease on Cardiac CT: Call to Action, or Wait and See?

Washington, DC—Do findings of nonobstructive coronary plaque on cardiac CT warrant aggressive action, or should the messaging for these patients be no different than it was prior? Those were the questions at the heart of a debate hosted here last weekend at the Society of Cardiovascular Computed Tomography (SCCT) 2017 Annual Scientific Meeting.

Given recent advances in imaging technology and the proliferation of scanners, more patients with nonobstructive disease are being diagnosed through routine screenings ordered by their primary care physicians, who then refer their patients for further evaluation. Cardiologists have the option of stepping up preventive medicine, including aspirin and statins, a strategy supported by observational studies but not in prospective, randomized controlled trials.

Nonobstructive Disease Is ‘Not a Risk Factor’

James K. Min, MD (Weill Cornell Medical College, New York, NY), arguing in favor of interventions at the time of diagnosis, reasoned in his presentation that “traditional coronary disease measures including high-grade stenosis and ischemia are simple end-stage surrogate measures of nonobstructive atherosclerotic plaque.”

Because “nonobstructive plaque identifies pathobiologically important processes,” he said, “we should be identifying patients who have nonobstructive coronary artery disease when they are starting to experience microvascular dysfunction and endothelial dysfunction and subendocardial perfusion abnormalities.”

Merely assessing patient risk factors and symptoms and urging them to be vigilant is not enough, Min argued. “We need to get past this point of calling it obstructive or nonobstructive. It's a misnomer. It's plaque or no plaque and the type of plaque that matters,” he stressed, claiming that even plaques that do not cause stenosis still put patients at higher risk for death.

We need to get past this point of calling it obstructive or nonobstructive. It's a misnomer. It's plaque or no plaque and the type of plaque that matters. James K. Min

In the future, Min said, “nonobstructive plaque evaluation will enable us to adopt innovative techniques to better identify risk even beyond traditional statistical measures.” Citing the emerging field of deep or machine learning, he foresees algorithms that will seek “to identify lesions or imaging features that presuppose risk so that you can identify and categorize patients who will versus will not have myocardial infarction.”

Nonobstructive plaques also allow for “comprehensive atherosclerotic plaque characterization that improves prognostic risk stratification,” Min said. “We're getting even better at diagnosing and characterizing nonobstructive plaque with dual energy CT methods where we can say not only that it's dark or black or gray, but we can actually tell you the exact material compositions of constituents within that plaque.”

He also argued that because about one-third of the lesions in the FAME trial that were considered “intermediate stenoses” (50%-70%) were shown to have coronary ischemia, “low-grade stenosis and nonobstructive plaque are related, but they're two entirely different concepts.” So acting on these plaques allows physicians to “employ atherosclerotic plaque characteristics to diagnose conventional things that we are looking for in symptomatic patients (ie, coronary ischemia).”

Lastly, Min pressed the idea that nonobstructive plaque is “not a risk factor” but rather “manifest disease.” Once that is established, he concluded, “you need to treat it.”

No Data, No Action

Taking the contrary view, Rita Redberg, MD (University of California, San Francisco), emphasized that “there is absolutely no data that you can improve cardiovascular outcomes, even morbidity or mortality, by identifying nonobstructive plaque in healthy people.”

There are even downsides to doing so, she continued. “The imaging can give us good pictures, . . . but it also leads to inappropriate and unnecessary costly and risky additional procedures in some cases.” The small but nontrivial added radiation risk is also something to consider, according to Redberg.

The availability of “very reliable office-based risk prediction tools” like the Framingham and other risk scores “actually give us intervenable targets,” she said. “I don’t know what we do to treat nonobstructive plaque besides what we already do to treat modifiable risk factors.”

Redberg described two relatively healthy patients she recently saw in the clinic who were diagnosed with nonobstructive plaque and given a “bag of medicines” to take, which resulted in disruptive memory loss and general anxiety. “The danger to me in diagnosing nonobstructive plaque is that you can diagnose it in people who don’t have risk factors and then they end up with a lot of medications and treatments that have no known benefit and definite harms,” she said.

The danger to me in diagnosing nonobstructive plaque is that you can diagnose it in people who don’t have risk factors and then they end up with a lot of medications and treatments that have no known benefit and definite harms. Rita Redberg

Instead of forcing these patients to continue taking the medications, Redberg said she focused instead on diet, exercise, and smoking cessation. “People aren’t given, what I would say, a sensible approach. You can do it without diagnosing nonobstructive plaque just based on office-based risk assessment. I advise all my patients, even low-risk, . . . [to] reduce their risk based on lifestyle modification,” she concluded. “That's the best balance of risk and benefits, and the best data supports this.”

Handling the Risk

Session co-chair Leslee Shaw, PhD (Emory University, Atlanta, GA), spoke with TCTMD after the debate and said that while Redberg “made some good points,” ultimately “there is risk in that plaque.”

True, many patients do make behavioral modifications on their own, she said. “If you know you have atherosclerosis, your future risk is not benign.” On the other hand, “nonobstructive disease is not a false positive. It's not benign. We do know that those folks can progress.”

Nonobstructive disease is not a false positive. It's not benign. We do know that those folks can progress. Leslee Shaw

The lack of clinical trials and guidelines in this space “is a glaring omission” given the breadth of patients who have nonobstructive disease who need medical management, Shaw said. “We don't know what’s the minimal therapy in order to retard progression so that they don't actually then have a heart attack or have progressive disease states where they develop obstructive disease. It's an issue where the lack of evidence really creates problems.”

Note: Min is a faculty member of the Cardiovascular Research Foundation, the publisher of TCTMD.