WASHINGTON, DC — Should clinicians take action when an asymptomatic patient has a coronary CT scan that shows nonobstructive plaque, or should these patients not have these scans in the first place?
This topic was debated at the Society of Cardiovascular Computed Tomography (SCCT) 2017 Annual Scientific Meeting, and since there was no vote, it was not clear who won the debate[1], but there are clearly two divergent ways to view nonobstructive coronary plaque on CT.
SCCT 2017 Gold Medal Award recipient Dr James K Min (Weill Cornell Medical College, New York, NY) took the stand that “nonobstructive coronary plaque requires action,” arguing that “having nonobstructive plaque presupposes that you’ve seen it. Once you have disease, you need to treat it.”
On the other side, JAMA Internal Medicine editor Dr Rita F Redberg (University of California San Francisco) defended why “nonobstructive disease on cardiovascular CT should not affect primary prevention” in asymptomatic people, who thus don’t have ischemia.
“There are absolutely no data that you can improve cardiovascular . . . morbidity or mortality by identifying nonobstructive plaque in healthy people, and there are downsides,” she stressed, including exposing patients to radiation, creating anxiety, and giving people unnecessary procedures or drugs with potential for harm.
To theheart.org | Medscape Cardiology she reiterated, “There are no outcome data that focusing on the [coronary CT] images leads to any better outcomes. . . . If you can’t make someone feel better or live longer with these [primary-prevention coronary CT scans and treatment] changes, I don’t think we should be doing them; we’re just making patients miserable.”
Invited to summarize the debate, session comoderator and incoming SCCT president Dr Todd C Villines (Uniformed Services University School of Medicine, Bethesda, MD) said that Min made a clear point that “when we see particularly large burdens of nonobstructive disease, particularly those who have vulnerable plaque characteristics, it compels us to counsel that patient more aggressively, to let them know that their risk is different from what we thought it was from risk factors.”
Clinicians need to “act on that, perhaps add preventive therapies and obviously engage [patients] in improving their habits and [having a] healthy lifestyle.”
Asked about Redberg’s points, he conceded, “We certainly don’t want to overtreat. When you look at the guidelines, it comes back to shared decision-making” between the patient and clinician.
Nonobstructive Plaque “a Misnomer”
Finding nonobstructive plaque “improves identification of at-risk patients who will experience MI or death,” Min began his arguments.
He cited 5-year follow-up results of the CONFIRM registry in more than 1800 patients without prior CAD or modifiable CAD risk factors assessed by CT angiography (CTA), in which nonobstructive plaques caused major adverse cardiac events at nearly the same rate as obstructive plaques[2].
“I think we need to get past this point of calling it ‘nonobstructive’ or ‘obstructive.’ It’s a misnomer. It’s ‘plaque’ or ‘no plaque,’ ” he said.
In another recent study of more than 6000 patients without CAD who underwent coronary CTA and coronary artery calcium (CAC) scoring, there was a twofold increase in 5-year mortality among patients with plaque but no stenosis[3].
“Nonobstructive plaque identifies pathobiologically important processes,” Min said. So “we should be identifying patients who have nonobstructive coronary artery disease when they are starting to experience microvascular dysfunction and endothelial dysfunction.
“It’s not ischemia; it’s not stenosis; it’s the atherosclerotic plaque characteristics that matter,” according to Min.
“The percent aggregate plaque volume [plaque burden] is what predicts the ischemia better than anything else that we have.”
Nonobstructive-Plaque Diagnosis Dangers
Cardiovascular CT imaging “certainly . . . can give us good pictures,” Redberg agreed, “but it also leads to inappropriate, unnecessary, costly, and risky additional procedures in some cases.”
Importantly, the procedure increases lifetime radiation-attributable risk of cancer. “Excess cancers and deaths due to our exuberant use of CT . . . is something consider,” she cautioned.
Instead of CT coronary imaging, “office-based risk scores such as Framingham and others . . . give us intervenable targets,” such as high blood pressure, high lipids, or smoking.
“I don’t know what we do to treat nonobstructive plaque besides what we would already do to treat modifiable risk factors,” she said.
“The danger to me . . . is that you can diagnose [nonobstructive plaque] 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, because there is no specific treatment for nonobstructive disease.”
To illustrate this, Redberg described two recent patients. The first, a 64-year old woman, had a few episodes of atypical chest pain and was sent for CAC scoring. Her CAC was 75, so she was sent for a coronary angiogram, diagnosed with a 30% ostial LAD lesion, and given “a bag of medicine”—aspirin, statins, calcium-channel blockers, and beta-blockers—that she did not take.
She had no cardiac risk factors; her total cholesterol was under 200 mg/dL; her LDL was around 100 mg/dL, and she “was very upset and concerned about why she had gotten all these medications,” Redberg said. “I told her that she really was low risk and reinforced diet, regular exercise, and not smoking, which she was already doing.”
A second similar patient had a similar experience, but she took the statin and experienced memory problems that ceased when she stopped taking the statin.
Redberg cited the 900-patient FACTOR-64 trial, in which coronary CTA screening of asymptomatic, high-risk diabetics did not reduce all-cause mortality, nonfatal MI, or unstable angina over 4 years.
Among 10,003 patients randomized to CTA or functional testing in the PROMISE trial, rates of coronary angiography, PCI, and CABG were much higher in the CTA arm “because imaging tends to lead to more imaging,” she said.
Also, the US Preventive Services Task Force and American College of Cardiology guidelines do not recommend screening asymptomatic low-risk patients to identify nonobstructive plaque.
No Randomized Trial
Finding nonobstructive plaque “guides therapy to improve event-free survival,” Min said in his rebuttal.
In a nonrandomized study of 10,000 patients by Cho and colleagues that looked at aspirin and statin in patients with nonobstructive coronary plaque, there was a marked reduction in mortality in a 2.5-year follow-up in patients who were taking statins and [had manifest CAD] diagnosed by a CT angiogram[3], he said.
“You didn’t show us the risk-factor score in that population,” Redberg countered.
“There is no randomized trial and no data showing a benefit for treating,” she said. “And what do you do to treat nonobstructive plaque? You are talking again about giving aspirin and statins, which we already do quite well based on risk factors.”
In a dramatic case published in the Archives of Internal Medicine[4] a 52- year-old woman with atypical chest pain but normal ECG, troponins, CRP, and other markers underwent coronary CTA “just for reassurance.” Both noncalcified and calcified plaque were identified, so she had a coronary angiogram that was complicated by a left main coronary dissection that required emergency CABG. Postoperatively the graft failed, stents thrombosed, and she ended up with refractory heart failure requiring a heart transplant.
“When it was published, people said the cardiac CT wasn’t used correctly, but this is not an atypical case,” Redberg said.
“All of our patients can reduce their risk with lifestyle modification, but I think it should be based on office-based risk assessment. A Mediterranean-style diet, physical activity, and no smoking, that’s the best balance of risks and benefits. and data support this.”
Min reports relationships with Cleerly, MDDX, and Arineta. Redberg and Villines had no relevant financial relationships.
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