Prominent Interventionalists Attack Appropriate Use Criteria For PCI 5

A group of leading interventional cardiologists has launched an attack on the growing role of appropriate use criteria (AUC) for PCI in the US. They argue that severe flaws in current guidelines render unreliable current attempts to assess the rate of appropriate procedures.

In a paper published in  JACC: Cardiovascular Interventions, Steven Marso and colleagues (Paul Teirstein, Dean Kereiakes, Jeffrey Moses, John Lasala, and J Aaron Grantham) criticize a study in JAMA published last year from the National Cardiovascular Data Registry (NCDR) that found a large degree of inappropriate or uncertain PCI procedures, as well as a wide range of variability among institutions. Marso et al write that the JAMA paper sensationalized the data by focusing attention on the low rate of appropriate indications for nonacute PCI– 50.4%– while failing to point out that the study found that 84.6% of procedures in the entire study population– acute and nonacute alike– were deemed appropriate. Furthermore, given the imprecision built into the system, they ask: what is the “acceptable threshold” of inappropriate PCI?

The authors write that the AUC panel “purposefully limited involvement of the interventional community during the development process, in order to avoid having a majority of committee members “whose livelihood is tied to the technology under study.” But the under-representation of interventionists may have biased the results, they argue. One particular case as graded by the AUC panel was the most common reason for cases to be categorized as inappropriate: the AUC committee decided that PCI was inappropriate for a patient with 1- to 2-vessel disease, no proximal LAD involvement or prior CABG, class I or II symptoms, low-risk noninvasive findings, and on no or minimal medications. But most clinicians believe this is an uncertain but not inappropriate indication, they say.  The AUC panel may have “got this one wrong,” they write.

Marso et al also point to the “lack of specific criteria for interpreting” stress tests in the NCDR database. In addition, they disagree with the inappropriate classification of most cases of class II angina before medical therapy has been attempted, arguing that both COURAGE and BARI 2D showed that PCI is a valid option for these patients. Finally, the authors argue that the NCDR database contains numerous inaccuracies, including misclassification of patients’ angina status or noninvasive risk assessment.

One striking feature of the controversy is that two of the authors of the JAMA paper (Paul Chan and John Spertus) and two of the authors of the  JACC: Cardiovascular Interventions paper (Steven Marso and Aaron Grantham) are all at the same institution: Saint Luke’s Mid America Heart Institute in Kansas City, Missouri. Marso and colleagues  state that 56% of cases classified as inappropriate at their institution “were misclassified due to incorrectly coding CCS class status, not documenting angina equivalents, or inaccurate documentation of the noninvasive risk assessment findings.”

Until the NCDR database is fixed, Marso et al write, “it could be argued” that the authors “should refrain from approving AUC-related clinical studies until such time that assurances are both valid and reliably collected.”

Sanjay Kaul sent the following comment to CardioBrief:

Because there are undesirable scientific, economic, logistic, & philosophical implications of unfocused broad (i.e., inappropriate) use of PCI, it is incumbent upon us as a professional society to track how often we use it judiciously. The PCI AUC, although far from perfect, are a step in the right direction. While some of the authors’ criticisms regarding the AUC in general and the Chan et al paper in particular are quite “appropriate”, I do not agree with their main contention that interventional cardiologists were underrepresented in the technical panel (4 out of 17) to minimize bias. Management of stable CAD is hardly the exclusive domain of interventional cardiologists!  They do, however, have some sage recommendations for refining the AUC. Ultimately, such ‘back and forth’ amongst the protagonists is a healthy exercise. I expect more light than heat will be generated as a consequence.

Editorial Comment: Since the publication of COURAGE and the subsequent Mark Midei scandal, no issue has been more explosive than the problem of possible overuse of PCI in non-urgent cases. No one really knows the full scope of the problem. As I hope to write in a future post, it is unclear whether Mark Midei was an outlier who went far beyond the bounds of acceptable practice (though as the Marso paper makes clear, there is no clear consensus on what exactly defines “acceptable practice”) or a scapegoat who was severely punished for doing what many other interventional cardiologists were also doing at the same time.

The full scope of the problem will not be measured by one paper from the NCDR, or by one response from interventional cardiologists. It’s going to be a long time and a lot of hard work will have to be done before we have a clear idea of the situation. But one thing is certain: there’s no chance that we will be going back anytime soon to the wild west days of interventional cardiology.

Marso et al score a number of valid points about the deficiencies of the NCDR and AUC. But they don’t propose a real alternative, except to suggest that interventional cardiologists are perfectly good at policing themselves and should be allowed to decide for themselves what procedures are appropriate. Outside scrutiny is clearly unwelcome in their view. This perspective may gain them some popularity within the interventional cardiology community but it is unlikely to get much traction in the larger world.

It’s easy to ridicule and criticize guidelines, appropriate use criteria, and the like. They will never be perfect. The documents will need to be continually updated and revised. And there will be legitimate differences of opinion about the details.

It’s understandable that fiercely independent physicians chafe when they’re told what to do. Several years ago, after COURAGE but before the Midei scandal broke, one of the co-authors of the Marso paper responded to a question on National Public Radio about stent overuse:

I definitely have a bias toward stents because I have a lot of experience with stents and I’ve seen patients do so much better.

One of his colleagues responded:

…sometimes there’s a tendency to believe in your procedures too much… most of the time interventional cardiologists are like that, they are going to say, well I can fix the artery. The question of course is, in some cases, should you?

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5 comments

  1. The interventionalusts are trying desperately to obscure the science of the pathophysiolgy of atherosclerotic plaque. MIs and resultant deaths are caused by rupture of early, unstable plaques most of which are not even seen on angiography. PCI of the older, more stable plaques seen on angiography will not prevent MIs as shown by COURAGE. So the guidelines should be very simple. In stable or stabilized patients PCI is indicated only for documented ischemic symptoms intractable to lifestyle change and drugs.

    • Dr. Rose — This assertion flies in the face of the documented evidence from FAME and FAME II. Verifiable ischemia should be revascularized. Enrollment in FAME II was stopped on ethical grounds precisely because ischemic patients who were randomized to OMT had a significantly higher rate of ACS. So if ischemia has been documented (not “symptoms” intractable to lifestyle changes and drugs) the patient should be revascularized. At least that is the data.

      • The only criterion for entry in FAME was multi vessel disease and there was no attempt to treat FFR diagnosed ischemia with lifestyle change or changes in drugs. 30% still smoked, 60% were hypertensive, 25% were diabetic, presumably type 2. So most of these patients had self-destructive lifestyles. Only 76% were on a beta blocker and only 36% were on a nitrate.

        About 30% of patients in FAME had unstable angina, half with dynamic ECG changes. So this was not entirely a group of stable or stabilized angina as was studied in the COURAGE trial. It could well be that this group of very symptomatic patients got most of the benefit from FFR guided PCI. The offending lesion causing the unstable angina should have been obvious anyway without FFR. The results are not broken down according to symptoms.

        FAME was funded by the FFR manufacturers and stent makers and the patient selection, medical treatment and reporting was designed consciously or unconsciously to show benefit. Even publications in the NEJM must be carefully assessed before assuming that the conclusions are justified by the data!

        FAME II was stopped because of reduced subjective “need” for revascularization not because of reduced MI or mortality.

        COURAGE is still the best study of PCI in truly stable or stabilized patients but even that study did not use documented, proven lifestyle change and so did not use optimal medical therapy possibly because it was funded by statin makers.

  2. Dr. Rose — We both covered this ground with back & forths on other forums, so I’ll only say that your facts are incorrect on several items. FAME was funded by Radi Systems, a relatively small European manufacturer of FFR that was subsequently purchased by St. Jude. No stent makers funded either FAME trials. Why would they? The take-away from FAME was that “stenting inappropriate lesions (as guided by FFR) showed higher costs and worse outcomes”. I would think this message would resonate with you. As for FAME II, the enrollment was stopped early — the trial goes on as planned. The DSMB (a high level independent entity from the sponsors or investigators) alerted the PIs that they could stop enrolling because the results were so strong that further enrollment would not change the outcomes but randomizing patients to OMT would involve ethical issues of knowingly undertreating. The need for urgent revascularization in these patients was not subjective. The great majority of them had progressed into ACS. As for MI and mortality, as of now there was no difference. It will be interesting to see the 1, 2 and longer data.

    • Reversible ischemia of whatever degree, detected by whatever method never caused an MI or killed anyone. MIs and coronary deaths are caused by plaque rupture. Obstructive plaques can rupture but are much less likely to do so compared to much more common early, more unstable, non-obstructive plaques, invisible on angiography. So MIs can only be efficiently prevented by reducing the chance of plaque rupture by regression of plaque with significant lifestyle change and drugs if necessary, not by PCI which should be reserved for treating acute plaque rupture.

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