January 19th, 2011

What PROSPECT Doesn’t Tell Us


The PROSPECT trial provides some interesting insights about the mechanisms of thrombotic coronary artery disease, but how, if at all, should it change practice? Here are what the findings do and do not demonstrate:

What the PROSPECT study says:

In ACS patients treated with PCI, major adverse cardiovascular events that occurred during a median follow-up of 3.4 years were as likely to result from a nonculprit ( i.e., other than the originally stented) lesion as  from the culprit lesion.  These nonculprit lesions often were angiographically mild (≈30% stenosis) and were characterized (with IVUS) as having thin-cap fibroatheroma, a large plaque burden, a small luminal area, or some combination of these.

What the PROSPECT study doesn’t say:

  1. ACS most commonly results from mild lesions. Major cardiovascular events were equally attributable to recurrence at the site of PCI and to nonculprit lesions.
  2. Mild lesions with thin caps, large plaque burdens, and small lumens carry a high risk of causing MI and death. In fact, of the lesions with all three of these characteristics, only 18% resulted in a cardiovascular event, the most frequent of which was hospitalization for unstable or progressive angina (in 93% of patients).  Death, MI, or cardiac arrest occurred in only 7% of patients.
  3. Patients should have IVUS of their entire coronary tree to identify “high risk” lesions. In this study, 1.6% of patients had complications (dissection or perforation) related to the 3-vessel imaging procedure.  Furthermore, of the 222 lesions leading to events, only 55 were prospectively “identified” by IVUS; 118 occurred at the sites of lesions treated with PCI, and 49 occurred in distal vessels inaccessible to IVUS.
  4. Mild angiographic stenoses should undergo revascularization. No data exist to suggest that revascularization of “vulnerable” lesions prevents acute events.  In fact, revascularization may be harmful: 13% of stented lesions were subsequently the site of a cardiovascular event.

Do you see any expanded role for IVUS after this study? Will you do anything different in your practice on the basis of these results?

4 Responses to “What PROSPECT Doesn’t Tell Us”

  1. Andre Paixao, MD says:

    In my mind this signals the need for more effective medical treatment. CAD being a diffuse or at least multi-segmental process efforts should me aimed at targeting the entire coronary vasculature and not necessarily identifying vulnerable plaque.

  2. I think that PCI of the culprit lesion is not the end of the story,, that is why post PCI optimal medical therapy including aggressive Statins therapy and indefinite therapy of Plt P2Y12 receptor antagonist in addition to a strict follow up all are mandatory for avoidance of vulnerable plaque rupture in the future.

  3. I agree with the previous unknown member: the most important issue is to treat more aggressive as possible with OMT (statins high-doses high-efficacy, ASA plus clopidogrel, betablockers, etc) in order to reduce the future (3 or 5 years) events, related both the stented lesions and the non culprit but ‘vulnerable’ plaques. I don’t think more PCI and stents at the first ACS can change the…story.

    Competing interests pertaining specifically to this post, comment, or both:

  4. David Powell , md, facc says:

    One question not well answered. Once the IRA is stented; what’s the evidence for stenting a non-IRA severe stenosis. They often get” staged” procedures. There were only 14 unstented in this trial. But if they are doing well, I’m not sure they need more stents. This type of patient was not in COURAGE. Interventionalists overwhelmingly recommend a return trip. I must admit: sometimes I do a perfusion study (is this even needed?) and, in the absence of ischemia in the nonculpret territory I don’t send them back.

    Competing interests pertaining specifically to this post, comment, or both: