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Implications for Patient Management
Assuming that the vulnerable plaque (VP) concept is, on the whole, accurate, then the current medical therapy, as it is effective in preventing coronary artery disease (CAD), is presumably also effective in preventing these plaques from developing or in stabilizing existing plaques. As discussed above, current therapies frequently used in CAD in which the mechanism of action may include stabilization of the plaque include, most notably, statin therapy and angiotensin converting enzyme (ACE) inhibition, as well as beta-blockade. Additionally, as described above, percutaneous transluminal coronary angioplasty (PTCA) and carotid endarterectomy have been recommended. Although by no means a major theme in the scientific literature that we reviewed, there appears to be considerable interest in stenting as a potential treatment, as evidenced by a recent report on CBS News:
Daniel Simon, M.D., director of interventional cardiology at Brigham &
Women's Hospital in Boston, in a recent analyst call, referred to drug-eluting
stents as the 'perfect pacifying device' for VP. He said that the use of drug-eluting
stents in treating VP could triple annual stent procedures (Anonymous, CBS
news, Sept 20, 2002).
Whether Dr. Simon's prophecy will prove to be true is a matter of speculation. However, we believe there are considerable barriers to evidence-based prophylactic stenting of VPs, some of which we highlight below.
- These plaques are typically asymptomatic, since they are, by definition, precursor lesions; many of the methods proposed to diagnose these plaques (e.g., optical coherence tomography [OCT], intravenous ultrasound [IVUS], and angioscopy) are invasive procedures, typically reserved for patients with clinical syndromes such as unstable angina and acute myocardial infarction (AMI). Apparently, the great majority of such plaques occur in patients who do not present such clinical syndromes.
- In this review, we did not identify any large scale, population-based natural history studies using a priori defined plaque characteristics. Thus, although it may be that plaques that were structurally vulnerable cause most clinical events, the probability that a plaque with "vulnerable" characteristics (using any of the emerging technologies) will cause a clinically significant event is still unknown. Furthermore, since it may be hard to justify research protocols requiring invasive testing on asymptomatic individuals, even those at relatively highrisk of atherosclerosis, natural history studies are problematic to contemplate. Regarding natural history, we speculate that if the condition is common, then the risk that any identified plaque will rupture must be rather low. On the other hand, if the risk that a plaque will rupture is high, then VP resulting in clinical events should be relatively rare.
- Prophylactic stenting of VP would have considerable competition from pharmacological treatments. First-line treatment for patients at risk for symptomatic CAD is aspirin, statins, and ACE inhibitors. Since stenting presumably would not replace pharmacotherapy, stenting would have to show significant benefit compared to medication. Furthermore, pharmacologic therapies themselves are evolving. For example, intravenous administration of recombinant HDL (ApoA-1 Milano) (Nissen 2003—a variant of apolipoprotein-caused regression of coronary atherosclerosis. This suggests that pharmacologic therapies may improve substantially, even further reducing the risk that an identified VP will lead to a clinical event. Indeed, the concept of the VP may produce other effective pharmacologic approaches, such as inhibitors of MMP activity, which might further diminish any putative benefits to prophylactic stenting.
The concept of VP is still evolving. We can only speculate about its course since no studies have been designed to accurately describe the natural history based on plaque characteristics. In such a context it is not surprising that there is only limited inferential evidence regarding methods of diagnosis and treatment modalities of this condition.
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