Stockholm, Sweden - Confirmation that thin-cap fibroatheromas (TCFAs) are focally distributed in the proximal left anterior descending (LAD) coronary artery is good news, according to the authors of a study using both computed tomography angiography (CTA) and virtual histology intravascular ultrasound (VH IVUS)
Dr Joëlla Van Velzen (Leiden University Medical Center, the Netherlands) and colleagues evaluated 168 patients with chest pain with coronary CTA to assess the frequency and distribution of mixed-composition plaques, which previous studies have shown are the most likely to rupture. All of the patients were then examined with VH IVUS to determine the frequency and distribution of high-risk plaque features, including the amount of necrotic core and presence of TCFAs.
The study results, presented as an abstract at the recent European Society of Cardiology (ESC) 2010 Congress, show that most TCFAs are located in the proximal segments of each vessel, primarily in the proximal LAD (p=0.03), and the average volume of necrotic core per vessel is greatest in the LAD (0.59 mm2), followed by the right coronary artery (0.55 mm2) and left circumflex artery (0.35 mm2) (p<0.001).
The VH IVUS exams found 602 plaques with 84 TCFA plaques, most of which were in the LAD, clustering mainly in the proximal part of the LAD. CTA found 984 plaques with 401 mixed-composition plaques, mostly located in the proximal segments of each vessel (p<0.001). Just under half of the mixed plaques were in the LAD.
Prior to this study, most of the existing information on the natural history and location of potentially high-risk plaques is retrospective autopsy data, according to the study authors. Van Velzen told heartwire that these results should be considered "encouraging," because plaques located proximally are more accessible to local invasive imaging techniques and local treatment options, such as PCI, than downstream plaques or diffuse disease.
Because CTA is a noninvasive technique and IVUS is invasive, a CTA technology that could identify vulnerable plaques would be helpful; however, Van Velzen cautioned that current CT technology cannot detect as many TCFAs as VH IVUS.
Commenting on the study, Dr Armin Zadeh (Johns Hopkins University, Baltimore, MD) agreed that "it's fairly well established that CTA is not as sensitive as VH IVUS to detect TCFAs; thus, [IVUS's] role does not seem to be diminished quite yet." On the other hand, the spatial resolution of VH IVUS is insufficient to detect TCFA as defined by pathology (<65-µm cap thickness), so VH IVUS "is not really a good standard to compare with" for the true assessment of TCFA, Zadeh said.
Many unanswered questions
Despite the encouraging findings, researchers have a long way to go before detection and treatment of vulnerable plaques can be routine. Commenting on the study, Dr Jonathan Lindner (Oregon Health and Science University, Portland) pointed out, " Right now, there is no specific therapy—drug or intervention—that has ever been shown to preventively treat [coronary disease] on the basis of [a] high-risk plaque phenotype."
Zadeh told heartwire that although this study confirms that problematic lesions are most common in the proximal LAD, "We don't know how troublesome these TCFAs really are. In reality, many of them eventually rupture clinically silently—evidence from pathology—and don't cause ACS." Further, Zadeh agrees with Lindner that "we don't know how to treat them even if we knew that they were troublesome—that is, we do not have any evidence yet that doing anything based on this information is associated with better outcomes. Particularly, it is unclear if doing anything beyond standard measures—cholesterol control, other risk-factor interdiction, etc—is helpful, let alone coronary stenting, which is associated with significant risks itself."
The future of research on identification and treatment of high-risk lesions before they become culprit lesions is "only conjecture at this point," Lindner said. "There is a parallel development of new treatment paradigms that will require new identification methods. The two are not happening in a vacuum independently of each other," he said.
Zadeh suggests that "we need outcome studies showing that identifying 'vulnerable plaques' significantly adds to our ability to predict risk over assessments with established track records," such as coronary atherosclerotic plaque burden, stenosis severity, stenosis location, and simple plaque characteristics. "More important, we need outcome studies showing that there is additional treatment in response to identifying 'vulnerable plaques' that improves outcome. Thus, we are quite a bit away from implementing some of these concepts into clinical practice."
Source:
Van Velzen JE, Schuiff JD, De Graaf FR, et al. Frequency and distribution of the vulnerable plaque in the coronary arteries: evaluated invasively by virtual histology intravascular ultrasound and non-invasively by multislice computed tomography. European Society of Cardiology 2010 Congress; August 29-September 1, 2010; Stockholm, Sweden. Abstract P4631.
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