3.3 Funciones de aptitud
4.1.4 Reductor de Ruido SUSAN
Previous histological studies have demonstrated that lesions containing a considerable amount of necrotic core tissue without evidence of an overlying fibrous cap (TCFA lesions) may be considered as a precursor of coronary plaque rupture.18 In vivo, TCFA
may be detected by VH IVUS and have indeed been more frequently observed in patients with acute coronary syndromes as compared with those with stable CAD. In a study by Rodriguez-Granillo et al,10 nonculprit, nonobstructive lesions were examined by VH
IVUS in 23 patients presenting with acute coronary syndromes and in 32 patients with stable CAD, demonstrating significantly higher incidence of TCFA in patients with acute coronary syndromes. An important finding of the present study is that TCFA were most frequently located in mixed plaques on MSCT. Accordingly, one could argue that mixed plaques might resemble high-risk lesions, because these lesions were also associated with other features of vulnerability on VH IVUS, such as an elevated amount of necrotic core tissue and less extensive calcification.18 Moreover, in studies comparing plaque
type on MSCT between patients presenting with acute coronary syndromes and stable CAD, completely calcified plaques were less prevalent in patients presenting with acute coronary syndromes.5–7 Finally, a recent study exploring potential prognostic predictors
of cardiovascular events on MSCT showed that mixed lesions were associated with adverse events on follow-up.19 Ideally, features of TCFA would be determined on MSCT
directly. Indeed, previous studies have attempted to characterize features of TCFA on MSCT.3 In comparison to grayscale IVUS, lipid core was identified on MSCT with an
accuracy of 70%.3 Nevertheless, it is important to realize that the insufficient spatial
resolution of MSCT precludes exact location of lipid accumulation in the plaque as well as visualization of the thin fibrous cap. Accordingly, direct identification of TCFA on MSCT is at present not feasible.
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Study limitations
Several limitations of the study should be acknowledged. First, noninvasive and invasive examinations were performed within 1 month. Accordingly, minor changes in plaque burden and composition may have occurred. Second, no validation of lesion length or distance measurements on MSCT and IVUS was performed and differences between modalities may have affected the accuracy of our results to a minor extent. Third, VH IVUS is a relatively new technique. Therefore, more extensive validation in larger patient populations and with the different VH IVUS systems that are available remains to be seen, while also more standardized representation of VH IVUS data is needed. Fourth, no plaque density measurements were performed on MSCT as it remains uncertain whether these measurements are reproducible. Indeed, operator dependency as well as potential variations in contrast attenuation may highly influence measurements.20 Finally, MSCT is
still associated with a substantial radiation dose, and administration of contrast material is required.
Conclusions
This study demonstrated a good correlation between quantification of calcium on MSCT and VH IVUS. In addition, plaque classification on MSCT paralleled relative plaque composition on VH IVUS, although VH IVUS provided more precise plaque characterization. Mixed plaques on MSCT were associated with high-risk features on VH IVUS, which suggests that MSCT observations might be useful for risk stratification. Further studies are needed to confirm the results.
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