Quantifying Plaque Burden and Morphology Using Coronary Computed Tomography Angiography to Predict Coronary Physiology
2015; Lippincott Williams & Wilkins; Volume: 8; Issue: 10 Linguagem: Inglês
10.1161/circimaging.115.004058
ISSN1942-0080
AutoresMarcelo F. Di Carli, Ron Blankstein,
Tópico(s)Advanced MRI Techniques and Applications
ResumoHomeCirculation: Cardiovascular ImagingVol. 8, No. 10Quantifying Plaque Burden and Morphology Using Coronary Computed Tomography Angiography to Predict Coronary Physiology Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBQuantifying Plaque Burden and Morphology Using Coronary Computed Tomography Angiography to Predict Coronary PhysiologyHelpful…But Is It Sufficient? Marcelo F. Di Carli, MD and Ron Blankstein, MD Marcelo F. Di CarliMarcelo F. Di Carli From the Noninvasive Cardiovascular Imaging Program, Heart and Vascular Institute, Division of Cardiovascular Medicine, Department of Medicine, Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. and Ron BlanksteinRon Blankstein From the Noninvasive Cardiovascular Imaging Program, Heart and Vascular Institute, Division of Cardiovascular Medicine, Department of Medicine, Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. Originally published14 Oct 2015https://doi.org/10.1161/CIRCIMAGING.115.004058Circulation: Cardiovascular Imaging. 2015;8:e004058Now this is not the end. It is not even the beginning of the end. But it is, perhaps, the end of the beginning.—Winston ChurchillCoronary computed tomography angiography (CTA) is a powerful noninvasive technique that can be used to visualize the presence, extent, and severity of both noncalcified and calcified plaque. When compared with other noninvasive imaging approaches, coronary CTA has the highest sensitivity to detect anatomic stenosis and, consequently, the highest negative predictive value to exclude obstructive coronary artery disease (CAD).1 However, once a coronary stenosis is identified, a limitation of CTA—which is equally problematic for invasive coronary angiography—is that the physiological consequences associated with those stenoses cannot be determined with any degree of accuracy.2,3 On the other hand, the presence and severity of ischemia are essential for understanding the pathophysiology of patient's symptoms and determining the potential role of coronary revascularization. Consequently, multiple techniques have been introduced to harness physiological data from CTA and infer whether a stenosis is hemodynamically significant. Some investigators have applied computational fluid dynamic modeling to estimate coronary pressure gradients and calculation of the fractional flow reserve across stenosis.4 Others have relied on the use of iodinated contrast at rest and during pharmacological stress to assess myocardial perfusion (computed tomography [CT] perfusion)5 in a similar manner to radionuclide scintigraphy and magnetic resonance imaging–based myocardial perfusion techniques. Recent clinical trials have demonstrated that in carefully selected patients, these techniques can provide useful information to understand the physiological significance of stenoses.6–9 So, it is clear that the paradigm of isolated stenosis quantification with angiography (noninvasive or invasive) has provided insufficient and, sometimes, misleading information for diagnosis and management of CAD. However, there is limited data addressing the question of whether a more complete quantification of the atherosclerotic burden with coronary CTA, including all stenosis dimensions and other plaque characteristics, can improve discrimination of flow-limiting lesions.See Article by Dey et alIn this issue of Circulation: Cardiovascular Imaging, Dey et al10 evaluated the quantitative relationship between stenosis dimensions and x-ray–based characteristics of coronary plaques and myocardial blood flow and coronary flow reserve (CFR)—a validated measure of the functional severity of coronary stenosis. The study included 51 symptomatic patients with known or suspected CAD undergoing vasodilator stress positron emission tomography (PET) myocardial perfusion imaging followed by coronary CTA on an integrated PET/CT system. Coronary flow reserve was calculated as the ratio of myocardial blood flow (in mL/min/g) during vasodilator stress over that at rest. Total coronary plaque volume and burden (plaque volume index by vessel volume), percent stenosis, plaque length, vessel remodeling, and x-ray–based plaque characteristics (calcified and noncalcified) were also quantified from coronary CTA. Overall, 19/51 patients and 41/151 vessels showed reduced coronary flow reserve (ie, <2.0). Compared with myocardial territories with normal CFR, those with reduced flow reserve were supplied by vessels containing larger total and noncalcified plaque burden and lesions that were longer and more angiographically obstructive. As expected, each of these CT angiographic features correlated inversely with vessel-based CFR. In multivariable analysis, the burden of noncalcified plaque but not the percent stenosis, lesion length, or vessel remodeling associated with reduced CFR. Using machine learning, they showed that a composite risk score integrating age, sex, and CT-based plaque characteristics (noncalcified plaque) was a better discriminator of vessels with impaired CFR than the stenosis severity alone. These results are consistent with a recent study by Park et al11 demonstrating that total plaque volume and an aggregate model, including plaque volume, lesion length, and low attenuation plaques on coronary CTA, improved identification of stenosis associated with abnormal invasive fractional flow reserve.How does one interpret the fact that the noncalcified plaque burden, not percent stenosis or lesion length, was a significant predictor of impaired CFR?The authors hypothesized that noncalcified plaque, a marker of clinical risk pathologically linked with inflammation, may be an anatomic surrogate of vascular endothelial cell dysfunction and impaired vascular reactivity. Although this is an appealing and certainly plausible theory, it cannot be determined from this study because noncalcified plaques accounted for almost 90% of the total plaque burden in this cohort. A more likely explanation is that the total plaque burden, which was almost entirely noncalcified, was inversely correlated with CFR primarily because of its adverse fluid dynamic effect on the functional pressure–flow characteristics of those plaques. This is likely the underlying mechanism for the association between low attenuation plaque and reduced fractional flow reserve in the study by Park et al11 because this association was restricted to vessels with ≥50% stenosis.Assessing the functional significance of stenosis from invasive or noninvasive quantitative coronary angiography is challenging because the individual pressure–flow characteristics of a coronary plaque depend in part on a variety of anatomic descriptors, including its minimal luminal diameter, length, and degree of lesion asymmetry. There is general agreement that no single anatomic feature or measurement can describe the stenosis appearance or account for the different anatomic shapes that have important hemodynamic consequences. Like in Park's study,11 the current analysis demonstrates that the logical integration of various anatomic descriptors of a coronary stenosis into a risk score can improve predictions of abnormal coronary hemodynamics. Although this is a step forward in the field of coronary CT imaging and a strength of the study, the concept is not new. More than 25 years ago, Gould and colleagues have demonstrated the validity of invasive quantitative coronary angiography for predicting the hemodynamic significance of stenoses if all the dimensions of the lesion are taken into account.12Although statistically significant, the observed correlations between the various anatomic descriptors of stenosis by CTA and coronary flow reserve in the current study were modest. This was also the case in Park's study,11 as well as in other studies using quantitative coronary angiography.13–15 It is important to recognize that myocardial blood flow is dependent on many other factors besides proximal coronary stenosis, such as aortic pressure,12 diffuse coronary atherosclerosis,16 microvascular function,17 and collateral blood flow.12 All these factors are more difficult to measure by coronary CTA. The prediction model incorporating coronary stenosis dimensions as used in this study, and in Park's,11 represents only one component of the complex anatomic–physiological model system, whereas myocardial tissue perfusion and patient symptoms depend on the response of the total integrated system. For example, a stenosis that does not produce a flow limitation and chest pain in one patient with preserved microvascular function or robust downstream collateral flow might result in severe functional limitation and ischemia in another with diffuse atherosclerosis or microvascular dysfunction.18What are the clinical implications of the integrated CT-based prediction model? The first question is whether the integrated anatomic stenosis model will be able to identify patients with flow-limiting CAD in need of revascularization as suggested by the authors. Of course, it is too early to tell. From a clinical viewpoint, however, the binary prediction of normal or abnormal coronary flow reserve is unlikely to be useful because decisions regarding the need of potential revascularization are rarely binary. Rather, these decisions are based on the severity of symptoms, clinical risk, and importantly, quantitative measurements of the severity of blood flow deficit and resulting myocardial ischemia. Therefore, the direct measurement of coronary flow reserve is a more appealing concept because it integrates all the geometric characteristics of a stenosis combined with the downstream effect of diffuse atherosclerosis, vessel remodeling, collateral flow, and microvascular function into a single measure of tissue perfusion and myocardial ischemia. Indeed, a normal CFR effectively excludes the presence of high risk angiographic CAD19,20 and helps reclassify risk in patients with known or suspected CAD.21–23 More importantly, emerging evidence suggests that a reduced CFR may help identify patients who benefit most from revascularization.18A potentially more promising application of the comprehensive CTA model of plaque characterization is for risk assessment and, potentially, guiding the intensity of preventative medical therapy. Over the last decade, multiple important studies have shown that increasing burden and severity of CAD on CTA is associated with incident all-cause death as well as adverse cardiovascular outcomes.24–27 Most of these studies showed these associations for patients who had stenosis on their CTA. More recently, it has been recognized that even nonobstructive plaque, especially when extensive, may be associated with adverse outcomes, including myocardial infarction and all-cause death.27,28 More recently, risk scores that incorporate the volume, anatomic extent, location, and type of plaque by CTA have demonstrated their potential value in risk assessment,29 especially in patients with angiographically nonobstructive CAD. The increased risk associated with having diffuse plaque has also been observed in patients undergoing invasive angiography.30 It has been hypothesized that clinical risk in these patients may be related to heightened activity of disease biology, which is difficult to ascertain by anatomic descriptors of CAD alone. In fact, circulating inflammatory biomarkers (including C-reactive protein, interleukin-6, fibrinogen, matrix metalloproteinase-9, membrane cofactor protein-1, tumor necrosis factor-α, and others) have been found to have only a weak association with the burden of atherosclerosis.31 This has been identified as a potential role for molecularly targeted imaging.32 This also opens the door for a complementary role of measures of coronary vasodilator function (eg, coronary flow reserve),33 reflecting the integrated effects of diffuse atherosclerosis and endothelial dysfunction. Quantitative coronary flow reserve provides a sensitive, accurate, and reproducible measure of the effects of disease biology that, unlike circulating biomarkers, is specific to the coronary circulation. Thus, CFR may be a useful surrogate marker of disease activity that reflects active pathophysiologic changes, which are more readily reversible with medical and lifestyle interventions.In summary, advances in noninvasive imaging are paving the way for precise and individualized quantitative phenotyping of CAD burden and risk. The comprehensive quantitative approach with coronary CT described by Dey et al represents a step forward from the traditional binary interpretation of stenosis severity, which has provided only partial answers to diagnosis, risk stratification, and most importantly, patient management. However, it is increasingly clear from this and other studies that the answers to these challenges will likely require the integration of quantitative information that describes both structure and function. Connecting the powerful, complementary biomarkers emerging from noninvasive imaging about CAD structure and function will offer a unique opportunity to better interpret the dynamic nature of the complex anatomic–physiological system, which will enable more informed decisions about patient management. Perhaps only then we will realize that the whole is greater than the sum of the parts.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Correspondence to Marcelo F. Di Carli, MD, Brigham and Women's Hospital, ASB-L1 037-C, 75 Francis St, Boston, MA 02115. E-mail [email protected]References1. 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