Elsevier

Atherosclerosis

Volume 219, Issue 2, December 2011, Pages 588-595
Atherosclerosis

Vulnerable plaque features on coronary CT angiography as markers of inducible regional myocardial hypoperfusion from severe coronary artery stenoses

https://doi.org/10.1016/j.atherosclerosis.2011.07.128Get rights and content

Abstract

Objective

We explored whether the presence of 3 known features of plaque vulnerability on coronary CT angiography (CCTA) – low attenuation plaque content (LAP), positive remodeling (PR), and spotty calcification (SC) – identifies plaques associated with greater inducible myocardial hypoperfusion measured by myocardial perfusion imaging (MPI).

Methods

We analyzed 49 patients free of cardiac disease who underwent CCTA and MPI within a 6-month period and were found on CCTA to have focal 70–99% stenosis from predominantly non-calcified plaque in the proximal or mid segment of 1 major coronary artery. Presence of LAP (≤30 Hounsfield Units), PR (outer wall diameter exceeds proximal reference by ≥5%), and SC (≤3 mm long and occupies ≤90° of cross-sectional artery circumference) was determined. On MPI, reversible hypoperfusion in the myocardial territory corresponding to the diseased artery was quantified both as percentage of total myocardium (RevTPDART) by an automatic algorithm and as summed difference score (SDSART) by two experienced readers. RevTPDART  3% and SDSART  3 defined significant inducible hypoperfusion in the territory of the diseased artery.

Results

Plaques in patients with RevTPDART  3% more frequently exhibited LAP (70% vs. 14%, p < 0.001) and PR (70% vs. 24%, p = 0.001) but not SC (55% vs. 34%, p = 0.154). RevTPDART increased from 1.3 ± 1.2% in arteries with LAP−/PR− plaques to 3.2 ± 4.3% with LAP+/PR− or LAP−/PR+ plaques to 8.3 ± 2.4% with LAP+/PR+ plaques (p < 0.001); SDSART showed a similar increase: 0.3 ± 0.7 to 2.3 ± 2.8 to 6.0 ± 3.8 (p < 0.001). Using the same LAP/PR categorization, there was a marked increase in the frequency of significant hypoperfusion as determined by both RevTPDART  3% (1/19 to 10/21 to 9/9, p < 0.001) and SDSART  3 (1/19 to 8/21 to 8/9, p < 0.001). LAP and PR, but not SC, were strong predictors of RevTPDART and SDSART in regression models adjusting for potential confounders.

Conclusions

Presence of low attenuation plaque and positive remodeling in severely stenotic plaques on CCTA is strongly predictive of myocardial hypoperfusion and may be useful in assessing the hemodynamic significance of such lesions.

Introduction

Presence of severe coronary artery stenosis (≥70% diameter) is often used as a surrogate for myocardial blood flow compromise, based on hemodynamic studies demonstrating that severe coronary artery stenosis leads to stress-induced myocardial hypoperfusion [1], [2]. Yet, a substantial proportion of severe coronary artery stenoses do not produce significant hypoperfusion on myocardial perfusion imaging (MPI) [3], [4]. In the nuclear sub-study of the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial, 40% of patients with ≥70% diameter stenosis on invasive coronary angiography exhibited none or mild myocardial hypoperfusion on single-photon emission computed tomographic MPI (SPECT-MPI) [4].

Processes that can increase myocardial hypoperfusion, including arterial wall injury and endothelial dysfunction, have been associated with specific changes in coronary plaque appearance, such as development of intra-plaque lipid core and positive vessel remodeling [5]. Non-invasive detection of lipid core (appearing as “low-attenuation” plaque, LAP), outward or “positive” vessel remodeling (PR), and spotty calcification (SC) on coronary computed tomographic angiography (CCTA) has been linked to the risk of acute coronary syndrome, denoting these findings as markers of plaque vulnerability [6]. However, whether these 3 features have impact on myocardial perfusion has not been evaluated. We conducted an exploratory study to test the hypothesis that severe coronary artery stenoses caused by plaques exhibiting LAP, PR, and/or SC result in greater myocardial hypoperfusion than similar stenoses caused by plaques that do not exhibit these features.

Section snippets

Patient population

From April 2006 through March 2011, we identified 49 consecutive patients who met all of the following criteria: no prior myocardial infarction or coronary artery revascularization, underwent both CCTA and SPECT-MPI or positron-emission tomography (PET)-MPI within a 6-month period at our center, CCTA showed severe single-vessel coronary artery stenosis from a discrete, predominantly non-calcified atherosclerotic plaque (<50% calcified component by visual estimation of whole plaque volume)

Results

Of the 49 patients studied, 34 were men (69%), and median age was 66 years. Ten patients had RevTPDART = 0%, and 34 had RevTPDART  1%, including 20 with RevTPDART  3% (range 3.2–11.4%). Locations of the severely stenotic plaques in these 20 patients were: 10 proximal and 3 mid LAD, 1 proximal and 2 mid LCX, and 3 proximal and 1 mid RCA. Reference luminal diameter on CCTA ranged between 2 and 5.5 mm with a median of 3.25 mm. Comparisons of demographic and coronary artery plaque anatomic

Discussion

In this study we demonstrated a novel relationship between coronary artery plaque morphology and myocardial hypoperfusion. In severely stenotic plaques, noninvasive detection of LAP and PR – 2 vulnerable plaque features linked to risk of acute coronary syndrome – was highly associated with increased myocardial hypoperfusion by quantitative MPI. Severe stenoses from plaques without LAP and PR produced low amounts of myocardial hypoperfusion. Importantly, these strong relationships were found

Conclusions

In this exploratory study, severe coronary arterial stenoses on CCTA from plaques exhibiting low-attenuation plaque and positive remodeling were strongly related to greater inducible myocardial hypoperfusion. These findings were independent of stenosis severity and indicate that plaque content and morphology may be useful in assessing the hemodynamic significance of severe stenoses.

Funding

Fellowship grant, American Physician-Fellowship for Medicine in Israel (Dr. Shmilovich); National Heart, Lung, and Blood Institute (Dr. Cheng, 1K23HL107458-01); American Heart Association Grant-in-Aid (Dr. Dey, 09GRNT2330000); The Lincy and Glazer Foundations (Beverly Hills, California, USA). Funding sources had no role in research conduct or preparation of the manuscript.

Disclosures

Drs. Berman, Germano, and Slomka receive QPS software royalties (Cedars-Sinai Medical Center, Los Angeles, CA, USA).

References (31)

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These authors contributed equally.

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