Key result
Lesions with both adverse plaque and hemodynamic characteristics on coronary CTA had a significantly higher risk of causing subsequent ACS compared to those with neither (HR 11.75; 95% CI 2.85-48.51).
Why the study?
Does the addition of noninvasive hemodynamic assessment to anatomical and plaque characteristics improve the identification of high-risk plaques destined to cause ACS?
Case-Control (n=72)
Does the addition of noninvasive hemodynamic assessment to anatomical and plaque characteristics improve the identification of high-risk plaques destined to cause ACS?
Hazard Ratio: 11.75 (95% CI 2.85–48.51)
p-value: p=0.001
Noninvasive hemodynamic assessment using coronary CTA and computational fluid dynamics significantly improves the identification of high-risk plaques destined to cause acute coronary syndrome.
Supports integrated CTA plaque-hemodynamic assessment for ACS risk stratification; hypothesis-generating and requires prospective validation.
Objectives The authors investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS). Background ACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known. Methods Seventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFR CT ], change in FFR CT across the lesion [△FFR CT ], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFR CT , △FFR CT , WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC). Results The culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p < 0.001) and higher prevalence of APC (80.3% vs. 42.0%; p < 0.001) than nonculprit lesions. Regarding hemodynamic parameters, culprit lesions showed lower FFR CT and higher △FFR CT , WSS, and axial plaque stress than nonculprit lesions (all p values <0.01). Among the 3 models, model 3, which included hemodynamic parameters, showed the highest c-index, and better discrimination (concordance statistic [c-index] 0.789 vs. 0.747; p = 0.014) and reclassification abilities (category-free net reclassification index 0.287; p = 0.047; relative integrated discrimination improvement 0.368; p < 0.001) than model 2. Lesions with both APC and AHC showed significantly higher risk of the culprit for subsequent ACS than those with no APC/AHC (hazard ratio: 11.75; 95% confidence interval: 2.85 to 48.51; p = 0.001) and with either APC or AHC (hazard ratio: 3.22; 95% confidence interval: 1.86 to 5.55; p < 0.001). Conclusions Noninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775 )
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Lee et al. (2018) conducted a case-control in Acute Coronary Syndrome (n=72). Adverse plaque characteristics (APC) and adverse hemodynamic characteristics (AHC) vs. No APC/AHC was evaluated on Culprit for subsequent ACS (HR 11.75, 95% CI 2.85-48.51, p=0.001). Lesions with both adverse plaque and hemodynamic characteristics on coronary CTA had a significantly higher risk of causing subsequent ACS compared to those with neither (HR 11.75; 95% CI 2.85-48.51).
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