Dataset Information

Non-lipid-rich low attenuation plaque with intraplaque haemorrhage assessed by multimodality imaging: a case report.

ABSTRACT:

Background

The lipid-rich necrotic core is a major pathological hallmark of acute coronary syndrome. Low attenuation plaque (LAP) on coronary computed tomography angiography (CCTA), defined as plaque CT attenuation of <30 Hounsfield units, is commonly believed to correspond to the lipid component. This report presents a non-lipid-rich LAP with intraplaque haemorrhage of the left main coronary artery (LM), as assessed by CCTA, near-infrared spectroscopy (NIRS), and non-contrast magnetic resonance imaging (MRI) using coronary atherosclerosis T1-weighted characterization with integrated anatomical reference technique, recently developed by our group.

Case summary

A 75-year-old woman presented with chest discomfort on exertion. Coronary computed tomography angiography revealed severe stenosis of the mid-left circumflex coronary artery and minimal stenosis with a large eccentric LM plaque. The LM lesion had an LAP, with a minimum plaque attenuation of 25 Hounsfield units. On non-contrast T1-weighted MRI, a high-intensity plaque with a plaque-to-myocardium signal intensity ratio of 3.02 was observed within the vessel wall, indicating intraplaque haemorrhage. Near-infrared spectroscopy categorized the lesion as non-lipid-rich, with a maximum lipid core burden index in 4 mm of 169.

Discussion

Intraplaque haemorrhage is a key feature of plaque instability, which is different from the lipid-rich necrotic core. Non-contrast T1-weighted MRI is ideal for detecting intraplaque haemorrhage with short T1 values. The imaging findings suggest that LAP on CCTA may represent not only lipid-rich plaques but also intraplaque haemorrhage. Magnetic resonance imaging provides a unique insight into plaque vulnerability from a different perspective than lipid assessment. Multimodality imaging, including MRI, facilitates the understanding of complicated plaque morphologies.

Keywords

Atherosclerosis • Case report • Computed tomography • Intraplaque haemorrhage • Lipid-rich plaque • Magnetic resonance imaging • Near-infrared spectroscopy-intravascular ultrasound.

SUBMITTER: Matsumoto H

PROVIDER: S-EPMC8728716 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundIntraplaque hemorrhage (IPH) is associated with plaque progression and ischemic events, and plaque lipid content (% lipid core) predicts the residual atherosclerotic cardiovascular disease risk. This study examined the impact of IPH on lipid content change in the setting of intensive lipid-lowering therapy.MethodsIn total, 214 AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low High-Density Lipoprotein/High Triglycerides: Impact on Global Health Outcomes) participants with clinically established ASCVD and low high-density lipoprotein cholesterol received cartoid MRI at baseline and 2 years to assess changes in carotid morphology and composition. Patients were randomized to extended-release niacin or placebo, and all received simvastatin with optional ezetimibe as necessary to lower low-density lipoprotein cholesterol to 40 to 80 mg/dL. Changes in lipid content and carotid morphology were tested using the Wilcoxon signed-rank test. Differences between subjects with and without IPH and between subjects assigned extended-release niacin or placebo were tested using the Wilcoxon rank-sum test. Linear regression was used to test the association of IPH and lipid content changes after adjusting for clinical risk factors.ResultsAmong 156 patients (61±9 years; 81% men) with complete MRI, prior statin use: <1 year, 26%; 1 to 5 years, 37%; >5 years, 37%. Triglycerides and ApoB decreased significantly, whereas high-density lipoprotein cholesterol and ApoA1 increased significantly over time. Plaque lipid content was significantly reduced (-0.5±2.4 %/year, P = 0.017) without a significant difference between the 2 treatment groups. However, the lipid content increased in plaques with IPH but regressed in plaques without IPH (1.2±2.5 %/year versus -1.0±2.2, P = 0.006). Additionally, IPH was associated with a decrease in lumen area (-0.4±0.9 mm2/year versus 0.3±1.4, P = 0.033). IPH remained significantly associated with increase in lipid content in multivariable analysis (54.4%, 95% CI: 26.8, 88.0, P < 0.001).ConclusionsCarotid plaques under continued intensive lipid-lowering therapy moved toward stabilization. However, plaques with IPH showed greater increases in lipid content and greater decreases in lumen area than plaques without IPH.RegistrationURL: https://www.Clinicaltrialsgov; Unique identifier: NCT01178320.