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Stabilization of symptomatic carotid atherosclerotic plaques by statins: a clinico-pathological analysis.

ABSTRACT: Human and animal studies have revealed a stabilization of atherosclerotic plaques by statins. However, the stabilization of human carotid plaques has not been thoroughly described pathologically. This analysis explored the relationship between statin therapy and plaque stability in carotid endarterectomy (CEA) specimens. We analyzed specimens harvested between May 2015 and February 2017, from 79 consecutive patients presenting with?>?70% carotid artery stenoses, of whom 66 were untreated (group 1) and 13 treated (group 2) with a statin. Immunohistochemistry was performed, using an endothelial specific antibody to CD31, CD34 and platelet derived growth factor receptor-?. The prevalence of plaque ruptures (P?=?0.009), lumen thrombi (P?=?0.009), inflammatory cells (P?=?0.008), intraplaque hemorrhages (P?=?0.030) and intraplaque microvessels (P??1.0 cm3 on magnetic resonance imaging, the mean infarct volume was significantly smaller (P?=?0.031) in group 2 (4.2?±?2.5 cm3) than in group 1 (8.2?±?7.1 cm3). The difference in mean concentration of low-density lipoprotein cholesterol between group 1 (121?±?32 mg/dl) and group 2 (105?±?37 mg/dl) was non-significant (P?=?0.118). This analysis of plaques harvested from patients undergoing CEA suggests that statin therapy mitigates the plaque instability, which, in patients presenting with strokes, might decrease infarct volume.

SUBMITTER: Konishi T

PROVIDER: S-EPMC6208692 | biostudies-other | 2018 Nov

REPOSITORIES: biostudies-other

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Stabilization of symptomatic carotid atherosclerotic plaques by statins: a clinico-pathological analysis.

Konishi Takao T Funayama Naohiro N Yamamoto Tadashi T Hotta Daisuke D Nomura Ryota R Nakagaki Yusuke Y Murahashi Takeo T Kamiyama Kenji K Yoshimoto Tetsuyuki T Aoki Takeshi T Tanaka Shinya S

Heart and vessels 20180522 11

Human and animal studies have revealed a stabilization of atherosclerotic plaques by statins. However, the stabilization of human carotid plaques has not been thoroughly described pathologically. This analysis explored the relationship between statin therapy and plaque stability in carotid endarterectomy (CEA) specimens. We analyzed specimens harvested between May 2015 and February 2017, from 79 consecutive patients presenting with > 70% carotid artery stenoses, of whom 66 were untreated (group ...[more]

PMID: 29789903

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Project description:To determine if black-blood 3 T cardiovascular magnetic resonance (bb-CMR) can depict differences between symptomatic and asymptomatic carotid atherosclerotic plaques in acute ischemic stroke patients.In this prospective monocentric observational study 34 patients (24 males; 70 ±9.3 years) with symptomatic carotid disease defined as ischemic brain lesions in one internal carotid artery territory on diffusion weighted images underwent a carotid bb-CMR at 3 T with fat-saturated pre- and post-contrast T1w-, PDw-, T2w- and TOF images using surface coils and Parallel Imaging techniques (PAT factor = 2) within 10 days after symptom onset. All patients underwent extensive clinical workup (lab, brain MR, duplex sonography, 24-hour ECG, transesophageal echocardiography) to exclude other causes of ischemic stroke. Prevalence of American Heart Association lesion type VI (AHA-LT6), status of the fibrous cap, presence of hemorrhage/thrombus and area measurements of calcification, necrotic core and hemorrhage were determined in both carotid arteries in consensus by two reviewers who were blinded to clinical information. McNemar and Wilcoxon's signed rank tests were use for statistical comparison. A p-value <0.05 was considered statistically significant.Symptomatic plaques showed a higher prevalence of AHA-LT6 (67.7% vs. 11.8%; p?<?0.001; odds ratio?=?12.5), ruptured fibrous caps (44.1% vs. 2.9%; p?<?0.001; odds ratio?=?15.0), juxtaluminal thrombus (26.5 vs. 0%; p?<?0.01; odds ratio?=?7.3) and intraplaque hemorrhage (58.6% vs. 11.8%; p?=?0.01; odds ratio?=?3.8). Necrotic core and hemorrhage areas were greater in symptomatic plaques (14.1 mm2 vs. 5.5 mm2 and 13.6 mm2 vs. 5.3 mm2; p?<?0.01, respectively).3 T bb-CMR is able to differentiate between symptomatic and asymptomatic carotid plaques, demonstrating the potential of bb-CMR to differentiate between stable and vulnerable lesions and ultimately to identify patients with low versus high risk for cardiovascular complications. Best predictors of the symptomatic side were a ruptured fibrous cap, AHA-LT 6, juxtaluminal hemorrhage/thrombus, and intraplaque hemorrhage.

Project description:BACKGROUND:The identification of patients with high-risk atherosclerotic plaques prior to the manifestation of clinical events remains challenging. Recent findings question histology- and imaging-based definitions of the "vulnerable plaque," necessitating an improved approach for predicting onset of symptoms. METHODS:We performed a proteomics comparison of the vascular extracellular matrix and associated molecules in human carotid endarterectomy specimens from 6 symptomatic versus 6 asymptomatic patients to identify a protein signature for high-risk atherosclerotic plaques. Proteomics data were integrated with gene expression profiling of 121 carotid endarterectomies and an analysis of protein secretion by lipid-loaded human vascular smooth muscle cells. Finally, epidemiological validation of candidate biomarkers was performed in two community-based studies. RESULTS:Proteomics and at least one of the other two approaches identified a molecular signature of plaques from symptomatic patients that comprised matrix metalloproteinase 9, chitinase 3-like-1, S100 calcium binding protein A8 (S100A8), S100A9, cathepsin B, fibronectin, and galectin-3-binding protein. Biomarker candidates measured in 685 subjects in the Bruneck study were associated with progression to advanced atherosclerosis and incidence of cardiovascular disease over a 10-year follow-up period. A 4-biomarker signature (matrix metalloproteinase 9, S100A8/S100A9, cathepsin D, and galectin-3-binding protein) improved risk prediction and was successfully replicated in an independent cohort, the SAPHIR study. CONCLUSION:The identified 4-biomarker signature may improve risk prediction and diagnostics for the management of cardiovascular disease. Further, our study highlights the strength of tissue-based proteomics for biomarker discovery. FUNDING:UK: British Heart Foundation (BHF); King's BHF Center; and the National Institute for Health Research Biomedical Research Center based at Guy's and St Thomas' NHS Foundation Trust and King's College London in partnership with King's College Hospital. Austria: Federal Ministry for Transport, Innovation and Technology (BMVIT); Federal Ministry of Science, Research and Economy (BMWFW); Wirtschaftsagentur Wien; and Standortagentur Tirol.

Dataset Information

Stabilization of symptomatic carotid atherosclerotic plaques by statins: a clinico-pathological analysis.

Publications

Stabilization of symptomatic carotid atherosclerotic plaques by statins: a clinico-pathological analysis.

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