Dataset Information

Comparison of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation.

ABSTRACT:

Background

The renin-angiotensin system plays an important role in promoting atherosclerotic plaque inflammation, which may be inhibited by angiotension-II receptor blockers.

Hypothesis

We investigated the effects of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation using ¹⁸ F-fluorodeoxyglucose (¹⁸ FDG) positron emission tomography (PET) imaging.

Methods

Fifty patients with acute coronary syndrome (ACS) and at least one lesion with ¹⁸ FDG uptake in the carotid artery (target-to-background ratio [TBR] ≥ 1.6) were randomly assigned to receive either fimasartan (60 mg once a day) or amlodipine (5 mg once a day). ¹⁸ FDG PET examinations were performed in all patients at baseline and 6 months. The primary endpoint was the percent change in the index vessel TBR for the most diseased segment (MDS TBR).

Results

The two groups had similar baseline characteristics. At the 6-month follow-up, index vessel and aorta MDS TBR significantly decreased in both groups. However, the percent change in index vessel MDS TBR was similar between the two groups (-9.33 ± 14.2% vs -7.73 ± 19.1%, respectively, P = 0.9). No significant difference was found for the percent change in the whole vessel TBR for the index vessel between the two groups, with similar findings for changes in MDS TBR or whole vessel TBR for the aorta. Total cholesterol, low-density lipoprotein cholesterol levels, and blood pressure improved to a similar degree in both groups.

Conclusions

Fimasartan and amlodipine reduce carotid atherosclerotic plaque inflammation similarly in patients with ACS, offering the same level of effectiveness.

SUBMITTER: Oh M

PROVIDER: S-EPMC6712325 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Publications

Comparison of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation.

Oh Minyoung M Lee Cheol Whan CW Ahn Jung-Min JM Park Duk-Woo DW Kang Soo-Jin SJ Lee Seung-Whan SW Kim Young-Hak YH Moon Dae Hyuk DH Park Seong-Wook SW Park Seung-Jung SJ

Clinical cardiology 20181220 2

<h4>Background</h4>The renin-angiotensin system plays an important role in promoting atherosclerotic plaque inflammation, which may be inhibited by angiotension-II receptor blockers.<h4>Hypothesis</h4>We investigated the effects of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation using <sup>18</sup> F-fluorodeoxyglucose (<sup>18</sup> FDG) positron emission tomography (PET) imaging.<h4>Methods</h4>Fifty patients with acute coronary syndrome (ACS) and at least one ...[more]

PMID: 30537083

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Project description:ObjectiveCarotid endarterectomy for symptomatic carotid stenosis is recommended for patients with >70% stenosis, but not in those with <50%. Because non-significant, low-degree stenoses may still cause strokes, refined risk stratification is necessary, which could be improved by assessing biological features of plaque instability. To challenge risk-stratification based on luminal narrowing, we compared biological features of carotid plaques from symptomatic patients with low-degree (<50%) vs high-degree (>70%) stenosis and explored potential mechanisms behind plaque instability in low-degree stenoses.MethodsEndarterectomy specimens were taken from symptomatic patients with high-degree (n = 204) and low-degree (n = 34) stenosis, all part of the Biobank of Karolinska Endarterectomies. Patient demographics, image-derived plaque morphology, and gene expression analyses of extracted lesions were used for comparisons. Plaque biology was assessed by transcriptomics using dimensionality reduction, differential gene expression, and gene-set enrichment analyses. Immunohistochemistry was used to study proteins corresponding to upregulated genes.ResultsThe demographics of the two groups were statistically similar. Calcification, lipid-rich necrotic core, intraplaque hemorrhage, plaque burden, and fibrous cap thickness were similar in both groups, whereas the sum of lipid-rich necrotic core and intraplaque hemorrhage was higher (P = .033) in the high-degree stenosis group. Dimensionality reduction analysis indicated poor clustering separation of plaque gene expression in low-compared with high-degree stenosis lesions, whereas differential gene expression showed upregulation of hypoxia-inducible factor 3A (log2 fold change, 0.7212; P = .0003), and gene-set enrichment analyses identified pathways related to tissue hypoxia and angiogenesis in low-degree stenoses. Hypoxia-inducible factor 3-alpha protein was associated with smooth muscle cells in neo-vascularized plaque regions.ConclusionsPlaques from symptomatic patients with non-significant low-degree carotid stenoses showed morphologic and biological features of atherosclerotic plaque instability that were comparable to plaques from patients with high-degree stenoses, emphasizing the need for improved stroke risk stratification for intervention in all patients with symptomatic carotid stenosis irrespective of luminal narrowing. An increased expression of hypoxia-inducible factor 3A in low-degree stenotic lesions suggested mechanisms of plaque instability associated with tissue hypoxia and plaque angiogenesis, but the exact role of hypoxia-inducible factor 3A in this process remains to be determined.Clinical relevanceCarotid plaques from symptomatic patients with <50% stenosis show morphologic and biological features of plaque instability, comparable to high-degree stenosis, which emphasizes the need for improved stroke risk stratification beyond stenosis severity.

Dataset Information

Comparison of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation.

Background

Hypothesis

Methods

Results

Conclusions

Publications

Comparison of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation.

Similar Datasets

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