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Association of HIV infection with age and symptomatic carotid atherosclerotic disease at the time of carotid intervention in the United States.

ABSTRACT: The primary objectives of this work were: (1) to describe trends in HIV prevalence among those undergoing carotid intervention (carotid endarterectomy or carotid artery stenting) in the United States; and (2) to determine if HIV infection is independently associated with symptomatic carotid atherosclerotic disease or age at the time of carotid intervention. In a nationally representative inpatient database from 2004 to 2014, HIV infection was associated with younger age at the time of carotid intervention (59 years [SE 0.2] vs 71 years [SE 0.01], p < 0.001), male sex (83% vs 58%, p < 0.001), black race (21% vs 4%, p < 0.001), and symptomatic carotid atherosclerotic disease (18.8% vs 11.0%, p < 0.001). Among those undergoing carotid intervention, there was a significant increase in the prevalence of HIV from 0.08% in 2004 to 0.17% in 2014 ( p < 0.001). After adjustment for patient demographics, comorbidities and other covariates, HIV infection remained significantly associated with younger age (-8.9 years; 95% CI: -9.7 to -8.1; p < 0.001) at the time of carotid intervention, but HIV infection was not independently associated with symptomatic carotid atherosclerotic disease.

SUBMITTER: Lin TC

PROVIDER: S-EPMC6380352 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Association of HIV infection with age and symptomatic carotid atherosclerotic disease at the time of carotid intervention in the United States.

Lin Timothy C TC Burton Brittany N BN Barleben Andrew A Hoenigl Martin M Gabriel Rodney A RA

Vascular medicine (London, England) 20180813 5

The primary objectives of this work were: (1) to describe trends in HIV prevalence among those undergoing carotid intervention (carotid endarterectomy or carotid artery stenting) in the United States; and (2) to determine if HIV infection is independently associated with symptomatic carotid atherosclerotic disease or age at the time of carotid intervention. In a nationally representative inpatient database from 2004 to 2014, HIV infection was associated with younger age at the time of carotid in ...[more]

PMID: 30101684

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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

Association of HIV infection with age and symptomatic carotid atherosclerotic disease at the time of carotid intervention in the United States.

Publications

Association of HIV infection with age and symptomatic carotid atherosclerotic disease at the time of carotid intervention in the United States.

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