Hipertension in Patients Submitted to Carotid Endarterectomy. Does Hypertension Predispose of Trigger Intraplaque Carotid Hemorrhage?

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Abstract

Background

It was suggested that hypertension (HT) may be a predisposing factor in the rupture of the neoformed vessels and the development of intraplaque hemorrhage (IPH). However, few attempts have been made to characterize the pathogenesis of these lesions.

Objective

In order to obtain information about the role of HT in the genesis of complicated carotid plaques (CCP) 195 endarterectomies from 191 patients were studied.

Material and methods

Specimens belonged to 143 hypertensives (age: 68.6 ± 8 years) and 48 non-hypertensives (age: 67.8± 8.9 years). Aside from histological staining, immunophenotyping of cells, apoptosis by DNA nick end labelling and chromosomes 7 and11, and FGF-3 gene amplification by FISH were per-formed.

Results

No differences were found among groups regarding the plaque type. CCP showed at the site of erosion loss of endothelial cells CD34+ &CD31+,a large number of macrophages and T-cells. In the IPH neoformed vessels (CD34+ & CD31+) surrounded by mononuclear infiltrates, high percentages of trisomy and tetrasomy of chromosome 7 and monosomy of chromosome 11 and gene amplification of locus 11q13.3 were ob-served. Apoptosis was very frequent (10-30%) in the high cellularity regions, where the infiltration of smooth muscle cells and macrophages was evident. Neither apoptosis (0-0.5%, p < 0.001)nor chromosomal and FGF-3 alterations were ob-served in non-CCP.

Conclusions

These findings suggest that the IPH might be due to the breakdown of neoformed vessels related to inflammatory infiltrates; imbalance between clonal cell growth and high rate apoptosis may account for the evolution of CCP, independent from HT.