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Diffuse calcifications protect carotid plaques regardless of the amount of neoangiogenesis and related histological complications.

Vasuri F, Fittipaldi S, Pini R, Degiovanni A, Mauro R, D'Errico-Grigioni A, Faggioli G, Stella A, Pasquinelli G - Biomed Res Int (2015)

Bottom Line: Diffusely calcified plaques (13/73) were found predominantly in females (P = 0.017), with a significantly lower incidence of symptoms (TIA/stroke (P = 0.019) than noncalcified plaques but with the same incidence of histological complications (P = 0.156)).Nestin density, but not CD34, correlated with the occurrence of intraplaque hemorrhage.These results can be applied in a future presurgical identification of patients at major risk of developing symptoms.

View Article: PubMed Central - PubMed

Affiliation: Pathology Unit, Department of Experimental, Diagnostic and Specialty Medicine (DIMES), S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, 40138 Bologna, Italy.

ABSTRACT

Background: Neoangiogenesis is crucial in plaque progression and instability. Previous data from our group showed that Nestin-positive intraplaque neovessels correlated with histological complications. The aim of the present work is to evaluate the relationship between neoangiogenesis, plaque morphology, and clinical instability of the plaque.

Materials and methods: Seventy-three patients (53 males and 20 females, mean age 71 years) were consecutively enrolled. Clinical data and 14 histological variables, including intraplaque hemorrhage and calcifications, were collected. Immunohistochemistry for CD34 and Nestin was performed. RT-PCR was performed to evaluate Nestin mRNA (including 5 healthy arteries as controls).

Results: Diffusely calcified plaques (13/73) were found predominantly in females (P = 0.017), with a significantly lower incidence of symptoms (TIA/stroke (P = 0.019) than noncalcified plaques but with the same incidence of histological complications (P = 0.156)). Accordingly, calcified and noncalcified plaques showed similar mean densities of positivity for CD34 and Nestin. Nestin density, but not CD34, correlated with the occurrence of intraplaque hemorrhage.

Conclusions: Plaques with massive calcifications show the same incidence of histological complications but without influencing symptomatology, especially in female patients, and regardless of the amount of neoangiogenesis. These results can be applied in a future presurgical identification of patients at major risk of developing symptoms.

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Difference in Nestin mRNA expression between type V (uncomplicated) and type VI (complicated) plaques (*P < 0.001).
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fig3: Difference in Nestin mRNA expression between type V (uncomplicated) and type VI (complicated) plaques (*P < 0.001).

Mentions: At RT-PCR, the total mean extracted mRNA from healthy tissue and type V and type VI plaques was 8764 ng, 5069.4 ng, and 2172 ng, respectively. The mean CT values of endogenous control GUSB were 36.28 ± 0.21 in healthy tissue, 31.36 ± 0.32 in type V plaques, and 34.20 ± 0.22 in type VI plaques. Mean CT for tested gene Nestin were 33.04 ± 0.06 in healthy tissue, 32.37 ± 0.12 in type V plaques, and 34.21 ± 0.30 in type VI plaques. ΔΔCT Nestin was significantly different from 0 (P = 0.0001); thus the hypothesis was rejected, which indicated a change in Nestin gene expression among healthy, type V and type VI plaques. In type V and type VI plaques, the mean ΔΔCT Nestin was, respectively, 4.25 and 3.25; this corresponds to 2−(ΔΔCT) of 0.05 for Nestin gene expression in type V plaques and 0.11 in type VI plaques. The type VI plaques showed a 2-fold expression increase for Nestin gene compared to type V plaques, as a confirmation of the IHC results (Figure 3).


Diffuse calcifications protect carotid plaques regardless of the amount of neoangiogenesis and related histological complications.

Vasuri F, Fittipaldi S, Pini R, Degiovanni A, Mauro R, D'Errico-Grigioni A, Faggioli G, Stella A, Pasquinelli G - Biomed Res Int (2015)

Difference in Nestin mRNA expression between type V (uncomplicated) and type VI (complicated) plaques (*P < 0.001).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4389976&req=5

fig3: Difference in Nestin mRNA expression between type V (uncomplicated) and type VI (complicated) plaques (*P < 0.001).
Mentions: At RT-PCR, the total mean extracted mRNA from healthy tissue and type V and type VI plaques was 8764 ng, 5069.4 ng, and 2172 ng, respectively. The mean CT values of endogenous control GUSB were 36.28 ± 0.21 in healthy tissue, 31.36 ± 0.32 in type V plaques, and 34.20 ± 0.22 in type VI plaques. Mean CT for tested gene Nestin were 33.04 ± 0.06 in healthy tissue, 32.37 ± 0.12 in type V plaques, and 34.21 ± 0.30 in type VI plaques. ΔΔCT Nestin was significantly different from 0 (P = 0.0001); thus the hypothesis was rejected, which indicated a change in Nestin gene expression among healthy, type V and type VI plaques. In type V and type VI plaques, the mean ΔΔCT Nestin was, respectively, 4.25 and 3.25; this corresponds to 2−(ΔΔCT) of 0.05 for Nestin gene expression in type V plaques and 0.11 in type VI plaques. The type VI plaques showed a 2-fold expression increase for Nestin gene compared to type V plaques, as a confirmation of the IHC results (Figure 3).

Bottom Line: Diffusely calcified plaques (13/73) were found predominantly in females (P = 0.017), with a significantly lower incidence of symptoms (TIA/stroke (P = 0.019) than noncalcified plaques but with the same incidence of histological complications (P = 0.156)).Nestin density, but not CD34, correlated with the occurrence of intraplaque hemorrhage.These results can be applied in a future presurgical identification of patients at major risk of developing symptoms.

View Article: PubMed Central - PubMed

Affiliation: Pathology Unit, Department of Experimental, Diagnostic and Specialty Medicine (DIMES), S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, 40138 Bologna, Italy.

ABSTRACT

Background: Neoangiogenesis is crucial in plaque progression and instability. Previous data from our group showed that Nestin-positive intraplaque neovessels correlated with histological complications. The aim of the present work is to evaluate the relationship between neoangiogenesis, plaque morphology, and clinical instability of the plaque.

Materials and methods: Seventy-three patients (53 males and 20 females, mean age 71 years) were consecutively enrolled. Clinical data and 14 histological variables, including intraplaque hemorrhage and calcifications, were collected. Immunohistochemistry for CD34 and Nestin was performed. RT-PCR was performed to evaluate Nestin mRNA (including 5 healthy arteries as controls).

Results: Diffusely calcified plaques (13/73) were found predominantly in females (P = 0.017), with a significantly lower incidence of symptoms (TIA/stroke (P = 0.019) than noncalcified plaques but with the same incidence of histological complications (P = 0.156)). Accordingly, calcified and noncalcified plaques showed similar mean densities of positivity for CD34 and Nestin. Nestin density, but not CD34, correlated with the occurrence of intraplaque hemorrhage.

Conclusions: Plaques with massive calcifications show the same incidence of histological complications but without influencing symptomatology, especially in female patients, and regardless of the amount of neoangiogenesis. These results can be applied in a future presurgical identification of patients at major risk of developing symptoms.

Show MeSH
Related in: MedlinePlus