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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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Flowchart illustrating the hypothetical plaque progression in relation to the Nestin-positive neoangiogenesis and calcification features. According to AHA classification [10], type V plaque is the uncomplicated fibroatheroma, type VI is the complicated plaque, type VII is the calcified plaque, and type VIII is the fibrotic plaque.
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fig5: Flowchart illustrating the hypothetical plaque progression in relation to the Nestin-positive neoangiogenesis and calcification features. According to AHA classification [10], type V plaque is the uncomplicated fibroatheroma, type VI is the complicated plaque, type VII is the calcified plaque, and type VIII is the fibrotic plaque.

Mentions: The reason why in the massively calcified plaques the neoangiogenesis and the histological complications do not affect symptomatology remains unclear, but it is possible that the hemorrhages and erosions found in these plaques might have a different pathogenesis. For example, it is possible that they can be due directly by the mechanical stresses of the calcified mass and not by immature neoangiogenesis and endothelial damage. Another possible explanation is that the “calcified type VI” plaques can represent an early stage of type VII plaques, in which the regressive process is more recent, and the complications have not disappeared yet (Figure 5).


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)

Flowchart illustrating the hypothetical plaque progression in relation to the Nestin-positive neoangiogenesis and calcification features. According to AHA classification [10], type V plaque is the uncomplicated fibroatheroma, type VI is the complicated plaque, type VII is the calcified plaque, and type VIII is the fibrotic plaque.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: Flowchart illustrating the hypothetical plaque progression in relation to the Nestin-positive neoangiogenesis and calcification features. According to AHA classification [10], type V plaque is the uncomplicated fibroatheroma, type VI is the complicated plaque, type VII is the calcified plaque, and type VIII is the fibrotic plaque.
Mentions: The reason why in the massively calcified plaques the neoangiogenesis and the histological complications do not affect symptomatology remains unclear, but it is possible that the hemorrhages and erosions found in these plaques might have a different pathogenesis. For example, it is possible that they can be due directly by the mechanical stresses of the calcified mass and not by immature neoangiogenesis and endothelial damage. Another possible explanation is that the “calcified type VI” plaques can represent an early stage of type VII plaques, in which the regressive process is more recent, and the complications have not disappeared yet (Figure 5).

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