Impact of Femoral Ossification on Local and Systemic Cardiovascular Patients' Condition.


Journal

Annals of vascular surgery
ISSN: 1615-5947
Titre abrégé: Ann Vasc Surg
Pays: Netherlands
ID NLM: 8703941

Informations de publication

Date de publication:
Oct 2019
Historique:
received: 08 08 2018
revised: 22 02 2019
accepted: 01 03 2019
pubmed: 15 6 2019
medline: 24 12 2019
entrez: 15 6 2019
Statut: ppublish

Résumé

Vascular calcifications are associated with a high cardiovascular morbi-mortality in the coronary territory. In parallel, femoral arteries are more calcified and develop osteoid metaplasia (OM). This study was conducted to assess the predictive value of OM and local inflammation on the occurrence of mid- and long-term adverse cardiovascular events. Between 2008 and 2015, 86 atheromatous samples were harvested during femoral endarterectomy on 81 patients and processed for histomorphological analyses of calcifications and inflammation (monocytes and B cells). Histological findings were compared with the long-term follow-up of patients, including major adverse cardiac event (MACE), major adverse limb event (MALE), and mortality. Frequencies were presented as percentage, and continuous data, as mean and standard deviation. A P-value < 0.05 was considered statistically significant. Median follow-up was 42.4 months (26.9-58.8). Twenty-eight percent of patients underwent a MACE; a MALE occurred in 18 (21%) limbs. Survival rate was 87.2% at 36 months. OM was found in 41 samples (51%), without any significant impact on the occurrence of MACE, MALE, or mortality. Preoperative white blood cell formulae revealed a higher rate of neutrophils associated with MACE (P = 0.04) and MALE (P = 0.0008), correlated with higher B cells counts in plaque samples. OM is part of femoral calcifications in almost 50% of the cases but does not seem to be an independent predictive variable for MACE or MALE. However, a higher rate of B cell infiltration of the plaque and preoperative neutrophil blood count may be predictive of adverse events during follow-up.

Sections du résumé

BACKGROUND BACKGROUND
Vascular calcifications are associated with a high cardiovascular morbi-mortality in the coronary territory. In parallel, femoral arteries are more calcified and develop osteoid metaplasia (OM). This study was conducted to assess the predictive value of OM and local inflammation on the occurrence of mid- and long-term adverse cardiovascular events.
METHOD METHODS
Between 2008 and 2015, 86 atheromatous samples were harvested during femoral endarterectomy on 81 patients and processed for histomorphological analyses of calcifications and inflammation (monocytes and B cells). Histological findings were compared with the long-term follow-up of patients, including major adverse cardiac event (MACE), major adverse limb event (MALE), and mortality. Frequencies were presented as percentage, and continuous data, as mean and standard deviation. A P-value < 0.05 was considered statistically significant.
RESULTS RESULTS
Median follow-up was 42.4 months (26.9-58.8). Twenty-eight percent of patients underwent a MACE; a MALE occurred in 18 (21%) limbs. Survival rate was 87.2% at 36 months. OM was found in 41 samples (51%), without any significant impact on the occurrence of MACE, MALE, or mortality. Preoperative white blood cell formulae revealed a higher rate of neutrophils associated with MACE (P = 0.04) and MALE (P = 0.0008), correlated with higher B cells counts in plaque samples.
CONCLUSIONS CONCLUSIONS
OM is part of femoral calcifications in almost 50% of the cases but does not seem to be an independent predictive variable for MACE or MALE. However, a higher rate of B cell infiltration of the plaque and preoperative neutrophil blood count may be predictive of adverse events during follow-up.

Identifiants

pubmed: 31200045
pii: S0890-5096(19)30397-8
doi: 10.1016/j.avsg.2019.03.035
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

335-345

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Aurore Danvin (A)

CHU Nantes, l'institut du thorax, service de chirurgie vasculaire, Nantes, France.

Thibaut Quillard (T)

Laboratoire de Physiopathologie de la Résorption Osseuse, Inserm UMR S 1238, Nantes, France.

Olivier Espitia (O)

Laboratoire de Physiopathologie de la Résorption Osseuse, Inserm UMR S 1238, Nantes, France; CHU Nantes, unité de médicine vasculaire, Nantes, France; Université de Nantes, Nantes, France.

Céline Charrier (C)

Laboratoire de Physiopathologie de la Résorption Osseuse, Inserm UMR S 1238, Nantes, France.

Béatrice Guyomarch (B)

CHU Nantes, institut du thorax, INSERM, CNRS, UNIV Nantes, Nantes, France.

Yann Gouëffic (Y)

CHU Nantes, l'institut du thorax, service de chirurgie vasculaire, Nantes, France; Laboratoire de Physiopathologie de la Résorption Osseuse, Inserm UMR S 1238, Nantes, France; Université de Nantes, Nantes, France.

Blandine Maurel (B)

CHU Nantes, l'institut du thorax, service de chirurgie vasculaire, Nantes, France; Laboratoire de Physiopathologie de la Résorption Osseuse, Inserm UMR S 1238, Nantes, France. Electronic address: blandine.maurel@chu-nantes.fr.

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