Acute Q Fever Endocarditis: A Paradigm Shift Following the Systematic Use of Transthoracic Echocardiography During Acute Q Fever.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
13 11 2019
Historique:
received: 16 09 2018
accepted: 04 02 2019
pubmed: 21 2 2019
medline: 15 9 2020
entrez: 21 2 2019
Statut: ppublish

Résumé

As Q fever, caused by Coxiella burnetii, is a major health challenge due to its cardiovascular complications, we aimed to detect acute Q fever valvular injury to improve therapeutic management. In the French national reference center for Q fever, we prospectively collected data from patients with acute Q fever and valvular injury. We identified a new clinical entity, acute Q fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae, and valve or chorda tendinae thickness. To determine whether or not the disease was superimposed on an underlying valvulopathy, patients' physicians were contacted. Aortic bicuspidy, valvular stenosis, and insufficiency were considered as underlying valvulopathies. Of the 2434 patients treated in our center, 1797 had acute Q fever and 48 had acute Q fever endocarditis. In 35 cases (72%), transthoracic echocardiography (TTE) identified a valvular lesion of acute Q fever endocarditis without underlying valvulopathy. Positive anticardiolipin antibodies (>22 immunoglobulin G-type phospholipid units [GPLU]) were independently associated with acute Q fever endocarditis (odds ratio [OR], 2.7 [95% confidence interval {CI}, 1.3-5.5]; P = .004). Acute Q fever endocarditis (OR, 5.2 [95% CI, 2.6-10.5]; P < .001) and age (OR, 1.7 [95% CI, 1.1-1.9]; P = .02) were independent predictors of progression toward persistent C. burnetii endocarditis. Systematic TTE in acute Q fever patients offers a unique opportunity for early diagnosis of acute Q fever endocarditis and for the prevention of persistent endocarditis. Transesophageal echocardiography should be proposed in men, aged >40 years, with anticardiolipin antibodies >60 GPLU when TTE is inconclusive or negative.

Sections du résumé

BACKGROUND
As Q fever, caused by Coxiella burnetii, is a major health challenge due to its cardiovascular complications, we aimed to detect acute Q fever valvular injury to improve therapeutic management.
METHODS
In the French national reference center for Q fever, we prospectively collected data from patients with acute Q fever and valvular injury. We identified a new clinical entity, acute Q fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae, and valve or chorda tendinae thickness. To determine whether or not the disease was superimposed on an underlying valvulopathy, patients' physicians were contacted. Aortic bicuspidy, valvular stenosis, and insufficiency were considered as underlying valvulopathies.
RESULTS
Of the 2434 patients treated in our center, 1797 had acute Q fever and 48 had acute Q fever endocarditis. In 35 cases (72%), transthoracic echocardiography (TTE) identified a valvular lesion of acute Q fever endocarditis without underlying valvulopathy. Positive anticardiolipin antibodies (>22 immunoglobulin G-type phospholipid units [GPLU]) were independently associated with acute Q fever endocarditis (odds ratio [OR], 2.7 [95% confidence interval {CI}, 1.3-5.5]; P = .004). Acute Q fever endocarditis (OR, 5.2 [95% CI, 2.6-10.5]; P < .001) and age (OR, 1.7 [95% CI, 1.1-1.9]; P = .02) were independent predictors of progression toward persistent C. burnetii endocarditis.
CONCLUSIONS
Systematic TTE in acute Q fever patients offers a unique opportunity for early diagnosis of acute Q fever endocarditis and for the prevention of persistent endocarditis. Transesophageal echocardiography should be proposed in men, aged >40 years, with anticardiolipin antibodies >60 GPLU when TTE is inconclusive or negative.

Identifiants

pubmed: 30785186
pii: 5315521
doi: 10.1093/cid/ciz120
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1987-1995

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

Auteurs

Cléa Melenotte (C)

Aix-Marseille Université, Institut de Recherche pour le Développement, Assistance publique-Hôpitaux de Marseille, Microbes Evolution Phylogénie et Infections, Institut Hospitalo Universitaire-Méditerranée Infection, Cayenne.

Loïc Epelboin (L)

Unité de Maladies infectieuses et Tropicales, Centre Hospitalier André Rosemon, Cayenne.

Matthieu Million (M)

Aix-Marseille Université, Institut de Recherche pour le Développement, Assistance publique-Hôpitaux de Marseille, Microbes Evolution Phylogénie et Infections, Institut Hospitalo Universitaire-Méditerranée Infection, Cayenne.

Sandrine Hubert (S)

Department of Cardiology, Aix-Marseille Université, Marseille.

Thierry Monsec (T)

Department of Cardiologie, Centre Hospitalier de Valence, France.

Félix Djossou (F)

Unité de Maladies infectieuses et Tropicales, Centre Hospitalier André Rosemon, Cayenne.

Jean-Louis Mège (JL)

Aix-Marseille Université, Institut de Recherche pour le Développement, Assistance publique-Hôpitaux de Marseille, Microbes Evolution Phylogénie et Infections, Institut Hospitalo Universitaire-Méditerranée Infection, Cayenne.

Gilbert Habib (G)

Unité de Maladies infectieuses et Tropicales, Centre Hospitalier André Rosemon, Cayenne.

Didier Raoult (D)

Aix-Marseille Université, Institut de Recherche pour le Développement, Assistance publique-Hôpitaux de Marseille, Microbes Evolution Phylogénie et Infections, Institut Hospitalo Universitaire-Méditerranée Infection, Cayenne.

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