Valvular heart disease associated with benfluorex

Valvular heart disease associated with benfluorex

Archives of Cardiovascular Disease (2010) 103, 342—343 IMAGE Valvular heart disease associated with benfluorex Valvulopathies associées à la prise de...

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Archives of Cardiovascular Disease (2010) 103, 342—343

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Valvular heart disease associated with benfluorex Valvulopathies associées à la prise de benfluorex Jean-Pierre Gueffet a,b,c,∗, Nicolas Piriou a,b,c, Jean-noël Trochu a,b,c a

UMR 915, Inserm, 44000 Nantes cedex, France Université de Nantes, 44000 Nantes cedex, France c Service de cardiologie, institut du thorax, CHU de Nantes, boulevard J.-Monod, 44093 Nantes cedex, France b

Received 22 September 2009; received in revised form 29 September 2009; accepted 29 September 2009 Available online 13 May 2010

KEYWORDS Benfluorex; Valvular fibrosis; Amphetamines; Pulmonary hypertension; Adverse drug reaction

MOTS CLÉS Benfluorex ; Fibrose valvulaire ; Amphétamines ; Hypertension valvulaire ; Effets secondaires médicamenteux



A 57-year-old woman was referred for dyspnoea during mild exercise, especially during the past year. Electrocardiogram and chest X-ray demonstrated no significant anomaly. Ntpro brain natriuretic peptide was moderately elevated to 319 ng/L (range: 0—290 ng/L). Echocardiographic examination showed normal left ventricle function and anatomy, mild regurgitations of the aortic and mitral valves and a severe regurgitation of the tricuspid valve (Figs. 1 and 2), with an estimated systolic pulmonary pressure of 60 mmHg. The mechanism of the valvular regurgitations corresponded to valvular fibrosis and subsequently restriction motion. Right heart catheterization confirmed pulmonary arterial hypertension with normal pulmonary wedge pressure and cardiac output. Thoracic tomodensitometry ruled out pulmonary embolism. There was also no clinical or biological evidence for a carcinoid syndrome. The patient had no previous medical history, but she had taken benfluorex (150 mg tid) for the past 8 years because of excessive weight (159 cm, 82 kg) and hypertriglyceridaemia. In addition to withdrawal of the drug, and because of elevated right atrial pressure, we started furosemide 40 mg per day but no specific treatment was given for pulmonary artery hypertension. Three months later, echocardiography showed consistently severe tricuspid regurgitation with an estimated systolic pulmonary pressure of 50 mmHg. No other right heart catheterization was done, in accordance with the patient’s wishes, as she felt better and had dyspnoea class II in the New York Heart Association classification.

Corresponding author. E-mail address: [email protected] (J.-P. Gueffet).

1875-2136/$ — see front matter © 2010 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.acvd.2009.09.015

Valvular heart disease associated with benfluorex

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Figure 2. Transthoracic echocardiography (apical 4-chamber plane) showing continuous Doppler of tricuspid insufficiency.

Figure 1. Transthoracic echocardiography (apical 4-chamber plane) showing (A) dilatation of the right cavities, fibrosis of the tricuspid valves responsible for a hiatus during systole and (B) severe tricuspid regurgitation in colour Doppler. RA: right atrium; RV: right ventricle; LA: left atrium; LV: left ventricle.

Fenfluramine-derivative diet pills were withdrawn from the market in 1997 because of an association with valvular regurgitation and pulmonary hypertension. The similarity of the echocardiographic lesions observed in our patient with those reported with fenfluramine makes us discuss the imputability of benfluorex, which is structurally related to other amphetamines. This observation underlines a potentially underestimated adverse drug reaction with benfluorex of which every cardiologist should be aware. Additionally, since this first observation we have seen two other cases of plurivalvular regurgitation (in particular severe tricuspid insufficiency) and pulmonary hypertension in patients on benfluorex.

Conflict of interest statement None.