Abstract
Background
Uric acid (UA) has been shown to be an independent risk factor for various cardiovascular
diseases. However, its significance in hypertrophic cardiomyopathy (HCM) has not yet
been evaluated. The objective of the present study was to evaluate clinical implications
of plasma UA levels on the prognosis of patients with HCM.
Methods
A total of 588 adult patients with HCM were enrolled at FuWai Hospital from 1999-2011
and followed until 2014. The plasma levels of UA were measured at enrollment.
Results
During the follow-up of 5.2 ± 2.4 years, 44 (7.5%) patients had cardiovascular-related
deaths, and 100 (17.0%) patients had cardiac events. Compared with the first tertile
of UA concentration (< 284.6 μmol/L), patients in the highest tertile (> 358.7 μmol/L)
had a higher risk for the development of adverse events: cardiovascular death (adjusted
hazard ratio [HR], 3.10; 95% confidence interval [CI], 1.37-7.04; P = 0.007), all-cause mortality (adjusted HR, 2.33; 95% CI, 1.11-4.89; P = 0.025), cardiac events (adjusted HR, 4.20, 95% CI, 2.38-7.42; P < 0.001), heart failure events (adjusted HR, 3.46; 95% CI, 1.86-6.45; P < 0.001), and arrhythmic events (adjusted HR, 9.19; 95% CI, 2.40-35.25; P = 0.001). Similarly, the continuous variable of UA (for every 1 mg/dL higher concentration)
was also an independent predictor for adverse outcomes: cardiovascular death (adjusted
HR, 1.29; 95% CI, 1.11-1.49; P = 0.001), all-cause mortality (adjusted HR, 1.23; 95% CI, 1.07-1.41; P = 0.004), cardiac events (adjusted HR, 1.27; 95% CI, 1.15-1.41; P < 0.001), heart failure events (adjusted HR, 1.19; 95% CI, 1.06-1.33; P = 0.003), and arrhythmic events (adjusted HR, 1.60; 95% CI, 1.30-1.98; P < 0.001).
Conclusions
Our results indicate that UA is an independent predictor of adverse outcomes in patients
with HCM.
Résumé
Introduction
Il a été démontré que l’acide urique (AU) est un facteur de risque indépendant de
plusieurs maladies cardiovasculaires. Cependant, son importance dans la cardiomyopathie
hypertrophique (CMH) n’a pas encore été évaluée. L’objectif de la présente étude était
d’évaluer les implications cliniques des concentrations plasmatiques de l’AU sur le
pronostic des patients souffrant de CMH.
Méthodes
Un total de 588 patients adultes souffrant de CMH ont été inscrits à l’hôpital FuWai
de 1999 à 2011 et suivis jusqu’en 2014. Les concentrations plasmatiques de l’AU ont
été mesurées à l’inscription.
Résultats
Durant le suivi de 5,2 ± 2,4 ans, 44 (7,5 %) patients ont connu une mort d’origine
cardiovasculaire et 100 (17,0 %) patients ont subi des événements cardiaques. Comparativement
au premier tertile de la concentration en AU (< 284,6 μmol/l), les patients dans le
tertile le plus élevé (> 358,7 μmol/l) étaient exposés à un risque plus élevé de développer
des événements indésirables : la mort d’origine cardiovasculaire (rapport de risque
[RR] ajusté, 3,10; intervalle de confiance [IC] à 95 %, 1,37-7,04; P = 0,007), la mortalité toutes causes confondues (RR ajusté, 2,33; IC à 95 %, 1,11-4,89;
P = 0,025), les événements cardiaques (RR ajusté, 4,20, IC à 95 %, 2,38-7,42; P < 0,001), les événements liés à l’insuffisance cardiaque (RR ajusté, 3,46; IC à 95
%, 1,86-6,45; P < 0,001) et les événements arythmiques (RR ajusté, 9,19; IC à 95 %, 2,40-35,25; P = 0,001). De la même façon, la variable continue de l’AU (pour chaque concentration
supérieure à 1 mg/dl) était également un prédicteur indépendant des résultats cliniques
défavorables : la mort cardiovasculaire (RR ajusté, 1,29; IC à 95 %, 1,11-1,49; P = 0,001), la mortalité toutes causes confondues (RR ajusté, 1,23; IC à 95 %, 1,07-1,41;
P = 0,004), les événements cardiaques (RR ajusté, 1,27; IC à 95 %, 1,15-1,41; P < 0,001), les événements liés à l’insuffisance cardiaque (RR ajusté, 1,19; IC à 95
%, 1,06-1,33; P = 0,003) et les événements arythmiques (RR ajusté, 1,60; IC à 95 %, 1,30-1,98; P < 0,001).
Conclusions
Nos résultats indiquent que l’AU est un prédicteur indépendant des résultats cliniques
défavorables chez les patients souffrant de CMH.
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Article info
Publication history
Published online: February 20, 2015
Accepted:
February 16,
2015
Received:
October 19,
2014
Footnotes
See page 1257 for disclosure information.
Identification
Copyright
© 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.