Usefulness of Carvedilol in the Treatment of Chronic Aortic Valve Regurgitation

Zendaoui, Adnane; Lachance, Dominic; Roussel, Élise; Couët, Jacques; Arsenault, Marie

doi:10.1161/circheartfailure.110.958512

Cited by 38 publications

(31 citation statements)

References 23 publications

(17 reference statements)

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“…In a murine model of severe AR, Plante and colleagues showed that after 180 days, the end systolic diameter was smaller and the LVEF higher in rats treated with metoprolol compared with untreated animals, whereas the end diastolic diameter was not significantly different 17. Similar results were found by Zendaoui and co-workers 19. These results suggest that β-blocker therapy does indeed protect the LV in AR.…”

Section: Discussionsupporting

confidence: 55%

Controlled release metoprolol for aortic regurgitation: a randomised clinical trial

Broch

Urheim

Lønnebakken

et al. 2015

Heart

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Objective Chronic aortic regurgitation (AR) creates a volume load on the left ventricle, which induces adaptive responses. With time, excessive left ventricular (LV) dilatation may precipitate heart failure. β-adrenergic receptor antagonists (β-blockers) are beneficial in patients with heart failure, but their effect in AR is unclear. This trial was designed to evaluate the effect of controlled release metoprolol on LV remodelling in patients with AR. Methods In this double blind trial, 75 asymptomatic patients aged 44±14 years, 89% males, fulfilling at least two echocardiographic criteria for moderate or severe chronic AR, were randomised to receive metoprolol CR/ XL up-titrated to 200 mg/day, or matching placebo. The primary endpoint was LV end diastolic volume, measured by MRI after 6 months of treatment. Results After 6 months, the difference in the baselineadjusted LV end diastolic volume between patients allocated to metoprolol and those allocated to placebo was 8 (95% CI −8 to 25) mL ( p=0.32). The adjusted LV ejection fraction was 2.7 (95% CI 0.1 to 5.3) percentage points higher in the metoprolol group than in the placebo group ( p=0.04). The exercise capacity and peak oxygen consumption did not differ between treatment arms. Serum concentrations of N-terminal pro-B-type natriuretic peptide were 138 (95% CI 71 to 205) pg/mL higher in the metoprolol group ( p<0.001). There were no serious adverse events in either treatment arm. Conclusions Treatment with metoprolol of adults with chronic, moderate to severe AR had no effect on LV volumes. Trial registration number ClinicalTrials.gov Identifier: NCT01157572-results.

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Section: Discussionsupporting

confidence: 55%

Controlled release metoprolol for aortic regurgitation: a randomised clinical trial

Broch

Urheim

Lønnebakken

et al. 2015

Heart

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“…To our knowledge it is the first report of a pharmacological treatment influencing LV remodeling in an animal model but with little influence on LV hypertrophy (Plante et al 2004a,b;Plante et al 2009;Plante et al 2008;Zendaoui et al 2011). However, considering the short duration of our study, it is not totally excluded that a preventive effect on LVH would appear after a longer follow-up.…”

Section: Discussionmentioning

confidence: 68%

Fenofibrate reduces cardiac remodeling and improves cardiac function in a rat model of severe left ventricle volume overload

et al. 2013

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Aims: Fenofibrate is a peroxisome proliferator associated receptor alpha agonist (PPAR) used clinically for the management of dyslipidemia and is a myocardial fatty acid oxidation stimulator. It has also been shown to have cardiac anti-hypertrophic properties but the effects of fenofibrate on the development of eccentric LVH and ventricular function in chronic left ventricular (LV) volume overload (VO) are unknown.This study was therefore designed to explore the effects of fenofibrate treatment in a VO rat model caused by severe aortic valve regurgitation (AR) with a focus on cardiac remodeling and myocardial metabolism.Main Methods: Male Wistar rats were divided in four groups (13-15 animals / group):Shams (S) treated with fenofibrate (F; 100 mg/kg/d PO) or not (C) and severe AR receiving or not fenofibrate. Treatment was started one week before surgery and the animals were sacrificed 9 weeks later.Key findings: AR rats developed severe LVH (increased LV weight) during the course of the protocol. Fenofibrate did not reduce LV weight. However, eccentric LV remodeling was strongly reduced by fenofibrate in AR animals. Fractional shortening was significantly less affected in ARF compared to ARC group. Fenofibrate also increased the myocardial enzymatic activity of enzymes associated with fatty acid oxidation while inhibiting glycolytic enzyme phosphofructokinase.Significance: Fenofibrate decreased LV eccentric remodeling associated with severe VO and helped maintain systolic function. Studies with a longer follow-up will be needed to assess the long-term effects of fenofibrate in chronic volume overload caused by aortic regurgitation.

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“…Para los pacientes que después de la cirugía siguen sufriendo insuficiencia cardiaca o hipertensión, son útiles los inhibidores de la enzima de conversión de la angiotensina (IECA), los antagonistas del receptor de la angiotensina II (ARA-II) y los bloqueadores beta 68,69 . En pacientes con síndrome de Marfan, los bloqueadores beta y el losartán pueden reducir la dilatación de la raíz aórtica y el riesgo de complicaciones aórticas, por lo que se debe considerarlos antes y después de la cirugía [70][71][72] .…”

Section: Tratamiento Médicounclassified