Key result
Carvedilol fails to improve LV remodeling or function in preclinical severe aortic regurgitation.
Why the study?
Beta-blockade is contraindicated in severe aortic regurgitation due to concerns of prolonging diastole and worsening regurgitation, but this has not been scientifically proven and some studies suggest benefits of targeting the sympathetic system in AR.
Does carvedilol improve left ventricular remodeling or function in rats with surgically induced aortic regurgitation?
Does carvedilol improve left ventricular remodeling or function in rats with surgically induced aortic regurgitation?
In a rat model of aortic regurgitation, carvedilol neither improved nor worsened left ventricular remodeling and function, suggesting beta-blockade may not be as detrimental in severe AR as traditionally feared.
Answers are grounded in this paper and cite their sources.
No remodeling benefit with carvedilol in AR rats; hypothesis-generating for human aortic regurgitation trials.
BACKGROUND: Beta-blockade is contraindicated in severe aortic regurgitation (AR) due to the fear of prolonging diastole and thus aggravate regurgitation. However, this has never been scientifically proven and positive effects of targeting the sympathetic system in AR has been demonstrated in several studies. METHOD: Thirty-nine Sprague-Dawley rats with AR were randomized to ten weeks of medical treatment with carvedilol or no treatment. Treatment was initiated either early or late after AR induction. The effect of carvedilol was assessed by serial echocardiography and invasive hemodynamic measurements. RESULTS: AR resulted in eccentric hypertrophy and left ventricular (LV) dysfunction. LV remodeling and function as measured by echocardiography was unaffected by treatment. LV dimensions were similar between treated and untreated groups and measures of LV performance (including strain and strain rate) were also unaltered. This result was confirmed by invasive measurements showing maximal and minimal pressure-time development, LV volumes, and LV pressures, to be unaltered by treatment. On the contrary, despite relative bradycardia carvedilol did not reflect any negative impact on the heart. CONCLUSION: Carvedilol did not improve left ventricular remodeling or function in rats with surgically induced AR. Despite relative bradycardia, we did not find carvedilol to negatively impact the heart, either when treatment was initiated early or late in the course of disease.
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Eskesen et al. (2015) studied Aortic regurgitation (n=39). Carvedilol vs. No treatment was evaluated on Left ventricular remodeling and function (assessed by echocardiography and invasive hemodynamics). Carvedilol did not improve left ventricular remodeling or function in rats with surgically induced severe aortic regurgitation, regardless of whether treatment was initiated early or late.
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