Abstract
Background and aimsDronedarone is a new multichannel-blocking antiarrhythmic for the treatment of patients with atrial fibrillation. Our group has demonstrated that dronedarone produces regression of cardiac remodeling; however, its effect on the remodeling of the elastic arteries has not yet been reported. We aim to assess the effects of dronedarone on the regression of thoracic aortic remodeling in spontaneously hypertensive rats (SHRs).MethodTen-month-old male SHRs were randomly assigned to an intervention group (SHR-D), where the animals received dronedarone treatment (100 mg/kg), to a control group (SHR) where rats were given vehicle, or to a group (SHR-A) where they were given amiodarone. A fourth group of normotensive control rats (Wistar-Kyoto rats, WKY) was also added. After two weeks of treatment, we studied the structure, the elastic fiber content of the thoracic aorta using histological techniques and confocal microscopy, and the vascular mechanical properties using an organ bath and isometric tension analysis. A mass spectrometric determination of symmetric dimethylarginine (SDMA) concentrations was performed.ResultsSHR group developed the classic remodeling expected from the experimental model: outward hypertrophic remodeling, increased elastic fiber content and wall stiffness. However, the SHR-D group showed statistically significantly lower values for aortic tunica media thickness, wall to lumen ratio, external diameter, cross-sectional area, volume density of the elastic fibers, wall stiffness, and aortic SDMA concentration when compared to the SHR group. These parameters were similar in the SHR and SHR-A groups. Interestingly, the values for tunica media thickness, volume density of the elastic fibers, wall stiffness, and SDMA concentration obtained from the SHR-D group were similar to those measured in the WKY group.ConclusionThese results suggest that dronedarone improves the structure and passive mechanical properties of the thoracic aorta in hypertensive rats, and that this protective effect could be associated with a reduction in the concentration of aortic SDMA.
Highlights
Hypertension is the most common cause of hypertensive heart disease [1]
The spontaneously hypertensive rats (SHR)-D group showed statistically significantly lower values for aortic tunica media thickness, wall to lumen ratio, external diameter, cross-sectional area, volume density of the elastic fibers, wall stiffness, and aortic symmetric dimethylarginine (SDMA) concentration when compared to the SHR group
The values for tunica media thickness, volume density of the elastic fibers, wall stiffness, and SDMA concentration obtained from the SHR-D group were similar to those measured in the WKY group
Summary
Hypertension induces cardiac remodeling, such as hypertrophy, which is related to arrhythmias (atrial and ventricular fibrillation), myocardial ischemia, and sudden cardiac death [2]. Dronedarone produces a reduction in the risk of stroke [10] and acute coronary syndrome [11] that may be related to reduced heart rate and arterial blood pressure [12,13]. Our group has previously demonstrated that dronedarone produces regression of left ventricular hypertrophy (LVH) in hypertensive rats after two weeks of treatment (resulting in reduced left ventricular mass, changes in the cardiomyocytes and collagen of the left ventricle, and an improvement in cardiac metabolism) [14]. Our group has demonstrated that dronedarone produces regression of cardiac remodeling; its effect on the remodeling of the elastic arteries has not yet been reported. We aim to assess the effects of dronedarone on the regression of thoracic aortic remodeling in spontaneously hypertensive rats (SHRs)
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