Key result
Renovascular hypertension induces mild aortic stenosis with ~15% lower aortic valve area in rabbits.
Why the study?
The molecular mechanisms linking hypertension and degenerative aortic valve stenosis remain unclear due to the absence of experimental models and lack of evidence for a cause-effect relationship.
Does the induction of hypertension cause the development of aortic valve stenosis in a rabbit model?
Does the induction of hypertension cause the development of aortic valve stenosis in a rabbit model?
Effect estimate: 14.6% reduction
p-value: p=<0.05
This study demonstrates a novel experimental rabbit model of aortic valve stenosis, providing evidence for a causal link between hypertension and the development of degenerative aortic valve disease.
OBJECTIVES: This study was designed to investigate the association between hypertension and aortic valve stenosis (AVS) in a rabbit model. BACKGROUND: Degenerative AVS is a prevalent disease in elderly persons. Its molecular mechanisms remain unclear, in part because of the absence of experimental models. Epidemiologic data suggest a link between hypertension and AVS. However, there has been no evidence of a cause-effect relationship. METHODS: New Zealand White rabbits were divided into two groups: 1) animals (n = 20) instrumented according to one-kidney/one-clip hypertensive model; and 2) control animals (n = 10) sham operated. Echocardiography (S12 MHz) was used to assess aortic valve (AV) morphology and function as well as left ventricular mass at baseline and after two and four months of hypertension. RESULTS: Blood pressure and left ventricular mass increase were highly significant in the animal model but not in controls at two months, without noticeable AV function abnormalities. After 4 months, however, 14 hypertensive survived animals showed a 14.6% reduction of AV area (0.240 +/- 0.063 cm2 vs. 0.205 +/- 0.060 cm2, p < 0.05), a 19.6% increase of AV thickness (0.056 +/- 0.011 cm vs. 0.067 +/- 0.010 cm, p < 0.001), a 40.4% increase of transvalvular mean gradient (5.35 +/- 2.26 mm Hg vs. 7.51 +/- 3.73 mm Hg, p < 0.05) and a 63.6% increase of transvalvular maximal gradient (10.56 +/- 3.68 mm Hg vs. 17.28 +/- 10.95 mm Hg, p < 0.05). Control animals did not show significant changes. CONCLUSIONS: We report a novel experimental model of AVS in rabbits that may prove useful in studying the progression of the disease and the efficacy of new treatments. The present findings support the hypothesis of a causal link between hypertension and AVS.
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Cuniberti et al. (2006) studied Aortic Valve Stenosis (n=30). One-kidney/one-clip hypertensive model vs. Sham operated was evaluated on Aortic valve area (14.6% reduction, p=<0.05). The one-kidney/one-clip hypertensive rabbit model induced mild aortic valve stenosis after 4 months, characterized by a 14.6% reduction in aortic valve area (p<0.05) and increased transvalvular gradients.
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