Development of mild aortic valve stenosis in a rabbit model of hypertension

被引:31
作者
Cuniberti, LA
Stutzbach, PG
Guevara, E
Yannarelli, GG
Laguens, RP
Favaloro, RR
机构
[1] Univ Favaloro, Lipid & Atherosclerosis Res Lab, Dept Pathol, RA-1078 Buenos Aires, DF, Argentina
[2] Favaloro Fdn, Inst Cardiol & Cardiovasc Surg, Buenos Aires, DF, Argentina
关键词
D O I
10.1016/j.jacc.2005.12.070
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-chp 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 2 animals showed a 14.6% reduction of AV area (0.240 +/- 0.063 cm(2) vs. 0.205 +/- 0.060 cm(2) 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 min 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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页码:2303 / 2309
页数:7
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