Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2935094 | International Journal of Cardiology | 2007 | 6 Pages |
ObjectivesTo analyze the potential contribution of contractility state and ventricular geometry to the development of heart failure in rats with aortic stenosis.MethodsRats were divided into three groups: compensated aortic stenosis (AS, n = 11), heart failure AS (n = 12) and control rats (C, n = 13).ResultsAfter 21 weeks, failing AS rats presented higher systolic (C = 36.6 ± 3.1, AS = 78.6 ± 4.8⁎, failing AS = 104.6 ± 7.8⁎†) and diastolic meridian stress (C = 6.9 ± 0.4, AS = 20.1 ± 1.1⁎, failing AS = 43.2 ± 3.2⁎†), hydroxyproline (C = 3.6 ± 0.7 mg/g, AS = 6.6 ± 0.6⁎ mg/g, failing AS = 9.2 ± 1.4⁎† mg/g) and cross-sectional area (C = 338 ± 25 μm2, AS = 451 ± 32⁎ μm2, failing AS = 508 ± 36⁎† μm2), in comparison with control and compensated AS animals (⁎p < 0.05 vs. control, †p < 0.05 vs. AS). In the isometric contraction study, considering the time from peak tension to 50% relaxation (RT50), the relative variation responses, following post-rest contraction and increase in Ca2+ concentration, were higher in failing AS than compensated AS animals. In contrast, following post-rest contraction, compensated AS group presented higher values of the peak developed tension (DT) than failing AS group. Following beta-adrenergic stimulation, control animals presented higher values of + dT/dt and − dT/dt than AS animals. In addition, failing AS animals presented higher TPT values than compensated AS animals.ConclusionMyocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.