Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis

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.