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

Objectives To analyze the potential contribution of contractility state and ventricular geometry to the development of heart failure in rats with aortic stenosis. Methods Rats were divided into three groups: compensated aortic stenosis (AS, n = 11), heart failure AS (n = 12) and control rats (C, n = 13). Results After 21 weeks, failing AS rats presented higher systolic (C = 36.6 ± 3.1, AS = 78.6 ± 4.8low asterisk, failing AS = 104.6 ± 7.8low asterisk†) and diastolic meridian stress (C = 6.9 ± 0.4, AS = 20.1 ± 1.1low asterisk, failing AS = 43.2 ± 3.2low asterisk†), hydroxyproline (C = 3.6 ± 0.7 mg/g, AS = 6.6 ± 0.6low asterisk mg/g, failing AS = 9.2 ± 1.4low asterisk† mg/g) and cross-sectional area (C = 338 ± 25 μm2, AS = 451 ± 32low asterisk μm2, failing AS = 508 ± 36low asterisk† μm2), in comparison with control and compensated AS animals (low asteriskp < 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. Conclusion Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.