This paper aims at studying the effects of the heart rate (HR) on the intraventricular hemodynamics and mitral valve dynamics for a healthy left ventricle of the human heart. The problem is tackled through direct numerical simulation of the Navier-Stokes equations, two–way coupled with a structural solver for the ventricle and mitral valve leaflets. Several HRs ranging from bradycardia to normal and up to tachycardia are considered and the resulting flow and structure dynamics analysed. Taking the physiological HR of 60 beats per minute (bpm) as reference case, it results that in the bradycardia regime the lower flow rates produce a weaker mitral jet with a lower blood kinetic energy and smaller wall shear stresses either on the valve leaflets and on the endocardium. In contrast, as the HR increases, the faster and thicker mitral jets are associated to increasing blood kinetic energy and the wall shear stress, which more than double increasing the HR from bradycardia to tachycardia. The altered wall shear stress distribution and amplitude, though not intense enough to produce immediate effects, are implied to induce, in the long-term, structure alteration or tissue remodelling via mechanotransduction mechanisms . Another relevant effect of the HR increase is the reduction of the diastasis duration until at HR=100 bpm the early diastole (E–wave) overlaps the late diastole (A–wave). This phenomenon produces an enhanced mitral leaflets mobility, which open more at higher HRs, thus yielding larger geometrical orifice area during diastole.
- Fluid-structure interaction
- Heart rate function