Timing of the aortic pulse wave inflection point is associated with mitral annular systolic motion.

Abstract

Introduction: The pressure wave inflection point (Ti) is widely considered the point of arrival of reflected arterial pressure waves and consequently a marker of arterial stiffness. Medial mitral annular motion measured by Tissue Doppler Imaging (TDI) is known to correlate with Ti. Additionally, peak S' velocity (S' max) is known to be proportional to ventricular contractility and inversely proportional to afterload. We sought to determine the effects of pharmacologically induced haemodynamic alterations on R wave - peak S' duration, peak S' velocity and Ti. Method(s): Twenty healthy male volunteers aged between 20 and 35 years were prospectively enrolled and underwent simultaneous carotid tonometry and echocardiographic evaluation using TDI. Measurements were repeated following the administration of salbutamol, glyceryl trinitrate, dobutamine, esmolol or sub-lingual nifedipine. We determined the timing of S' max and of Ti relative to the ECG R wave. Heart rate, Pulse Wave Velocity (PWV), augmentation index and left ventricular ejection time (LVET) were calculated from ensemble averaged carotid pressure waveforms. Result(s): Forty paired measurements were performed in 20 participants. Baseline R-S' duration correlated significantly with Ti (r = 0.63, p = 0.003), heart rate (r =-0.54, p = 0.01) and LVET (r = 0.52, p = 0.02). S' max was correlated with Ti (r = 0.46, p = 0.04) and heart rate (r = 0.58, p = 0.01). These correlations persisted following pharmacological intervention (Table 1).Augmentation index and PWV were not correlated with any other parameter in this cohort. Conclusion(s): This data supports the hypothesis that Ti is related to contractility and afterload. Measurement of the R-wave to S' interval and S' max may provide additional insights into ventricular-vascular interaction. (Table Presented).