A model based approach to estimate contractile force development using myocardial velocity imaging: a validation study during alterations in contractility and heart rate

Abstract

Forces within the myocardial wall may be described by a stress tensor that is the sum of passive/elastic (/spl sigma//sub P/) and active (/spl sigma//sub A/) stresses. We developed a mechanical model based approach to calculate these stress components separately using myocardial velocity imaging (MVI). The timing and shape of the extracted /spl sigma//sub A/ profiles match those in isolated muscle experiments. We wanted to validate further this model based approach to estimating active stress and see whether it could detect changes in active force development. Therefore, we compared peak active stress (/spl sigma//sub Amax/) with peak positive rule of pressure rise (dPdt/sub max/), a common clinical contractility index, during changes in heart rate (HR) and contractility. In closed-chest pigs, MVI and pressure data were recorded. HR was varied by atrial pacing (AP=120-180 bpm, n=9). Contractility was increased by incremental dobutamine infusion (DI=5-20 /spl mu/g/kg/min, n=9). Finally, contractility was decreased by esmolol infusion (0.5/spl plusmn/0.15 mg/kg/min) plus subsequent pacing (120-180 bpm) (EI group, n=6). /spl sigma//sub Amax/ increased significantly with each stage of DI. During AP, /spl sigma//sub Amax/ remained relatively constant while it decreased significantly with EI. /spl sigma//sub Amax/ correlates with dPdt/sub max/ (r=0.79 P<0.01). /spl sigma//sub Amax/ reflects changes in contractility while being relatively independent of heart rate.