Cardiac remodeling following acute myocardial infarction (MI) has been widely described. The single best predictor of adverse left ventricular remodeling (LVr) is infarct size (IS) determined by cardiac magnetic resonance (CMR). Recent developments in cardiac fluid-dynamics imaging have heightened the interest about hemodynamic forces (HDFs) patterns associated with cardi-ac adaptations. Evidences connecting fluid dynamics, embryological heart development and cardiac remodeling following pathological event or therapeutic interventions increased in last years.
In our study we aim to evaluate HDFs and their influence on post-infarction LVr in a cohort of patients with reperfused ST-segment elevation MI (STEMI) using a novel technique based on endocardial borders tracking of steady-state free-precession cine CMR datasets. Both hemodynamic forces directed along the "apex-to-base" (A-B, longitudinal) and "latero-septal" (L-S, horizontal) LV axis will be estimated. L-S/A-B HDFs ratio, computed as the ratio between L-S HDFs and A-B HDFs, will be calculated to assess the relative distribution of the hemodynamic force directions in the LV. Correlations with L-S/A-B HDFs ratio and the relative increase in LVESV at 4 months¿ follow-up will be evaluated.
Cardiac remodeling following acute myocardial infarction has been widely described. Several factors are implied in this adverse phenomenon. On the clinical point of view, adverse left ventricular remodeling is the main cause of heart failure and death after acute myocardial infarction. Thus, a comprehensive assessment of all parameters involved should be very important. Previous studies of our group clearly demonstrated the key role of intraventricular fluid dynamics in cardiac adaptations in several clinical conditions and in particular after acute myocardial infarction. Evidences connecting fluid dynamics, embryological heart development and cardiac remodeling following pathological event or therapeutic interventions increased in last years.
Using a new method for estimating hemodynamic forces from the motion of the LV endocardial boundary we will be able to calculate several new parameters, from a cardiac MR imaging, potentially involved in remodeling processes. From a better knolwledge of hemodinamics of LV remodeling we could improve treatment of this post-infarction adverse event, targeting drugs able to modify the direction of hemodynamic forces into the left ventricle