|| Checking for direct PDF access through Ovid
Purpose: Several studies, based on mathematical and computational models, demonstrated that LV diastolic filling is characterized by the formation of intraventricular rotational bodies of fluids, termed "vortex rings", that optimize the efficiency of LV ejection. The vortical blood motion in the LV supports redirection toward aortic outflow and the dynamic balance with the surrounding tissue. We hypothesized that a breaking of such a natural arrangement may be a concurrent cause of ventricular remodeling. At this aim, intraventricular blood flow was analyzed in healthy subjects and in acute myocardial infarction to evaluate morphology and dynamics of the LV diastolic vortex rings formation and to verify early indicators of blood-tissue unbalance.Methods: Ten healthy volunteers (mean age 27±2) and 15 patients (mean age 57±2) with a first acute myocardial infarction (AMI) were enrolled. The following examinations were performed: 2D and 3D echocardiography analysis to assess LV systolic and diastolic function, and Echo-PIV analysis to evaluate properties of swirling motion. E-PIV analysis was made by Hyper Flow 188.8.131.52, software which analyzes images of the myocardial contrast echocardiography obtained by tracking LV flow with an ultrasound contrast. By carrying out this analysis, we obtained the following parameters to evaluate and quantify vortex rings: Vortex depth, Vortex length, Vortex intensity, Vortex area and Energy dissipation.Results: As compared to AMI patients (LVEF-3D=47±2%), the healthy volunteers (LVEF-3D=56±0.7%) had a significant lower kinetic energy dissipation (0.46±0.04 vs 0.36±0.04, p=0.02, respectively). However, when AMI patients are divided into two subgroups according to LVEF (9 pts with LVEF>45% and 6 with LVEF<45%), we observed that energy dissipation was significantly higher in the first group (0.60±0.05 vs 0.43±0.05; p=0.043).Conclusions: Our preliminary data show that in AMI patients with preserved LV function there is a significant increase in energy dissipation, likely showing the presence of a broken fluid-tissue dynamical coupling despite the development of a compensatory mechanisms for maintaining the LVEF. In presence of a significant LV dysfunction, fluid-tissue interaction is closer to normal and energy dissipation is markedly reduced. Further data are needed to assess the role of these parameters in the development of LV remodeling.