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Funding Acknowledgements Type of funding sources: None. Background Mitral annular calcification (MAC) is a strong predictor of stroke but mechanism(s) are poorly defined. Severe MAC can produce a gradient across the mitral valve (MV) and, when studied in vitro, disturbs normal flow across the valve resulting in increased viscous energy dissipation. Purpose We hypothesized that severe MAC would increase shear stress on particles traveling across the MV into the left ventricle (LV). Given that shear stresses cause platelet activation this might represent a mechanism by which MAC could increase stroke risk. Methods A silicone model MV was created using a 3D TEE dataset. 3D printed calcium phantoms were incorporated into the valve simulate severe MAC. The valve was tested in a left heart duplicator under rest and exercise conditions and compared with a duplicate valve without the calcium phantoms. Fine particles suspended in a water/glycerol blood analogue allowed for measurement of vortex formation and shear stresses using particle image velocimetry (PIV). Particle residence time (PRT) maps were created to assess how long blood particles would remain in the LV. Particle residence index (PRI - ratio of remaining particles in LV/initial number of particles) is a more quantitative measure of how fast particles leave the LV. These calculations were used to approximate viscous shear stresses on blood particles. For each particle the induced viscous shear stress was evaluated for the entire duration of residence in the LV. Results For the normal MV all released particles left the LV by the 3rd cycle; with severe MAC particles completely left the LV shortly after the 7th cycle. PRI measurements confirmed that particles remained longer in the LV in the presence of severe MAC (figure 1). MAC also induced a shift in the accumulated shear stress levels from the high range > 0.4 Pa.s and the low range < 0.1 towards the middle region (0.16-0.32 Pa.s, figure 2). As shear stress is reported for one cycle, one may expect MAC to lead to higher accumulated higher viscous stresses as particles reside in the LV for a longer time. Conclusions In the presence of severe MAC blood particles remain longer in the LV and are exposed to greater cumulative shear stresses vs the normal situation. Given that shear stress is known to cause platelet activation this may be a mechanism by which MAC increases risk of ischemic stroke. Abstract Figure 1 Abstract Figure 2
Background Systolic anterior motion (SAM) of the mitral valve (MV) can develop after mitral valve repair with placement of an annuloplasty ring. It is occasionally seen in patients with mitral annular calcification (MAC) but mechanisms have not been carefully delineated. Using 2-dimensional echocardiography we explored morphologic parameters which may contribute to SAM in patients with MAC. Hypothesis We hypothesized that in cases of MAC where SAM is present there would be anterior displacement of the valve by the posterior annular calcification. Methods From our echocardiographic database we identified 20 patients with severe MAC who also had SAM with definite septal contact. Each subject was paired with 2 controls free of MAC and 1 control with severe MAC but no SAM. All controls were matched for age, sex, BSA, and septal wall thickness (±1.5 mm). 2-D echocardiographic measurements were taken from the parasternal long-axis (PLAX), apical 3-chamber and apical 4-chamber views. Results MAC+SAM vs MAC no-SAM. Three notable differences were observed: MAC+SAM patients, as compared with MAC no-SAM, had a smaller left ventricular outflow tract (LVOT), longer anterior mitral leaflet, and greater displacement of the MV coaptation point towards the interventricular septum (Figure 1). Median values for these 3 factors were determined using the no-MAC controls; each MAC subject was then scored for number of factors exceeding those values. MAC+SAM patients had a mean score of 2.7 vs 1.1 for MAC no-SAM patients. By combining anterior mitral leaflet length and coaptation point-septal distance as a ratio we could effectively separate MAC+SAM vs MAC no-SAM when >0.9 with one exception (Figure 2). We also observed a smaller anteroposterior annular dimension in the MAC+SAM group. MAC no-SAM vs no-MAC. Comparing these groups there were no differences in LVOT diameter or coaptation-septal distance; effective anterior mitral leaflet length was smaller in MAC no-SAM subjects vs no-MAC controls while anteroposterior dimension of the annulus was larger. Conclusions SAM develops in a subset of patients with severe calcification of the mitral annulus. These patients have a smaller anteroposterior annular dimension, possibly due to severe MAC. Other notable differences characterize MAC patients with SAM from those without. The LVOT is smaller, the effective anterior mitral leaflet length is longer, and the point of leaflet coaptation is displaced towards the septum. Using the ratio of anterior mitral leaflet length/coaptation point-septal distance in this study sample effectively separated those MAC patients with SAM from those without. FUNDunding Acknowledgement Type of funding sources: None. Figure 1 Figure 2
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