Abstract 1866: Assessment of Mechanical Dyssynchrony in Patients with Primary (AL) Systemic Amyloidosis and Cardiac Involvement
Background: In patients with cardiac amyloidosis infiltration of the conducting system may be a potential cause of mechanical dyssynchrony. The aim of this study was to assess the mechanical dyssynchrony in patients with cardiac amyloidosis (CA) using standard Doppler echocardiography and tissue Doppler imaging (TDI).
Methods: We included 103 patients with primary amyloidosis and 27 healthy controls. Patients were divided into two groups: 68 non CA, and 35 overt CA, according to left ventricular (LV) thickness (table⇓). We excluded patients with atrial fibrillation (n=5) or a pacemaker (n=5). Dyssynchrony assessment included:
atrio-ventricular (A-V) dyssynchrony (dys), the ratio between diastolic filling time and duration of a complete cardiac cycle (A LV filling time of < 40% cardiac cycle is indicative of A-V dys.),
interventricular dys., difference between the left and right ventricular pre-ejection interval (> 40 ms is considered abnormal), and
intraventricular dys. assessed by tissue velocity imaging (TVI), using the standard deviation of time to systolic peak (Ts-SD) of the 12 LV segments, and by the maximal difference in Ts between any two of the LV segments (> 32 msec and >100 msec, respectively, considered abnormal).
Results: Contrary to the hypothesis, the intraventricular dys. indices in overt CA patients were reduced as compared either to controls or to the non-CA group (p<0.05). The morphology of TVI curves was abnormal in the overt CA group and differed from controls and Non CA patients
Conclusions: Dys. indices in overt CA patients were reduced compared to controls and, more impressively, to the non-CA patients with systemic amyloidosis. The regional timing of systolic motion measured by tissue velocity was highly synchronized in the patients with overt cardiac amyloidosis. Further investigation will be needed to clarify the effect of super-normal synchrony on the hemodynamic abnormality in the cardiac amyloidosis