Aortic Valve Annular Properties in Cardiac Amyloidosis—Insights from the Three-Dimensional Speckle Tracking Echocardiographic MAGYAR-Path Study

<b>Introduction.</b> The etiology of cardiac amyloidosis (CA) involves the systemic or localized deposition of misfolded amyloid proteins within the myocardial interstitium and valvular structures. The primary objective of this study was to employ three-dimensional speckle-tracking echocardiography (3DSTE) to perform a detailed analysis of the aortic valve annulus (AVA) and left ventricular (LV) strains in CA patients and to compare these parameters with those of matched healthy controls. <b>Methods.</b> The initial cohort for this study comprised 35 individuals diagnosed with CA. However, 12 patients were subsequently excluded from the final analysis due to suboptimal image quality precluding accurate measurement of AVA dimensions and/or LV strains. The final analytical group, therefore, consisted of 23 CA patients (14 males), with a mean age of 64.6 ± 7.1 years. The results obtained from the CA patient group were compared with those of a healthy control cohort comprising 23 individuals (14 males; mean age: 53.2 ± 5.3 years). <b>Results.</b> In CA patients, AVA area was greater in end-diastole in 11 out of 23 cases (48%), and in end-systole in 8 out of 23 cases (35%), while it proved to be equal in 4 out of 23 cases (17%). The ratio of healthy controls with greater end-diastolic AVA area (12 out of 23, 52%) and greater end-systolic AVA area (11 out of 23, 48%) did not differ from that of CA patients. End-diastolic and end-systolic maximum and minimum AVA diameters, areas and perimeters did not differ between CA patients and matched controls. AVA plane systolic excursion (AAPSE) was found to be significantly impaired in all CA patients irrespective of AVA area size. Basal LV radial (RS), circumferential (CS) and longitudinal (LS) strains were reduced in CA patients compared with those of controls. End-systolic AVA dimensions tended to be reduced in CA patients with greater end-diastolic AVA area compared with those with greater end-systolic AVA area. While basal LV-RS and LV-CS proved to be similar between CA subgroups, basal LV-LS tended to be higher in CA patients with greater end-systolic AVA area. Controls with greater end-diastolic AVA area showed lower basal LV-RS and LV-LS compared with those with greater end-systolic AVA area. CA patients with equal end-diastolic and end-systolic AVA area (<i>n</i> = 4) showed similarly reduced AAPSE, basal LV-RS, basal LV-CS and LV-LS. <b>Conclusions.</b> In the presence of CA, the AVA is not dilated; however, its spatial displacement is reduced, suggesting its functional impairment, as represented by AAPSE, possibly due to the reduction in all concomitant LV strain parameters.