From a simplified pathophysiological point-of-view, cardiac AL is different from cardiac ATTR and not only characterized by “extracellular” accumulation of (light-chain) amyloid fibrils, but also by toxic effects that are caused by those light-chains, subsequently leading to myocardial inflammation as well as intra- and extracellular edema (including myocyte swelling). Here, TTR is linked to axial length measurement.