<h3>Purpose</h3> Transthyretin amyloidosis (ATTR) is an increasingly recognized cause of cardiomyopathy (CMY). Both genetic variant (v-ATTR) and wild-type (wt-ATTR) amyloidosis present with a restrictive phenotype characterized by thick ventricular walls, small ventricular cavity, and left atrial enlargement. We present a series of 4 patients (pts) with non-restrictive phenotypes that were identified to have cardiac amyloidosis at heart transplant (HT). <h3>Methods</h3> Between 11/2019 to 10/2020, 4/121 heart explants were identified with a non-restrictive phenotype and amyloid deposition. All 4 pts were male, 3 were black, and only Case 1 had a history of coronary artery disease. Pre-HT transthoracic echocardiograms (TTE) were reviewed. Explants were evaluated by gross examination, light microscopy, immunohistochemical staining (kappa light chains, lamba light chains, beta-2-microglobulin, amyloid A, transthyretin), and mass spectrometry. <h3>Results</h3> Pre-HT TTE demonstrated low EF, normal left ventricular (LV) wall thickness, and LV dilation in all cases (>95<sup>th</sup> percentile for height and gender). The mean LV end diastolic internal diameter (LVIDd) was 69 mm (range 61-80) and LVIDd adjusted for body surface area was 36 mm/m<sup>2</sup> (range 28-48). There was no evidence of ventricular wall thickening. Mean LV EF was 19% (range 15-25) and 3 pts had moderate right ventricular dysfunction. Explant pathology was notable for interstitial and perivascular Congo Red positive deposits. Mass spectrometry confirmed presence of v-ATTR (3 cases) and amyloidosis leukocyte chemotactic factor 2 (ALECT2) (1 case). In 2 cases, amyloid deposits were found diffusely throughout the myocardium. <h3>Conclusion</h3> Amyloid CMY can present with a dilated phenotype composed of marked LV dilation and normal wall thickness. Further research is needed to determine the contribution of amyloidosis to the development of dilated cardiomyopathy as seen in these cases. Additionally, the relationship of non-ATTR genetics to typical and atypical cardiac amyloid phenotypes is unknown.