Amyloidosis is a group of diseases caused by infiltration and deposition of abnormally folded proteins known as fibrils in a variety of tissues. The heart is a frequent and critical target. This cardiac deposition can result in mechanical disruption of cardiac function, resulting in restrictive cardiomyopathy and heart failure and electrical disruption, resulting in abnormal cardiac conduction. The vast majority of cases of amyloid cardiac disease are due to two etiologies, either light chain or AL amyloid and transthyretin (ATTR) amyloid which can be further subdivided into wild type (ATTRwt) and variant (ATTRv) forms. Specific mutations in ATTR are more likely to result in cardiac involvement. The diagnosis of cardiac amyloid in general and specific types relies on combination of clinical, lab, electrocardiographic, and imaging findings. Echocardiography, Cardiac Magnetic Resonance Imaging and scintigraphic (pyrophosphate) imaging have specific features which support the diagnosis of cardiac amyloid. Tissue biopsies, specifically endomyocardial or abdominal fat pad with congo red staining and negative birefringence, support the diagnosis of amyloid. For AL amyloid, serum and/or urine electrophoresis with the presence of light chains points to diagnosis with confirmation by bone marrow biopsy. Treatment depends on the type of amyloid with therapies for AL amyloid being directed toward reduction of the population of abnormal plasma cells which produce light chains. This therapy is either chemotherapy or stem cell transplantation. For ATTR amyloid, there are therapies directed against production of the abnormal transthyretin, either stabilizers which reduce the production of TTR protein. The therapies directed against TTR protein have been shown to improve cardiac function and improve survival.