The therapeutic landscape for cardiac amyloidosis is rapidly evolving. In the last decade, our focus has shifted from dealing with the inevitable complications of continued extracellular infiltration of amyloid fibrils to earlier identification of these patients with prompt initiation of targeted therapy to prevent further deposition. Although much of the focus on novel targeted therapies is within the realm of transthyretin amyloidosis, light chain amyloidosis has benefited due to an overlap particularly in the final common pathway of fibrillogenesis and extraction of amyloid fibrils from the heart. Here, we review the targeted therapeutics for transthyretin and light chain amyloidosis. For transthyretin amyloidosis, the list of current and future therapeutics continues to evolve; and therefore, it is crucial to become familiar with the underlying mechanistic pathways of the disease. Although targeted therapeutic choices in AL amyloidosis are largely driven by the hematology team, the cardiac adverse effect profiles of these therapies, particularly in those with advanced amyloidosis, provide an opportunity for early recognition to prevent decompensation and can help inform recommendations regarding therapy changes when required.

心脏淀粉样变性的治疗前景正在迅速发展。在过去十年中，我们的重点已从处理淀粉样原纤维持续细胞外浸润的不可避免的并发症转移到早期识别这些患者并迅速开始靶向治疗以防止进一步沉积。尽管对新型靶向治疗的大部分关注都在转甲状腺素蛋白淀粉样变性领域，但轻链淀粉样变性受益于重叠，特别是在原纤维发生和从心脏提取淀粉样原纤维的最终共同途径中。在这里，我们回顾了转甲状腺素蛋白和轻链淀粉样变性的靶向治疗。对于转甲状腺素蛋白淀粉样变性，当前和未来的治疗方法清单不断发展；因此，熟悉该疾病的潜在机制至关重要。尽管 AL 淀粉样变性的靶向治疗选择主要由血液学团队推动，但这些疗法的心脏不良反应特征，特别是在晚期淀粉样变性患者中，为早期识别以防止失代偿提供了机会，并有助于在需要时提供有关治疗改变的建议.