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Peer-reviewedCC BY 4.0JACC Case Reports

9-Year Serial CMR Monitoring of Cardiac AL Amyloidosis Regression After Teclistamab

  1. 1Department of Radiology and Cardiovascular Imaging, GHICL–Groupement des Hôpitaux de l’Institut Catholique de Lille, Lille, France
  2. 2Department of Hematology, GHICL–Groupement des Hôpitaux de l'Institut Catholique de Lille–Hôpital Saint-Vincent-de-Paul, Lille, France

Abstract

Background: Cardiac amyloid light-chain (AL) amyloidosis carries a poor prognosis and is considered largely irreversible once symptomatic. Long-term serial cardiovascular magnetic resonance (CMR) data following B-cell maturation antigen-directed therapy are lacking.

Case Summary: A 64-year-old man with biopsy-proven cardiac AL amyloidosis achieved sustained hematologic complete response after teclistamab following failure of 4 prior lines including daratumumab. Eleven CMR examinations over 9 years documented a biphasic trajectory: progressive infiltration through 2020 (left ventricular mass 186 g, wall thickness 18 mm, global longitudinal strain −4.8%), followed by sustained structural and functional regression through 2025 (left ventricular mass 127 g, wall thickness 13 mm, global longitudinal strain −13.7%).

Discussion: This represents the longest serial CMR follow-up in cardiac AL amyloidosis reported to date, demonstrating that cine-derived parameters reliably track cardiac regression in real-world conditions. Native T1 normalized while extracellular volume fraction (ECV) paradoxically increased, suggesting persistent fibril burden beyond hematologic clearance.

Take-Home Message: Serial CMR with cine-derived parameters provides robust longitudinal monitoring of cardiac AL amyloidosis regression following novel plasma cell–directed therapy, even without systematic contrast enhancement.

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BibTeX
@article{silvestri20269year,
  title = {{9-Year Serial CMR Monitoring of Cardiac AL Amyloidosis Regression After Teclistamab}},
  author = {Valentina Silvestri and Manuel Toledano and Bénédicte Hivert and Emmanuelle Bourgeois and Benjamin Carpentier and Jean Giraud and Alexandre Willaume and François Delelis and Laurent Pascal},
  journal = {JACC Case Reports},
  year = {2026},
  month = aug,
  doi = {10.1016/j.jaccas.2026.109553},
  url = {https://doi.org/10.1016/j.jaccas.2026.109553},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - 9-Year Serial CMR Monitoring of Cardiac AL Amyloidosis Regression After Teclistamab
AU  - Valentina Silvestri
AU  - Manuel Toledano
AU  - Bénédicte Hivert
AU  - Emmanuelle Bourgeois
AU  - Benjamin Carpentier
AU  - Jean Giraud
AU  - Alexandre Willaume
AU  - François Delelis
AU  - Laurent Pascal
PY  - 2026
DA  - 2026/08/27
JO  - JACC Case Reports
DO  - 10.1016/j.jaccas.2026.109553
UR  - https://doi.org/10.1016/j.jaccas.2026.109553
AB  - Background: Cardiac amyloid light-chain (AL) amyloidosis carries a poor prognosis and is considered largely irreversible once symptomatic. Long-term serial cardiovascular magnetic resonance (CMR) data following B-cell maturation antigen-directed therapy are lacking.  Case Summary: A 64-year-old man with biopsy-proven cardiac AL amyloidosis achieved sustained hematologic complete response after teclistamab following failure of 4 prior lines including daratumumab. Eleven CMR examinations over 9 years documented a biphasic trajectory: progressive infiltration through 2020 (left ventricular mass 186 g, wall thickness 18 mm, global longitudinal strain −4.8%), followed by sustained structural and functional regression through 2025 (left ventricular mass 127 g, wall thickness 13 mm, global longitudinal strain −13.7%).  Discussion: This represents the longest serial CMR follow-up in cardiac AL amyloidosis reported to date, demonstrating that cine-derived parameters reliably track cardiac regression in real-world conditions. Native T1 normalized while extracellular volume fraction (ECV) paradoxically increased, suggesting persistent fibril burden beyond hematologic clearance.  Take-Home Message: Serial CMR with cine-derived parameters provides robust longitudinal monitoring of cardiac AL amyloidosis regression following novel plasma cell–directed therapy, even without systematic contrast enhancement.
SN  - 2666-0849
ER  -