Ana Devesa1,2, Andrea Camblor Blasco1, Ana María Pello Lázaro1, Elham Askari3, Gregoria Lapeña4, Sandra Gómez Talavera1,2,5, Mikel Taibo Urquía1, Celia Rodríguez Olleros6, José Tuñón1,5,7, Borja Ibáñez1,2,5, Álvaro Aceña1,7. 1. Department of Cardiology, IIS - Fundación Jiménez Díaz University Hospital - Quironsalud, Av. Reyes Católicos, 2, Madrid, 28040, Spain. 2. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro, 3, Madrid, 28029, Spain. 3. Department of Hematology, Fundación Jiménez Díaz University Hospital- Quironsalud, Madrid, Spain. 4. Department of Nuclear Medicine, Fundación Jiménez Díaz University Hospital- Quironsalud, Madrid, Spain. 5. Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain. 6. Department of Internal Medicine, Fundación Jiménez Díaz University Hospital- Quironsalud, Madrid, Spain. 7. Universidad Autónoma de Madrid, Madrid, Spain.
Abstract
AIMS: As evidenced by scintigraphy imaging, the prevalence of transthyretin (TTR) cardiac amyloidosis in heart failure patients with preserved ejection fraction (HFpEF) and left ventricular hypertrophy (LVH) ranges between 13% and 19%. The natural evolution of cardiac amyloidosis begins with the deposition of amyloid material in the myocardium, with LVH ensuing at later stages. With current imaging modalities, it is possible to detect TTR cardiac amyloidosis before the hypertrophic stage. The aim of this study was to determine the prevalence of TTR cardiac amyloidosis in HFpEF patients without LVH. METHODS AND RESULTS: The study prospectively enrolled patients admitted for HF with LV ejection fraction (LVEF) ≥ 50% and LV wall thickness <12 mm. TTR cardiac amyloidosis was diagnosed according to accepted criteria, which include positive cardiac 99-Tc-DPD scintigraphy in the absence of monoclonal protein expansion in blood. Transthyretin gene sequencing was performed in positive patients. From July 2017 to January 2020, 329 patients with HFpEF and LV thickness <12 mm were identified. After exclusions, 58 patients completed the study with cardiac scintigraphy (79 years, 54% men; median LVEF 60% and LV wall thickness 10.5 mm). Three patients (5.2%) were positive for TTR cardiac amyloidosis; genetic analysis excluded the presence of hereditary TTR amyloidosis. Positive patients baseline characteristics (84 years, 67% men, LVEF 60%, and LV wall thickness 11 mm) were similar to patients without TTR, except for troponin levels (0.05 vs. 0.02 ng/mL, P = 0.03) and glomerular filtration rate (82 vs. 60 mL/min, P = 0.032), which were higher in TTR patients. CONCLUSIONS: In a cohort of patients with HFpEF without LVH, the prevalence of TTR cardiac amyloidosis was 5%. Early diagnosis of cardiac involvement in TTR amyloidosis (before manifest LVH) would seem recommendable because newly approved specific treatments can prevent additional deposition of amyloid material.
AIMS: As evidenced by scintigraphy imaging, the prevalence of transthyretin (TTR) cardiac amyloidosis in heart failurepatients with preserved ejection fraction (HFpEF) and left ventricular hypertrophy (LVH) ranges between 13% and 19%. The natural evolution of cardiac amyloidosis begins with the deposition of amyloid material in the myocardium, with LVH ensuing at later stages. With current imaging modalities, it is possible to detect TTRcardiac amyloidosis before the hypertrophic stage. The aim of this study was to determine the prevalence of TTRcardiac amyloidosis in HFpEF patients without LVH. METHODS AND RESULTS: The study prospectively enrolled patients admitted for HF with LV ejection fraction (LVEF) ≥ 50% and LV wall thickness <12 mm. TTRcardiac amyloidosis was diagnosed according to accepted criteria, which include positive cardiac 99-Tc-DPD scintigraphy in the absence of monoclonal protein expansion in blood. Transthyretin gene sequencing was performed in positive patients. From July 2017 to January 2020, 329 patients with HFpEF and LV thickness <12 mm were identified. After exclusions, 58 patients completed the study with cardiac scintigraphy (79 years, 54% men; median LVEF 60% and LV wall thickness 10.5 mm). Three patients (5.2%) were positive for TTRcardiac amyloidosis; genetic analysis excluded the presence of hereditary TTR amyloidosis. Positive patients baseline characteristics (84 years, 67% men, LVEF 60%, and LV wall thickness 11 mm) were similar to patients without TTR, except for troponin levels (0.05 vs. 0.02 ng/mL, P = 0.03) and glomerular filtration rate (82 vs. 60 mL/min, P = 0.032), which were higher in TTRpatients. CONCLUSIONS: In a cohort of patients with HFpEF without LVH, the prevalence of TTRcardiac amyloidosis was 5%. Early diagnosis of cardiac involvement in TTRamyloidosis (before manifest LVH) would seem recommendable because newly approved specific treatments can prevent additional deposition of amyloid material.
Authors: Svenja Ney; Peter Ihle; Thomas Ruhnke; Christian Günster; Guido Michels; Katharina Seuthe; Martin Hellmich; Roman Pfister Journal: Clin Res Cardiol Date: 2022-10-14 Impact factor: 6.138
Authors: Daniella Nagy; Katalin Révész; Gergely Peskó; Gergely Varga; Laura Horváth; Péter Farkas; András Dávid Tóth; Róbert Sepp; Hajnalka Vágó; Anikó Ilona Nagy; Tamás Masszi; Zoltán Pozsonyi Journal: Biomedicines Date: 2022-07-21