Chest pain in cardiac amyloidosis: occurrence, causes and prognostic significance.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 10 2023
Historique:
received: 30 03 2023
revised: 01 07 2023
accepted: 19 07 2023
medline: 8 9 2023
pubmed: 23 7 2023
entrez: 22 7 2023
Statut: ppublish

Résumé

Chest pain is experienced by patients with cardiac amyloidosis (CA), but a systematic investigation of its frequency, underlying etiologies and clinical significance is lacking. Clinical, echocardiographic, laboratory characteristics, available coronary arteries imaging and endomyocardial biopsy (EMB) findings of 174 patients with CA (n = 104 with transthyretin, ATTR; n = 70 with light chains, AL) were analyzed. Chest pain was reported in 66 (38%) CA patients. Compared to those without, patients with chest pain had more frequently a history of coronary artery disease (CAD) (27% vs 15%, p = 0.048) and heart failure (HF) symptoms (62% vs 43%, p = 0.015), higher high sensitivity troponin I (hs-cTnI, 101 vs 65 ng/L, p = 0.032) and higher brain natriuretic peptide (597 vs 407 ng/L, p = 0.024). Among CA patients with chest pain undergoing coronary arteries imaging (n = 37), obstructive CAD was detected in 14 (38%), 13 of whom with ATTR-CA. Of these 37 patients, EMB was available in 10 and vascular/perivascular amyloid deposition was detected in 4/5 (80%) of AL-CA patients and 1/5 ATTR-CA. Among patients with suspected acute coronary syndrome (n = 22), obstructive CAD was detected in 9/17 (53%) ATTR-CA and 0/5 AL-CA; hs-cTnI levels were similar between those with and without obstructive CAD. During a follow-up of 17 (8-34) months, chest pain was a significant predictor of HF hospitalization (HR1.86, 95% CI 1.02-3.39, p = 0.042), even after adjustment for CA subtype and CAD. Chest pain is a common symptom in patients with CA, reflects a more advanced cardiac impairment and predicts future HF hospitalization. The etiology of chest pain seems to differ, with obstructive CAD more frequent in ATTR-CA whilst amyloid vascular/perivascular involvement more common in AL-CA.

Sections du résumé

BACKGROUND
Chest pain is experienced by patients with cardiac amyloidosis (CA), but a systematic investigation of its frequency, underlying etiologies and clinical significance is lacking.
METHODS
Clinical, echocardiographic, laboratory characteristics, available coronary arteries imaging and endomyocardial biopsy (EMB) findings of 174 patients with CA (n = 104 with transthyretin, ATTR; n = 70 with light chains, AL) were analyzed.
RESULTS
Chest pain was reported in 66 (38%) CA patients. Compared to those without, patients with chest pain had more frequently a history of coronary artery disease (CAD) (27% vs 15%, p = 0.048) and heart failure (HF) symptoms (62% vs 43%, p = 0.015), higher high sensitivity troponin I (hs-cTnI, 101 vs 65 ng/L, p = 0.032) and higher brain natriuretic peptide (597 vs 407 ng/L, p = 0.024). Among CA patients with chest pain undergoing coronary arteries imaging (n = 37), obstructive CAD was detected in 14 (38%), 13 of whom with ATTR-CA. Of these 37 patients, EMB was available in 10 and vascular/perivascular amyloid deposition was detected in 4/5 (80%) of AL-CA patients and 1/5 ATTR-CA. Among patients with suspected acute coronary syndrome (n = 22), obstructive CAD was detected in 9/17 (53%) ATTR-CA and 0/5 AL-CA; hs-cTnI levels were similar between those with and without obstructive CAD. During a follow-up of 17 (8-34) months, chest pain was a significant predictor of HF hospitalization (HR1.86, 95% CI 1.02-3.39, p = 0.042), even after adjustment for CA subtype and CAD.
CONCLUSION
Chest pain is a common symptom in patients with CA, reflects a more advanced cardiac impairment and predicts future HF hospitalization. The etiology of chest pain seems to differ, with obstructive CAD more frequent in ATTR-CA whilst amyloid vascular/perivascular involvement more common in AL-CA.

Identifiants

pubmed: 37481000
pii: S0167-5273(23)01011-2
doi: 10.1016/j.ijcard.2023.131204
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

131204

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest Dr. De Michieli received honoraria from Pfizer Inc, Alnylam Pharmaceuticals, AstraZeneca Spa. Dr. Cipriani received honoraria from Pfizer Inc, Alnylam Pharmaceuticals, AstraZeneca Spa.  The other Authors report no relationships that could be construed as a conflict of interest.

Auteurs

Laura De Michieli (L)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy.

Monica De Gaspari (M)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiovascular Pathology Unit, University Hospital of Padua, Italy.

Giulio Sinigiani (G)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy.

Alessandro Lupi (A)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy.

Luca Vedovelli (L)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Unit of Biostatistics, Epidemiology and Public Health, University of Padua, Italy.

Alessandro Salvalaggio (A)

Department of Neurosciences, University of Padua, Italy; Padova Neuroscience Center (PNC), University of Padua, Italy.

Mila Della Barbera (M)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiovascular Pathology Unit, University Hospital of Padua, Italy.

Stefania Rizzo (S)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiovascular Pathology Unit, University Hospital of Padua, Italy.

Kalliopi Pilichou (K)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiovascular Pathology Unit, University Hospital of Padua, Italy.

Diego Cecchin (D)

Department of Medicine (DIMED), Nuclear Medicine Unit, University-Hospital of Padua, Italy.

Chiara Briani (C)

Department of Neurosciences, University of Padua, Italy.

Dario Gregori (D)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Unit of Biostatistics, Epidemiology and Public Health, University of Padua, Italy.

Giuseppe Tarantini (G)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiology Unit, University Hospital of Padua, Italy.

Tamara Berno (T)

Hematology And Clinical Immunology Branch, Department of Medicine, University of Padua, Italy.

Livio Trentin (L)

Hematology And Clinical Immunology Branch, Department of Medicine, University of Padua, Italy.

Cristina Basso (C)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiovascular Pathology Unit, University Hospital of Padua, Italy.

Domenico Corrado (D)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiology Unit, University Hospital of Padua, Italy.

Sabino Iliceto (S)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiology Unit, University Hospital of Padua, Italy.

Martina Perazzolo Marra (M)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiology Unit, University Hospital of Padua, Italy.

Alberto Cipriani (A)

Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Italy; Cardiology Unit, University Hospital of Padua, Italy. Electronic address: alberto.cipriani@unipd.it.

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