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The Prevalence of Advanced Interatrial Block and Its Relationship to Left Atrial Function in Patients with Transthyretin Cardiac Amyloidosis
Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.ORCID iD: 0000-0002-8192-9166
2021 (English)In: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 10, no 13, article id 2764Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Advanced interatrial block (aIAB), which is associated with incident atrial fibrillation and stroke, occurs in the setting of blocked interatrial conduction. Atrial amyloid deposition could be a possible substrate for reduced interatrial conduction, but the prevalence of aIAB in patients with transthyretin cardiac amyloidosis (ATTR-CA) is unknown. We aimed to describe the prevalence of aIAB and its relationship to left atrial function in patients with ATTR-CA in comparison to patients with HF and left ventricular hypertrophy but no CA.

METHODS: The presence of aIAB was investigated among 75 patients (49 patients with ATTR-CA and 26 with HF but no CA). A comprehensive echocardiographic investigation was performed in all patients, including left atrial strain and strain rate measurements.

RESULTS: Among patients with ATTR-CA, 27% had aIAB and in patients with HF but no CA, this figure was 21%, (p = 0.78). The presence of aIAB was associated with a low strain rate during atrial contraction (<0.91 s-1) (OR: 5.2 (1.4-19.9)), even after adjusting for age and LAVi (OR: 4.5 (1.0-19.19)).

CONCLUSIONS: Advanced interatrial block is common among patients with ATTR-CA, as well as in patients with heart failure and left ventricular hypertrophy but no CA. aIAB is associated with reduced left atrial contractile function.

Place, publisher, year, edition, pages
MDPI, 2021. Vol. 10, no 13, article id 2764
Keywords [en]
cardiac amyloidosis, interatrial block, left atrial strain, transthyretin amyloid
National Category
Other Clinical Medicine
Identifiers
URN: urn:nbn:se:umu:diva-185801DOI: 10.3390/jcm10132764ISI: 000671206000001PubMedID: 34201866Scopus ID: 2-s2.0-85114079822OAI: oai:DiVA.org:umu-185801DiVA, id: diva2:1578723
Funder
Swedish Heart Lung Foundation, 20160787, 20200160Swedish Research Council, 2019-01338.Available from: 2021-07-07 Created: 2021-07-07 Last updated: 2023-09-05Bibliographically approved

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Lindqvist, Per

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