Atrial cardiomyopathy and systemic organ crosstalk: from mechanisms to clinical implications

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Abstract
Atrial cardiomyopathy (ACMP) encompasses structural, electrical and functional atrial abnormalities that have been associated with ischaemic stroke, heart failure and mortality, independent of atrial fibrillation (AF). Increasing evidence suggests that AF, stroke and other adverse outcomes may represent parallel manifestations of ACMP. In the present narrative review, we synthesise current experimental and clinical evidence on the risk factors, pathophysiology, diagnosis and stages of ACMP, and summarise its bidirectional interactions with affected organs, including the left ventricle, lungs, brain, kidneys and gut. ACMP can be considered as an upstream disease process driven by fibrosis, inflammation, oxidative stress, hypercoagulability, metabolic stress and adipose tissue. Through haemodynamic, neurohormonal, inflammatory and thrombotic pathways, ACMP both contributes to and results from dysfunction in other organs, forming self-perpetuating cycles. ACMP can be characterised using complementary electrical, structural, functional and biomarker-based measures, although no single diagnostic standard exists. Disease progression appears staged, with earlier phases potentially reversible and advanced stages dominated by more permanent structural remodelling. Collectively, the evidence supports considering ACMP as a multiorgan disease, highlighting the need for an atrium-centred, integrated approach to risk stratification, preventive and therapeutic strategies.
Funding Information
  • Dutch Cardiovascular Alliance (01-002-2022-0118 EmbRACE)
  • Hartstichting (RACE V (CVON 2014–9))
  • Hartstichting (RED-CVD (CVON2017-11).)
  • Health~Holland (PPP Allowance; CVON-AI (2018B017))
  • European Union’s Horizon 2020 Research and Innovation Programme (EHRA-PATHS (945260))
  • ZonMw (DECISION project 848090001)

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