Bayes Syndrome and Myocardial Fibrosis: Mechanistic Links and Clinical Implications

Figures

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  Fig. 1.. The pathophysiological mechanisms underlying myocardial fibrosis and the subsequent pathway leading to IAB. This schematic provides a guided overview of the proposed pathway linking pressure overload/oxidative stress to inflammatory and pro-fibrotic remodeling. Pressure overload and oxidative stress activate NF-κB and TGF-β signaling, amplifying inflammatory cytokine production. Following myocardial injury, macrophage infiltration and phenotypic transitions enhance cytokine- and exosome-mediated communication with cardiac (atrial) fibroblasts, promoting myofibroblast differentiation. The resulting collagen/ECM accumulation drives fibrosis and collagen-based scar formation, which may impair interatrial conduction (including Bachmann’s bundle) and contribute to IAB. IAB, advanced interatrial block; TGF-β,transforming growth factor-β; NF-κB, nuclear factor kappaB; ECM, extracellular matrix; ROS, reactive oxygen species; TNF-α, tumor necrosis factor-alpha; IL-1β, interleukin-1beta. Figure created using Scientific Image and Illustration Software | BioRender.

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  Fig. 2.. Application of imaging modalities in the assessment of interatrial block and myocardial fibrosis. The upper panels summarize key imaging approaches—conventional echocardiography, CMR and advanced echocardiography (STE and TDI)—highlighting their major readouts, advantages, limitations, and typical clinical applications in evaluating atrial structure/function and fibrosis-related phenotypes. The lower schematic illustrates the complementary, stepwise strategy for integrated phenotyping and risk stratification: ECG (electrical phenotype; P-wave indices/A-IAB pattern) → echo/STE (mechanical phenotype; LA size and strain) → CMR (tissue phenotype; LGE fibrosis burden ± T1 mapping) → integrated assessment to estimate substrate severity and AF/stroke risk. LA, left atrium; AF, atrial fibrillation; IAB, interatrial block; FACM, fibrotic atrial cardiomyopathy; STE, speckle-tracking echocardiography; CMR, cardiac magnetic resonance; TDI, tissue Doppler imaging; EMD, electromechanical delay; ECG, electrocardiogram; LGE, late gadolinium enhancement. Figure created using Scientific Image and Illustration Software | BioRender.

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  Fig. 3.. Proposed coupling between Bayes syndrome (IAB) and atrial fibrosis. This schematic integrates major mechanistic domains—oxidative stress, ischemic injury, neurohumoral activation (RAAS/Ang II), and mechanical loading—to illustrate a proposed self-reinforcing remodeling loop between atrial fibrosis and A-IAB. The four quadrants organize pathways by domain, and the central loop summarizes the bidirectional coupling: fibrosis facilitates conduction discontinuity and interatrial conduction delay, whereas A-IAB–associated desynchronization and atrial pressure overload may further promote remodeling. Solid arrows denote better-supported links; dashed arrows indicate hypothesized or indirect pathways requiring further validation. ROS, reactive oxygen species; IAB, interatrial block; Ang II, angiotensin II; TGF-β, transforming growth factor β; RAAS, renin-angiotensin-aldosterone system; PLC, phospholipase C. Figure created using Scientific Image and Illustration Software | BioRender.

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  Fig. 4.. Integrated diagnostic workflow for Bayes syndrome (advanced interatrial block) and individualized management. Patients with clinical suspicion undergo 12-lead ECG to identify A-IAB (PWD ≥120 ms with biphasic P waves in inferior leads). Risk stratification and multimodality imaging (TTE ± STE; selective CMR for fibrosis) guide rhythm monitoring and individualized decisions on follow-up intensity, rhythm-control strategies, and antithrombotic management. A-IAB, advanced interatrial block; LA, left atrium; PWD, P-wave duration; TTE, transthoracic echocardiography; STE, speckle-tracking echocardiography; CMR, cardiac magnetic resonance; LGE, late gadolinium enhancement; TIA, transient ischemic attack. Figure created using Scientific Image and Illustration Software | BioRender.