ArticleJACC. Clinical electrophysiology2025
Microvascular Rarefaction in the Sinoatrial Node: A Potential Mechanism for Pacemaker Dysfunction in Early HFpEF.
Article in JACC. Clinical electrophysiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Beat-locked ATP microdomains in the sinoatrial node map a Ca2+-timed energetic hierarchy and regional pacemaker roles.The Journal of general physiology · 2026Article
- Demonstration of beat-to-beat, on-demand ATP synthesis in ventricular myocytes reveals sex-specific mitochondrial and cytosolic dynamics.The Journal of physiology · 2026Article
- Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model.The Journal of physiology · 2026Review
- Heart Rate Recovery Index as a Novel Marker in Heart Failure Assessment: A Comparative Analysis of Heart Rate Deceleration During Exercise Testing.International journal of general medicine · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundMicrovascular rarefaction is a feature of heart failure with preserved ejection fraction (HFpEF) that may underlie associated rhythm disturbances. Angiotensin II (AngII) signaling has been implicated, but its role in sinoatrial (SA) node dysfunction remains unclear.
objectivesThe authors tested whether changes in SA node microvascular architecture contribute to pacemaker dysfunction in early HFpEF.
methodsMice received a 28-day subcutaneous infusion of a sub-pressor dose of AngII. Electrocardiography, echocardiography, confocal imaging, spatial RNA detection, and optical mapping were used to assess SA node structure and function.
resultsHeart rate declined progressively during AngII infusion, with males falling from 605 ± 6 beats/min to 490 ± 6 beats/min and females from 646 ± 23 beats/min to 511 ± 10 beats/min by day 28. Bradycardia was accompanied by increased beat-to-beat variability: the percentage of consecutive heartbeats that differed in duration by >6 milliseconds increased from 3.5% ± 1.3% to 32.1% ± 4.5% in males and from 3.8% ± 1.1% to 27.7% ± 2.5% in females. These changes coincided with reduced microvessel density in the superior SA node (males: 6.1 ± 0.5 nm/μm
conclusionsThese findings highlight microvascular rarefaction in the superior SA node as a key early event in HFpEF pathology. The loss of redundant vascular loops compromises metabolic support for pacemaking, illustrating a broader principle: rarefaction can impair excitability in metabolically demanding excitable tissues.
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