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The current management paradigm for heart failure (HF) and cardiomyopathies predominantly emphasizes structural and ischemic etiologies, often overlooking the substantial role of electrical dyssynchrony in cardiac dysfunction and remodeling. This work introduces a novel conceptual framework that integrates existing evidence illustrating how electrical dyssynchrony induces mechanical dyssynchrony, culminating in regional cardiac impairment and structural remodeling. The myocardial area that activated early lacks proper afterload, impairing its ability to perform work effectively. Consequently, disuse atrophy gradually manifests in the early activation area over time. We propose the concept of early\u2010excitation segment atrophy (EESA) syndrome to address the HF caused by asynchronous conduction. For the left ventricle, whichever part contracts first will become disused and may contribute to or exacerbate HF. The conduction abnormalities known to induce EESA include left bundle branch block (LBBB), right ventricular pacing (RVP), bilateral bundle branch block (BBBB), Wolff\u2013Parkinson\u2013White (WPW) syndrome, and premature ventricular contractions (PVCs). Appropriate diagnosis and treatment will lead to improved left ventricular ejection fraction and reduced mortality. By integrating EESA into clinical practice, we aim to improve the recognition and management of dyssynchrony\u2010induced cardiomyopathies, ultimately enhancing patient outcomes. This review presents an update of the mechanisms, prevalence, incidence, and risk factors, as well as their diagnosis and management, while highlighting current gaps of knowledge.<\/jats:p>","DOI":"10.1111\/pace.70130","type":"journal-article","created":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T18:06:32Z","timestamp":1768845992000},"page":"425-434","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Early\u2010Excitation Segment Atrophy (EESA) Syndrome: Linking Electrical Dyssynchrony to Regional Myocardial Atrophy"],"prefix":"10.1111","volume":"49","author":[{"given":"Sanshuai","family":"Chang","sequence":"first","affiliation":[{"name":"Department of Cardiology Beijing Anzhen Hospital, Capital Medical University, National Clinical Research Centre for Cardiovascular Diseases  Beijing 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