Electromechanical reciprocity and arrhythmogenesis in long-QT syndrome and beyond.

Autor:	Odening KE; Translational Cardiology, Department of Cardiology, Inselspital, Bern University Hospital, University of Bern, Freiburgstrasse 18, 3010, Bern, Switzerland.; Institute of Physiology, University of Bern, Bühlplatz 5, 3012, Bern, Switzerland., van der Linde HJ; Janssen Research & Development, Division of Janssen Pharmaceutica N.V., Beerse, Belgium., Ackerman MJ; Department of Cardiovascular Medicine, Division of Heart Rhythm Services (Windland Smith Rice Genetic Heart Rhythm Clinic), Mayo Clinic, Rochester, MN, USA.; Department of Pediatric and Adolescent Medicine, Division of Pediatric Cardiology, Mayo Clinic, Rochester, MN, USA.; Department of Molecular Pharmacology & Experimental Therapeutics (Windland Smith Rice Sudden Death Genomics Laboratory), Mayo Clinic, Rochester, MN, USA., Volders PGA; Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center+, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands., Ter Bekke RMA; Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center+, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands.
Jazyk:	angličtina
Zdroj:	European heart journal [Eur Heart J] 2022 Aug 21; Vol. 43 (32), pp. 3018-3028.
DOI:	10.1093/eurheartj/ehac135
Abstrakt:	An abundance of literature describes physiological and pathological determinants of cardiac performance, building on the principles of excitation-contraction coupling. However, the mutual influencing of excitation-contraction and mechano-electrical feedback in the beating heart, here designated 'electromechanical reciprocity', remains poorly recognized clinically, despite the awareness that external and cardiac-internal mechanical stimuli can trigger electrical responses and arrhythmia. This review focuses on electromechanical reciprocity in the long-QT syndrome (LQTS), historically considered a purely electrical disease, but now appreciated as paradigmatic for the understanding of mechano-electrical contributions to arrhythmogenesis in this and other cardiac conditions. Electromechanical dispersion in LQTS is characterized by heterogeneously prolonged ventricular repolarization, besides altered contraction duration and relaxation. Mechanical alterations may deviate from what would be expected from global and regional repolarization abnormalities. Pathological repolarization prolongation outlasts mechanical systole in patients with LQTS, yielding a negative electromechanical window (EMW), which is most pronounced in symptomatic patients. The electromechanical window is a superior and independent arrhythmia-risk predictor compared with the heart rate-corrected QT. A negative EMW implies that the ventricle is deformed-by volume loading during the rapid filling phase-when repolarization is still ongoing. This creates a 'sensitized' electromechanical substrate, in which inadvertent electrical or mechanical stimuli such as local after-depolarizations, after-contractions, or dyssynchrony can trigger abnormal impulses. Increased sympathetic-nerve activity and pause-dependent potentiation further exaggerate electromechanical heterogeneities, promoting arrhythmogenesis. Unraveling electromechanical reciprocity advances the understanding of arrhythmia formation in various conditions. Real-time image integration of cardiac electrophysiology and mechanics offers new opportunities to address challenges in arrhythmia management. Competing Interests: Conflicts of interest: K.E.O, H.J.v.d.L, P.G.A.V., and R.M.A.t.B declare no conflict of interest. M.J.A. declares royalties from AliveCor, Anumana, Pfizer; consulting fees from Abbott, ARMGO Pharma, Boston Scientific, Bristol Myers Squipp, Daiichi Sankyo, Invitae, Medtronic, UpToDate; and a leadership role (President of Board) at the Sudden Arrhythmia Death Syndromes (SADS) Foundation. (© The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology.)
Databáze:	MEDLINE
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