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1. Mitral regurgitation impact on left atrial myopathy in hypertrophic cardiomyopathy

Author

Thomas Zegkos, Vasileios Kamperidis, Thomas Gossios, Dimitris Ntelios, Despoina Parcharidou, Christos A. Papanastasiou, Theofilos Panagiotidis, Theodora Tsianaka, Pavlos Rouskas, Sotiris Katranas, Haralambos Karvounis, and Georgios Efthimiadis

Subjects
Adult, Male, Muscular Diseases, Humans, Mitral Valve Insufficiency, Atrial Function, Left, Female, Radiology, Nuclear Medicine and imaging, Heart Atria, Cardiomyopathy, Hypertrophic, Middle Aged, Cardiology and Cardiovascular Medicine, Aged
Abstract

Recent studies have shown that mitral regurgitation (MR) represents a major determinant of left atrial (LA) function in patients with heart failure with preserved ejection fraction. The role of MR in determining LA myopathy in hypertrophic cardiomyopathy (HCM) is unknown. The aim of this study was to examine the association of MR with LA myopathy, assessed by LA strain values in HCM patients.In total 250 consecutive patients (mean age 51 ± 16 years, 67.2% male) with an established diagnosis of HCM and with sinus rhythm at index echocardiography evaluation were included. LA reservoir, conduit and booster strain were analyzed, besides LA size, left ventricular (LV) systolic and diastolic function. The predictors of LA strain values were identified with linear regression analysis.Significant (more than mild) MR was a significant univariate predictor of all the three LA strain values. In multivariate linear regression analysis, independent predictors of LA reservoir strain were more than mild MR (r = -.23), LV global longitudinal strain (r = -.49), LA volume index (r = -.27) and patient age (r = -.23). Significant MR was also an independent determinant of LA conduit (r = -.17) and booster strain (r = -.12). In patients with LA volume index 34 ml/mSignificant MR is associated with LA myopathy independently of the LV diastolic and systolic function and LA size.

Published
2022

2. Cardiac Outcomes in Adults With Mitochondrial Diseases

Author

Konstantinos Savvatis, Christoffer Rasmus Vissing, Lori Klouvi, Anca Florian, Mehjabin Rahman, Anthony Béhin, Abdallah Fayssoil, Marion Masingue, Tanya Stojkovic, Henri Marc Bécane, Nawal Berber, Fanny Mochel, Denis Duboc, Bertrand Fontaine, Bjørg Krett, Caroline Stalens, Julie Lejeune, Robert D.S. Pitceathly, Luis Lopes, Malika Saadi, Thomas Gossios, Vincent Procaccio, Marco Spinazzi, Céline Tard, Pascal De Groote, Claire-Marie Dhaenens, Claire Douillard, Andoni Echaniz-Laguna, Ros Quinlivan, Michael G. Hanna, Ali Yilmaz, John Vissing, Pascal Laforêt, Perry Elliott, Karim Wahbi, Queen Mary University of London (QMUL), IT University of Copenhagen (ITU), Association française contre les myopathies (AFM-Téléthon), University Hospital Münster - Universitaetsklinikum Muenster [Germany] (UKM), University College of London [London] (UCL), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Hôpital Raymond Poincaré [Garches], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université de Versailles Saint-Quentin-en-Yvelines - UFR Sciences de la santé Simone Veil (UVSQ Santé), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Université Paris Cité (UPCité), Sorbonne Université (SU), Hôpital Cochin [AP-HP], Aristotle University of Thessaloniki, MitoVasc - Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Département de Biochimie et Génétique [Angers], Université d'Angers (UA)-Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Lille Neurosciences & Cognition - U 1172 (LilNCog), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP), Hôpital Claude Huriez [Lille], CHU Lille, AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Handicap neuromusculaire : Physiopathologie, Biothérapie et Pharmacologies appliquées (END-ICAP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), MR/S005021/1, Association Française contre les Myopathies, AFM, Medical Research Council, MRC: MR/S002065/1, Department of Health and Social Care, DH, University College London Hospitals NHS Foundation Trust, UCLH, NIHR Cambridge Biomedical Research Centre, This study was funded by grants from the Association Française contre les Myopathies (French Alliance against Myopathies), which was not involved in the design and conduct of the study, the collection, management, analysis, and interpretation of the data, the preparation, review or approval of the manuscript, and nor in the decision to submit the manuscript for publication. Dr Pitceathly is supported by a Medical Research Council (United Kingdom) Clinician Scientist Fellowship (MR/S002065/1). Drs Pitceathly and Hanna receive funding from a Medical Research Council (United Kingdom) strategic award to establish an International Centre for Genomic Medicine in Neuromuscular Diseases (ICGNMD) (MR/S005021/1). Dr Lopes is supported by a Medical Research Council (United Kingdom) clinical academic partnership (CARP) award. Dr Quinlivan was funded by National Institute for Health and Care Research Biomedical Research Centre, University College Hospitals Foundation Trust. The University College London Hospitals/University College London Queen Square Institute of Neurology sequencing facility receives a proportion of funding from the Department of Health's National Institute for Health and Care Research Biomedical Research Centre’s funding scheme. The clinical and diagnostic 'Rare Mitochondrial Disorders' Service in London is funded by the U.K. NHS Highly Specialised Commissioners. Dr Elliott has received consultancy fees from Pfizer, Sanofi, Sarepta, DinaQor, Freeline, Novo Nordisk, and Bristol Myers Squibb. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Subjects
Adult, conduction disease, mitochondrial diseases, [SDV]Life Sciences [q-bio], heart failure, sudden death, Heart, Stroke Volume, Prognosis, DNA, Mitochondrial, Ventricular Function, Left, single large-scale deletions, Risk Factors, Humans, Hypertrophy, Left Ventricular, Cardiology and Cardiovascular Medicine, G%22">m3243A>G
Abstract

International audience; Background: Patients with mitochondrial diseases are at risk of heart failure (HF) and arrhythmic major adverse cardiac events (MACE). Objectives: We developed prediction models to estimate the risk of HF and arrhythmic MACE in this population. Methods: We determined the incidence and searched for predictors of HF and arrhythmic MACE using Cox regression in 600 adult patients from a multicenter registry with genetically confirmed mitochondrial diseases. Results: Over a median follow-up time of 6.67 years, 29 patients (4.9%) reached the HF endpoint, including 19 hospitalizations for nonterminal HF, 2 cardiac transplantations, and 8 deaths from HF. Thirty others (5.1%) reached the arrhythmic MACE, including 21 with third-degree or type II second-degree atrioventricular blocks, 4 with sinus node dysfunction, and 5 sudden cardiac deaths. Predictors of HF were the m.3243A>G variant (HR: 4.3; 95% CI: 1.8-10.1), conduction defects (HR: 3.0; 95% CI: 1.3-6.9), left ventricular (LV) hypertrophy (HR: 2.6; 95% CI: 1.1-5.8), LV ejection fraction

Published
2022

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