Objectives Atrial fibrillation (AF) is associated with increased morbidity and mortality in patients with hypertrophic cardiomyopathy (HCM). The primary aim of this study (HCM Risk-AF) was to determine the predictors of AF in a large multicentre cohort of patients with HCM. Exploratory analyses were performed to investigate the association between AF and survival and the efficacy of antiarrhythmic therapy in maintaining sinus rhythm (SR).
Methods A retrospective, longitudinal cohort of patients recruited between 1986 and 2008 in seven centres was used to develop multivariable Cox regression models fitted with preselected predictors. HCM was defined as unexplained hypertrophy (maximum left ventricular wall thickness of ≥15 mm or in accordance with published criteria for the diagnosis of familial disease). 28% of patients (n=1171) had coexistent hypertension. The primary end point was paroxysmal, permanent or persistent AF detected on ECG, Holter monitoring or implantable device interrogation.
Results Of the 4248 patients with HCM without pre-existing AF, 740 (17.4%) reached the primary end point. Multivariable Cox regression revealed an association between AF and female sex, age, left atrial diameter, New York Heart Association (NYHA) class, hypertension and vascular disease. The proportion of patients with cardiovascular death at 10 years was 4.9% in the SR group and 10.9% in the AF group (difference in proportions=5.9%; 95% CI (4.1% to 7.8%)). The proportion of patients with non-cardiovascular death at 10 years was 3.2% in the SR group and 5.9% in the AF group (difference in proportions=2.8%; 95% CI (0.1% to 4.2%)). An intention-to-treat propensity score analysis demonstrated that β-blockers, calcium channel antagonists and disopyramide initially maintained SR during follow-up, but their protective effect diminished with time. Amiodarone therapy did not prevent AF during follow-up.
Conclusion This study shows that patients with HCM who are at risk of AF development can be identified using readily available clinical parameters. The development of AF is associated with a poor prognosis but there was no evidence that antiarrhythmic therapy prevents AF in the long term.
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Collaborators Additional Hypertrophic Cardiomyopathy Outcomes investigators. Maite Tomé-Esteban1, Antonis Pantazis1, Shaughan Dickie1, Xusto Fernandez2, Angela Lopez2, Vasiliki Vlagkouli3, Antonio Romero4, Andrea Buono5, Giuseppe Pacileo5, Maria Gallego-Delgado6 and Marta Cobo-Marcos6: (1) The Inherited Cardiac Diseases Unit, The Heart Hospital/University College London, 16-18 Westmoreland St, London W1G8PH, UK; (2) Cardiology Department and Research Unit, A Coruña University Hospital, Galician Health Service, Spain; (3) Unit of Inherited Cardiovascular Diseases, First Department of Cardiology, University of Athens, 99 Michalakopoulou St, Athens 11527, Greece; (4) Cardiac Department, University Hospital Virgen Arrixaca, Murcia-Cartagena s/n. El Palmar, Murcia, 30120, Spain; (5) Monaldi Hospital, Second University of Naples, Via Leonardo Bianchi 1, Naples 80131, Italy; (6) Heart Failure and Inherited Cardiac Diseases Unit, Hospital Universitario Puerta del Hierro Majadahonda, Manuel de Falla, 1, 28222, Madrid, Spain.
Contributors OPG designed the study, collected and interpreted the data, carried out the descriptive statistical analysis and wrote the article. PME designed the study, interpreted the data and wrote the article. RZO was involved in study design, led the statistical aspects of the risk modelling and wrote the article. MP was involved in the study design and carried out the statistical analysis. COM, LM, AA, EB, JRG, GL, PG-P and CR collected and interpreted the data and critically reviewed the manuscript. WJM was involved in the drafting of the article and revised it critically for important intellectual content. Antonis Pantazis, Maite Tome-Esteban, Shaughan Dickie, Xusto Fernandez, Angela Lopez, Vasiliki Vlagkouli, Antonio Romero, Andrea Buono and Maria Gallego-Delgado and Marta Cobo-Marcos were involved in data collection and interpretation.
Funding This study was funded by the British Heart Foundation and by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. It was also partially supported by the Red Investigación Cardiovascular from the Instituto de Salud Carlos III, Spanish Ministry of Health (grants RD12/0042/0049, RD12/0042/0066 and RD12/0042/0069) and Project No. PI11/02604, integrated in the National Plan for Scientific Research, Development and Technological Innovation 2008–2011 and funded by the ISCIII-General Subdirection of Assessment and Promotion of the Research—European Regional Development Fund ‘A way of making Europe’. OPG received research support from the British Heart Foundation (FS/12/86/29841) and the National Institute for Health Research University College London Hospitals Biomedical Research Centre.
Competing interests None declared.
Ethics approval West of Scotland Research Ethics Committee.
Provenance and peer review Not commissioned; externally peer reviewed.
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