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Editorial
Ventricular arrhythmias in mitral valve prolapse: new explanations for an old problem
  1. Alberto Cipriani,
  2. Barbara Bauce
  1. Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padova, Italy
  1. Correspondence to Prof. Barbara Bauce, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padova 35128, Italy; barbara.bauce{at}unipd.it

https://doi.org/10.1136/heartjnl-2020-318086

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    Nearly 60 years after the first description by Barlow, mitral valve prolapse (MVP) still remains a diagnosis of great interest and intense controversy.

    This continuing concern is driven by the high prevalence of this valvular disorder, detected in 1.2%–2.4% of the general population,1 and its not infrequent association with symptoms including atypical chest pain, exertional dyspnoea, palpitations and anxiety (MVP syndrome) and clinical findings including mid-systolic click, low blood pressure, leaner build and ECG anomalies. It is also common in cardiovascular conditions including significant mitral regurgitation (MR), infective endocarditis, cerebrovascular ischaemic events, ventricular arrhythmias (VAs) and even sudden cardiac death (SCD).2

    On the other hand, strong controversy arises from the general lack of knowledge of the pathophysiological basis underlying most of these associations, especially with VAs and SCD, which might be coincidental in such a common disorder like MVP.

    MVPs are not all the same

    Over the last few years, however, we have learnt that MVPs are not all the same, and that the ‘arrhythmic MVP’ is a peculiar clinical entity, characterised by specific mitral valve apparatus abnormalities, such as myxomatous, redundant and prolapsing leaflets, mitral annular disjunction (MAD), replacement fibrotic changes in papillary muscles and basal myocardium. Furthermore, high electrical instability puts patients, especially young women, at risk of life-threatening VAs and SCD.

    The pathophysiological link between these features is far from being elucidated, although our group recently proposed a causal …

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    Footnotes

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    • Contributors Drafting of the manuscript: AC. Critical revision of the manuscript for important intellectual content: BB. All authors certify that this material or similar material has not been and will not be submitted to or published in any other publications.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Patient consent for publication Not required.

    • Provenance and peer review Commissioned; internally peer reviewed.

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