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Arrhythmias and sudden death
Original research article
Mitral valve prolapse and sudden cardiac death: a systematic review and meta-analysis
  1. Chrishan J Nalliah1,2,
  2. Rajiv Mahajan1,
  3. Adrian D Elliott1,
  4. Haris Haqqani3,
  5. Dennis H Lau1,
  6. Jitendra K Vohra2,
  7. Joseph B Morton2,
  8. Christopher Semsarian4,
  9. Thomas Marwick5,
  10. Jonathan M Kalman2,
  11. Prashanthan Sanders1
  1. 1 Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, South Australia, Australia
  2. 2 Department of Cardiology, Royal Melbourne Hospital and the University of Melbourne, Melbourne, Victoria, Australia
  3. 3 Prince Charles Hospital, Chermside, Queensland, Australia
  4. 4 Department of Cardiology, Royal Prince Alfred Hospital and the Centenary Institute, University of Sydney, Sydney, New South Wales, Australia
  5. 5 Baker IDI Heart and Diabetes Institute and the Alfred Hospital, Melbourne, Victoria, Australia
  1. Correspondence to Professor Prashanthan Sanders, Department of Cardiology, Centre for Heart Rhythm Disorders, Royal Adelaide Hospital, Adelaide, SA 5000, Australia; prash.sanders{at}adelaide.edu.au

Abstract

Objectives Mitral valve prolapse (MVP) is commonly observed as a benign finding. However, the literature suggests that it may be associated with sudden cardiac death (SCD). We performed a meta-analysis and systematic review to determine the: (1) prevalence of MVP in the general population; (2) prevalence of MVP in all SCD and unexplained SCD; (3) incidence of SCD in MVP and (4) risk factors for SCD.

Methods The English medical literature was searched for: (1) MVP community prevalence; (2) MVP prevalence in SCD cohorts; (3) incidence SCD in MVP and (4) SCD risk factors in MVP. Thirty-four studies were identified for inclusion. This study was registered with PROSPERO (CRD42018089502).

Results The prevalence of MVP was 1.2% (95% CI 0.5 to 2.0) in community populations. Among SCD victims, the cause of death remained undetermined in 22.1% (95% CI 13.4 to 30.7); of these, MVP was observed in 11.7% (95% CI 5.8 to 19.1). The incidence of SCD in the MVP population was 0.14% (95% CI 0.1 to 0.3) per year. Potential risk factors for SCD include bileaflet prolapse, ventricular fibrosis complex ventricular ectopy and ST-T wave abnormalities.

Conclusion The high prevalence of MVP in cohorts of unexplained SCD despite low population prevalence provides indirect evidence of an association of MVP with SCD. The absolute number of people exposed to the risk of SCD is significant, although the incidence of life-threatening arrhythmic events in the general MVP population remains low. High-risk features include bileaflet prolapse, ventricular fibrosis, ST-T wave abnormalities and frequent complex ventricular ectopy.

Trial registration PROSPERO (CRD42018089502).

  • cardiac arrest
  • premature ventricular beats
  • ventricular fibrillation
  • implanted cardiac defibrillators
  • echocardiography

https://doi.org/10.1136/heartjnl-2017-312932

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    Footnotes

    • Contributors CJN, RM, ADE and PS had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: CJN, RM, DHL, JMK and PS. Acquisition of data: CJN and RM. Analysis and interpretation of data: CJN, RM, ADE and PS. Drafting of the manuscript: CJN, RM and PS. Critical revision of the manuscript for important intellectual content: CJN, RM, ADE, HH, DHL, JKV, JBM, CS, TM, JMK and PS. Statistical analysis: CJN, RM and ADE. Study supervision: RM and PS.

    • Funding CJN is supported by a Postgraduate Scholarship funded by the National Health and Medical Research Council of Australia and the National Heart Foundation and by the BJ Amos Travelling Fellowship from the Westmead Association. RM is supported by the Leo J. Mahar Lectureship from the University of Adelaide and by an Early Career Fellowship jointly funded by the National Health and Medical Research Council of Australia and the National Heart Foundation of Australia. DHL is supported by a Robert J. Craig Lectureship from the University of Adelaide. CS, JMK and PS are supported by a Practitioner Fellowships from the National Health and Medical Research Council of Australia. PS is supported by the National Heart Foundation of Australia.

    • Disclaimer JMK reports having received research funding from St Jude Medical, Biosense-Webster, Medtronic and Boston Scientific. Dr Sanders reports having served on the advisory board of Biosense-Webster, Medtronic, CathRx and Abbott. PS reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Biosense-Webster, Medtronic, Abbott and Boston Scientific. PS reports that the University of Adelaide has received on his behalf research funding from Medtronic, Abbott, Boston Scientific, Biotronik and Liva Nova.

    • Competing interests JMK reports having received research funding from St Jude Medical, Biosense-Webster, Medtronic and Boston Scientific. Dr Sanders reports having served on the advisory board of Biosense-Webster, Medtronic, CathRx and St Jude Medical. PS reports having received lecture and/or consulting fees from Biosense-Webster, Medtronic, St Jude Medical, and Boston Scientific. PS reports having received research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik and Sorin.

    • Patient consent Not required.

    • Provenance and peer review Not commissioned; externally peer reviewed.