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Valvular heart disease
Original article
Diffuse myocardial fibrosis in patients with mitral valve prolapse and ventricular arrhythmia
  1. An H Bui1,2,
  2. Sébastien Roujol2,
  3. Murilo Foppa2,3,
  4. Kraig V Kissinger4,
  5. Beth Goddu4,
  6. Thomas H Hauser2,
  7. Peter J Zimetbaum1,2,
  8. Long H Ngo2,
  9. Warren J Manning2,4,
  10. Reza Nezafat2,
  11. Francesca N Delling2,5
  1. 1Cardiovascular Division, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
  2. 2Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
  3. 3Division of Cardiology, Hospital de Clinicas de Porto Alegre, Federal University of Rio Grande do Sul, Brazil
  4. 4Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
  5. 5Department of Medicine, Division of Cardiology, University of California, San Francisco, California, USA
  1. Correspondence to Dr Francesca N Delling, University of California San Francisco, 555 Mission Bay Blvd South, Room S352C, San Francisco, CA 94158, USA; Francesca.Delling{at}ucsf.edu

Abstract

Objective We aimed to investigate the association of diffuse myocardial fibrosis by cardiac magnetic resonance (CMR) T1 with complex ventricular arrhythmia (ComVA) in mitral valve prolapse (MVP).

Methods A retrospective analysis was performed on 41 consecutive patients with MVP referred for CMR between 2006 and 2011, and 31 healthy controls. Arrhythmia analysis was available in 23 patients with MVP with Holter/event monitors. Left ventricular (LV) septal T1 times were derived from Look-Locker sequences after administration of 0.2 mmol/kg gadopentetate dimeglumine. Late gadolinium enhancement (LGE) CMR images were available for all subjects.

Results Patients with MVP had significantly shorter postcontrast T1 times when compared with controls (334±52 vs 363±58 ms; p=0.03) despite similar LV ejection fraction (LVEF) (63±7 vs 60±6%, p=0.10). In a multivariable analysis, LV end-diastolic volume, LVEF and mitral regurgitation fraction were all correlates of T1 times, with LVEF and LV end-diastolic volume being the strongest (p=0.005, p=0.008 and p=0.045, respectively; model adjusted R2=0.30). Patients with MVP with ComVA had significantly shorter postcontrast T1 times when compared with patients with MVP without ComVA (324 (296, 348) vs 354 (327, 376) ms; p=0.03) and only 5/14 (36%) had evidence of papillary muscle LGE.

Conclusions MVP may be associated with diffuse LV myocardial fibrosis as suggested by reduced postcontrast T1 times. Diffuse interstitial derangement is linked to subclinical systolic dysfunction, and may contribute to ComVA in MVP-related mitral regurgitation, even in the absence of focal fibrosis.

https://doi.org/10.1136/heartjnl-2016-309303

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    Footnotes

    • Contributors FND conceived of the study. AHB and FND initiated the study design and AHB primarily drafted the manuscript. SR, MF, KVK, BG, PJZ, WJM, RN and FND helped with implementation. THH and LHN provided statistical expertise and conducted the primary statistical analysis. All authors contributed to refinement of the study protocol and approved the final manuscript.

    • Funding National Institutes of Health (NIH): National Heart, Lung, and Blood Institute. NIH K23HL116652 (FND).

    • Competing interests None declared.

    • Ethics approval Institutional Review Board.

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