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Evaluation of papillary muscle function using cardiovascular magnetic resonance imaging in mitral valve prolapse

Yuchi Han1, Dana C Peters, Kraig V Kissinger

  • 1Department of Medicine (Cardiovascular Division), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. yhan@bidmc.harvard.edu

The American Journal of Cardiology
|July 6, 2010
PubMed

Insights

Papillary muscle (PM) dysfunction in mitral valve prolapse (MVP) increases PM systolic velocity and excursion. However, these functional changes did not correlate with the presence of PM fibrosis in MVP patients.

Area of Science:

  • Cardiovascular Imaging
  • Cardiac Electrophysiology
  • Valvular Heart Disease

Background:

  • Abnormal papillary muscle (PM) motion in mitral valve prolapse (MVP) can impact myocardial electrophysiologic stability.
  • Cardiovascular magnetic resonance (CMR) can quantify PM mechanics and visualize fibrosis.

Purpose of the Study:

  • To prospectively assess papillary muscle (PM) excursion and velocity in patients with mitral valve prolapse (MVP) using cardiovascular magnetic resonance (CMR).
  • To investigate the relationship between PM mechanical function and the presence of myocardial fibrosis in MVP.

Main Methods:

  • Prospective study of 16 MVP patients and 9 healthy controls.
  • Phase-contrast and cine CMR were used to measure PM tip velocity and excursion during systole.
  • Late gadolinium enhancement (LGE) CMR was performed in 13 MVP patients to assess for PM fibrosis.

Main Results:

  • Patients with MVP exhibited significantly increased peak PM systolic velocity (12 ± 5 cm/s vs 5 ± 2 cm/s, p < 0.001) and maximum PM excursion (15 ± 5 mm vs 2 ± 3 mm, p < 0.001) compared to controls.
  • Definite PM LGE (fibrosis) was identified in 6 of 13 MVP patients (46%).
  • PM fibrosis did not correlate with increased PM systolic velocity or excursion.

Conclusions:

  • Functional CMR imaging reveals significantly increased PM systolic velocity and excursion in MVP patients.
  • The observed functional abnormalities in PM motion in MVP are not associated with detectable PM fibrosis.
  • CMR-derived PM mechanics may offer insights into MVP pathophysiology, independent of fibrotic substrate.

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