Use of Cardiac Magnetic Resonance (CMR) and Quantitative Myocardial Perfusion Mapping in a Patient with Mixed Valvular Heart Disease (QF_SA_139)

A 66-year-old man was referred to cardiology clinic for dyspnea on exertion for about 2 years, associated with bilateral lower extremity edema chest discomfort with exertion. He has history of hypertension and stage III CKD. Home medications are furosemide and lisinopril. TTE showed LVEF 74%, probably severe aortic regurgitation (AR), mild mitral regurgitation (MR) and mild to moderate tricuspid regurgitation (TR). He was referred to stress CMR for evaluation of myocardial ischemia and valvular heart disease (VHD).

Diagnostic Techniques and Their Most Important Findings:

The CMR was performed in a 1.5T magnet (Siemens MAGNETOM Aera, Siemens Healthineers, Erlagen, Germany). First-pass stress myocardial perfusion imaging was performed using Regadenoson (0.4 mg) with free breathing and motion correction. Inline quantitative myocardial perfusion mapping was used for quantification of myocardial blood flow at rest and stress. LGE imaging was obtained using phase-sensitive inversion recovery sequence. Native and post contrast T1 mapping were obtained to derive ECV. Phase contrast flow imaging was obtained for flow quantification.

The CMR showed a severely dilated LV (LVEDVi 187 ml/m², LVESVi 61 ml/m²), with eccentric hypertrophy (LV mass 104 g/m²) and preserved systolic function (LVEF 67%). RV was moderately dilated (RVEDVi 120 ml/m²) with reduced systolic function (RVEF 40%). There was a flail posterior mitral valve leaflet and severe MR with an eccenteric anteriorly directed MR jet (regurgitant volume [RVol] 115 ml, regurgitant fraction [RF] 42%) (Fig. 1). The aortic valve is bicuspid with fused left and right coronary cusps and prolapse of non-coronary cusp. There was severe AR (RVol 48 ml, RF 43%) with holodiastolic flow reversal in the descending aorta (Fig 2). There was mild to moderate TR (RVol 23 ml, RF 22%). Myocardial ECV was elevated at 31%. In the first-pass myocardial perfusion imaging, there was no subendocardial myocardial perfusion defect at stress. Global myocardial perfusion was 3.2 ml/min/g at stress and 0.9 ml/min/g at rest, with normal myocardial perfusion reserve 3.5 (Fig 3).

Learning Points from this Case:

This case highlights the advantage of CMR in the assessment of VHD. It is excellent for the assessment of all four valves, both stenotic and regurgitant lesions with the advantage of free choice of image planes, not limited by acoustic window. CMR provides detailed anatomical and functional assessment of the valves and chambers with high spatial and temporal resolution and accurate volumetric and flow quantification. It also provides additional prognostic information including LV mass, chamber volumes and myocardial fibrosis, which is critical to predict clinical outcome of asymptomatic patients and to guide treatment. Stress perfusion imaging and myocardial blood flow quantification provides added prognostic value. CMR complements the conventional imaging and is a crucial tool for the comprehensive and accurate assessment of VHD.