Haemodynamic Overestimation of Mitral Stenosis in Calcific Mitral Valve Disease: A Case Report Highlighting the Impact of Atrial Fibrillation, Mitral Regurgitation, and Volume Overload

Background: The echocardiographic assessment of mitral stenosis requires the integration of mitral valve morphology, mitral valve area, transmitral gradients, heart rate, rhythm, and haemodynamic conditions. Although the mean transmitral gradient is an important parameter, it is intrinsically flow-dependent. Tachycardia, atrial fibrillation, increased cardiac output, volume overload, and concomitant mitral regurgitation may increase transmitral flow and thereby elevate the measured gradient. This effect may lead to overestimation of mitral stenosis severity, particularly when direct planimetric assessment is technically limited by extensive mitral annular and leaflet calcification. Case Presentation: A 55-year-old man with diabetes mellitus, hypertension, and stage 5 chronic kidney disease presented with significant volume overload. Initial echocardiography demonstrated a thickened, calcified, non-rheumatic mitral valve with moderate mitral annular calcification. Atrial fibrillation with a fast ventricular response was present at a heart rate of approximately 120 beats/min. Moderate-to-severe mitral regurgitation was also present. Left ventricular ejection fraction was preserved at 60%. The left atrial dimension was 43 mm, and the estimated right ventricular systolic pressure was 60 mmHg. Extensive mitral valve calcification made accurate planimetric assessment of the mitral valve area technically difficult, while pressure half-time was considered unreliable under the prevailing haemodynamic conditions. A transmitral gradient of approximately 16/9 mmHg was recorded and, in the context of the calcified valve, was initially interpreted as indicating moderate mitral stenosis. The patient was subsequently treated for volume overload and heart failure. Following clinical and haemodynamic improvement, repeat echocardiography demonstrated substantial reductions in mitral regurgitation and pulmonary pressure. Normal sinus rhythm was present at a heart rate of approximately 80 beats/min. Mitral valve planimetry became feasible and demonstrated a mitral valve area of approximately 1.8 cm². The transmitral gradient was approximately 8/4 mmHg, mitral regurgitation had decreased to mild, and the estimated right ventricular systolic pressure had decreased to 32 mmHg. Left ventricular ejection fraction remained preserved at 60%. Conclusion: The findings demonstrate the potential for substantial overestimation of mitral stenosis severity when transmitral gradients are interpreted without adequate consideration of rhythm, heart rate, transvalvular flow, mitral regurgitation, and volume status. The marked reduction in the gradient after correction of volume overload and restoration of sinus rhythm, together with a planimetric mitral valve area of 1.8 cm², suggests that the initial gradient was influenced substantially by altered haemodynamic conditions rather than by moderate fixed mitral stenosis alone. In patients with calcific mitral valve disease, particularly in the presence of atrial fibrillation, significant MR, and fluid overload, treatment and haemodynamic stabilisation followed by repeat echocardiographic assessment may reduce the risk of inappropriate classification of mitral stenosis severity.