Figure 1.

Consequences of very severe calcific aortic stenosis (A) in a patient in their 60s without a history of systemic hypertension. Peak transvalvular gradient was 127 mm Hg (mean gradient of 84 mm Hg) (B) at a blood pressure of 120/70 mm Hg, with an estimated LV systolic pressure of 247 mm Hg and a calculated aortic valve area of 0.6 cm². As a result of severe pressure overload, there was significant concentric LV hypertrophy (A) with an indexed LV mass of 130 g/m² and a relative wall thickness of 0.55. Global systolic LV function was preserved (ejection fraction of 65%) while systolic myocardial velocities measured by tissue Doppler imaging were significantly reduced (septal s’ 5.2 cm/s)(D), indicating LV longitudinal dysfunction. There was significant LV diastolic dysfunction: impaired relaxation with a septal e’ of 4.8 cm/s (D) and increased filling pressure—pseudonormal mitral inflow (C) with elevated E/e' ratio of 16 and a moderately dilated left atrium. LV, left ventricular.