Aortic stenosis (AS) is the prototypical pressure overload lesion. The Gunther-Grossman paradigm of the 1970s dictates that as afterload increases, concentric hypertrophy—increases in left ventricular (LV) mass index and relative wall thickness—normalize systolic load and allow for normal ejection fraction despite markedly increased intraventricular systolic pressure. In some individuals, this compensatory process appears to be excessive and can be associated with poor outcome even with aortic valve replacement (AVR). Increasingly, attention has been focused on the malefic consequences for diastolic function of such ‘compensatory’ hypertrophy.