<qa>  What is the consequence of AVS?The consequence of AVS is increased pressure load on the left ventricle which causes changes in the ventricular structure. Pressure overload causes replication of the sarcomeres leading to left ventricular LV hypertrophy, and myocardial stretch will cause activation of cardiac peptides and activation of the renin angiotensin aldosterone system RAAS. With progression of disease, RAAS activation will, through stimulation of the angiotensin-II receptor mediate fibroblast proliferation, promote fibrosis and directly affect the extracellular matrix. The consequence of LV hypertrophy and interstitial fibrosis is increased chamber-stiffness and delayed active LV relaxation which initially will cause diastolic increased LV end-diastolic pressure and later in the disease progression also systolic dysfunction. In congestive heart failure and ischemic heart disease the degree of diastolic dysfunction has been demonstrated to correlate with functional class, neurohormonal activation and prognosis which also recently has been suggested for AVS. Thus, although not fully elucidated the transition from well compensated hypertrophy caused by pressure overload to symptomatic heart failure may be related to evolving diastolic dysfunction. With longstanding elevated filling pressures the left atrium will dilate due to chronically increased atrial afterload. Only limited data are available on the degree and importance of LA dilatation in AVS. 