Even severe AS may exist for many years without producing any symptoms because of the ability of the hyperophied LV to generate the elevated intraventricular pressures required to maintain a normal stroke volume. Most patients with pure or predominant AS have gradually increasing obstruction over years, but do not become symptomatic until the sixth to eighth decades. Exeional dyspnea, angina pectoris, and syncope are the three cardinal symptoms. Dyspnea results primarily from elevation of the pulmonary capillary pressure caused by elevations of LV diastolic pressures secondary to reduced left ventricular compliance and impaired relaxation. Angina pectoris usually develops somewhat later and reflects an imbalance between the augmented myocardial oxygen requirements and reduced oxygen availability. Exeional syncope may result from a decline in aerial pressure caused by vasodilation in the exercising muscles and inadequate vasoconstriction in nonexercising muscles in the face of a fixed CO, or from a sudden fall in CO produced by an arrhythmia. ( Harrison&;s principle of internal medicine,18th edition,pg no.1939 )