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The incidence of clinically significant aortic regurgitation (AR) increases with age, typically peaking in the fourth to sixth decade of life. It is more common in men than women. The prevalence of AR in the Framingham study was reported to be 4.9%, with regurgitation of moderate or greater severity occurring in 0.5%.
AETIOLOGY OF AORTIC REGURGITATION
AR may be caused by malfunction of the valve leaflets themselves, by dilatation of the aortic root and annulus, or may be due to a combination of these factors (table 1). Rheumatic disease is still the most common aetiology of AR in developing countries; however, in Western Europe and North America the leading cause of AR is either congenital (particularly due to bicuspid leaflets) or degenerative disease, including annuloaortic ectasia. Understanding the mechanism leading to AR is essential for proper patient management, including the surgical approach. Thus, knowledge of the morphology of the valve leaflets, the annulus and the ascending aorta are essential.
PATHOPHYSIOLOGY AND HAEMODYNAMIC CONSIDERATIONS
AR causes volume overload of the left ventricle (LV). The total stroke volume ejected by the LV (sum of effective stroke volume plus regurgitant volume) is increased; in severe AR regurgitant volume may equal or even exceed effective stroke volume. An increase in LV end-diastolic volume is the main compensatory mechanism needed to maintain a normal effective stroke volume. Left ventricular ejection fraction is initially normal, however, LV end-diastolic pressure rises. In time LV end-diastolic volume continues to increase further and ejection fraction drops; these changes may actually precede the development of clinical symptoms. Considerable eccentric myocardial hypertrophy can occur with chronic AR and at autopsy heart weights of up to 1000 g have been reported.
Acute AR can be life threatening, as LV dilatation and other compensatory mechanisms cannot develop rapidly enough to avoid haemodynamic deterioration. The same regurgitant …