Chronic aortic insufficiency (AI) is typically the result of congenital conditions such as a bicuspid aortic valve, rheumatic disease, connective tissue disorders (e.g., Marfan’s syndrome), or cystic medical necrosis. Acute AI is rarer and carries a poor prognosis. Aortic dissections, trauma, and bacterial endocarditis can lead to acute aortic insufficiency. Both processes lead to malcoaptation of the aortic valve leaflets by causing abnormalities in the leaflets themselves or dilation of the AV annulus, the aortic root, or both.
Aortic insufficiency is characterized by decreased forward flow due to regurgitation of part of the ejected stroke volume back into the left ventricular outflow tract across the incompetent valve. Left ventricular volume overload ensues, leading to eccentric hypertrophy and dilatation. Ventricular compliance increases to promote a larger diastolic capacity while maintaining a normal left ventricular end-diastolic pressure. Some concentric hypertrophy occurs in addition to the eccentric changes due to the increased wall stress from the increase in left ventricular radius. Due to the runoff of blood into the LV during diastole and increased ejected volume during systole, AI leads to a widened pulse pressure (Figure 66-1(A)). The lower aortic diastolic pressure allows for preservation of stroke volume and ejection fraction until late in the disease state.
Aortic insufficiency: pressure–time tracing (A) and pressure–volume loop (B). (A, Reproduced with permission from Hammer GD, McPhee SJ, eds. Pathophysiology of Disease: An Introduction to Clinical Medicine, 7th ed. New York, NY: McGraw-Hill Education, Inc.; 2014: Fig. 10-24 B&C. B, Reproduced with permission from Cheitlin MD et al. Clinical Cardiology, 6th ed. New York, NY: McGraw-Hill Companies; 1993: Fig. 13-1 A.)
Patients with chronic aortic regurgitation remain relatively asymptomatic, sometimes for decades. The work required to eject the increased volume across the incompetent valve is reduced due to the lower outflow impedance. Furthermore, a competent mitral valve confines these changes to the left ventricle. Over time, left ventricular dilatation leads to mitral regurgitation and left atrial enlargement. Once the LV reaches its limit of dilatation, intraventricular pressures rise as a result of the large diastolic volume. Decreased coronary perfusion and congestive heart failure result. In contrast, acute AI leads to a sudden increase in left ventricular work and wall tension. Because of a sudden rise in LVEDP, cardiac output drops along with decreased myocardial perfusion. Pulmonary edema, acute congestive heart failure, and cardiogenic shock ensue.
The pressure–volume loop in chronic aortic insufficiency shows an enlarged left ventricular volume with minimal change in end-diastolic pressure (Figure 66-1(B)). The entire loop is shifted to the right along the X-axis due to the increased volumes. Isovolumic relaxation is absent with chronic regurgitation because the incompetent valve allows back filling of the left ventricle from the aorta during diastole even before the mitral valve opens. Stroke volume is ...