Description
- The aortic valve, normally consisting of 3 leaflets, opens during ventricular systole and closes during diastole. Valve closure prevents backflow of blood from the aorta to the left ventricle (LV) and helps maintain aortic diastolic pressure and coronary perfusion pressure.
- Aortic regurgitation (AR) is the presence of a backflow leak through the valvular apparatus during diastole.
- Ranges in severity from trace, mild, moderate, or severe; it is classified by the amount of regurgitant volume, regurgitant orifice area size, and pressure equalization half-time by echocardiography.
- Regurgitation may be associated with any condition that alters aortic valve closure. Aortic dilation, aneurysm, dissection, and abscess are external causes of aortic valve dysfunction and account for about half of all AR cases. Rheumatic valve disease, collagen vascular diseases, connective tissue diseases (especially Marfan syndrome (1) [C]), congenital malformations, senile degeneration, and infective endocarditis are direct valvular conditions that commonly produce AR in the remainder of cases.
- Acute AR is the sudden onset of backflow leak usually due to an acute event such as aortic dissection or valvular trauma.
- Chronic AR has a gradual onset and may be sustained for many years.
- May also accompany aortic stenosis—a narrowing of the open valvular area
Epidemiology
Incidence
- Worldwide, rheumatic heart disease is the most common cause of AR.
- In the US, congenital and degenerative valvular and aortic disease is most common.
- Congenital bicuspid aortic valves occur in 1–2% of the US population and may contribute to AR.
Morbidity
- Acute AR has a higher rate of morbidity and mortality due to the underlying pathophysiology. This can result in diastolic and systolic dysfunction and eventually decompensation (CHF).
- Chronic AR mortality is related to the eventual decompensation of the LV; it is more common in severe AR. Decreased ejection fraction and LV function have a poor prognosis for recovery, even after repair.
- Surgical management becomes the common end point to both types of AR.
Mortality
- Acute AR has a high mortality due to sudden uncompensated cardiovascular changes usually requiring immediate surgical management.
- Chronic AR mortality relates to eventual decompensation of the LV and may occur at any age usually with severe AR. Decreased ejection fraction and LV function has a poor prognosis for recovery even after repair.
- Yearly mortality risk relates to NYHA classification for chronic severe AR:
- Asymptomatic: 2.8%
- NYHA Class I: 3.0%
- NYHA Class II: 6.3%
- NYHA Class III–IV: 24.6% (4)
Etiology/Risk Factors
- Male gender has a greater risk for AR with a related increased risk of hypertension, connective tissue and congenital valvular diseases, which may result in presentation at a younger age.
- Severe AR is most commonly diagnosed at age 60 and above.
Physiology/Pathophysiology
- Acute AR results in an acute increase in LV diastolic volume, decreased aortic diastolic pressure (forward flow), decreased coronary perfusion pressure, volume overload, and decreased diastolic function of the LV. This leads to an increase in myocardial demand, acute fulminant CHF, and cardiogenic shock. Common causes of acute AR, including aortic dissection, warrant emergent surgical repair.
- Chronic AR has a more insidious onset and may take years to become symptomatic. As regurgitant volume and AR worsen over time, the LV has time to remodel with eccentric hypertrophy and dilation. The increase in diastolic volume is compensated by the enlarged LV, increased heart rate, and decreased systemic vascular resistance (SVR). Ejection fraction is maintained and may prevent symptoms without exertion or positional changes. As time passes, the ventricle becomes "too enlarged" with resultant increases in wall stress and decreases in myocardial perfusion (leads to diminished EF, CHF, and end-organ hypoperfusion). Recall Laplace's law where Tension = (Pressure × Radius)/Wall Thickness; as the radius increases, tension also increases (increases myocardial oxygen consumption). Sympathetic stimulation increases SVR to maintain pressure but worsens AR; hinders forward flow. Without timely surgical repair the heart may not be able to significantly recover.
- Maintenance of cardiac output, coronary perfusion, and prevention of cardiac decompensation are the primary goals.
- Normal sinus rhythm and avoidance of bradycardia to minimize regurgitant time
- SVR may be mildly decreased, but should be balanced between facilitating forward flow (decreasing regurgitation) and maintaining adequate coronary and systemic perfusion pressure.
- Careful fluid management and inotropic support to prevent cardiovascular overload or collapse
Outline