AR, or aortic regurgitation, occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion/dilation of the aortic root. In developed countries, the most common causes are aortic root dilation or a congenital bicuspid aortic valve. AR is more common in men than women. Symptomatic patients or asymptomatic patients with reduced ejection fraction or increased left ventricular dimensions require surgical treatment such as aortic valve replacement. The prognosis depends on symptoms and left ventricular function, with asymptomatic patients having normal ejection fraction having an excellent long-term prognosis.

1. AORTIC
REGURGITATION
Dr. Adnan Ali Khan

2. • AR is a condition due to inadequate closure of the
aortic valve leaflets leading to abnormal retrograde
flow of blood through the aortic valve during cardiac
diastole.
• It can be induced either by damage to and dysfunction
of the aortic valve leaflets or by distortion or dilatation
of the aortic root and ascending aorta
• In the developing world, the most common cause of AR is
rheumatic heart disease. However, in developed
countries, AR is most often due to aortic root dilation or a
congenital bicuspid aortic valve.

3. Leaflet abnormalities Aortic root or ascending aorta
Rheumatic fever Systemic hypertension
Endocarditis Aortitis (eg, syphilis)
Trauma Reactive arthritis
Bicuspid aortic valve Ankylosing spondylitis
Rheumatoid arthritis Trauma/ Dissecting aneurysm
Myxomatous degeneration Osteogenesis imperfecta
Ankylosing spondylitis Marfan syndrome/ EDS
Acromegaly Inflammatory bowel disease
AR is seen more commonly in men than in women. As in the Framingham study, AR
wa 13% of men versus 8.5% of women. The greater prevalence of AR in men may
reflect, i the male preponderance of underlying conditions such as Marfan syndrome
or bicus valve[3] .

4. Sudden large regurgitant volume imposed
on LV of normal size with normal
compliance
1. Rapid ↑ LVEDP and ↑ LAP
2. LV attempts to maintain CO with ↑HR and
↑ Contractility
Angina
↓ Coronary perfusion
↑demand myocardial O2
Attempts to maintain forward SV/CO may be inadequate
Cardiogenic Shock
↓ Forward SV/CO
Pulmonary edema
↑ LVEDP and ↑ LAP

5. Regurgitant Volume Load
Compensatory Mechanisms:
Angina
↓ Coronary perfusion pressure & marked
LVH
1. ↑LV dilatation ↑ LVED vol and ↑chamber
compliance
2. ↑ LV hypertrophy
Decompensation
Steadily increasing regurgitant volume load
Further ventricular dilatation  ↑ wall stress
Inability to continue further hypertrophy
Contractile dysfunction  ↓ EF/SV/CO
CHF symptoms
Due to both congestion and ↓
CO

6. deMusset's sign A head bob occurring with each cardiac cycle
Mueller's sign Systolic pulsations of the uvula.
Becker's sign Visible pulsations of the retinal arteries and pupils.
Quincke's
pulses
visible Capillary pulsations in the nailbeds after holding the tip
of the nail.
Duroziez's sign A systolic and diastolic bruit heard when the femoral artery is
partially compressed.to and fro murmur
Traube's sign A pistol shot murmur (systolic and diastolic sounds) heard over
the femoral arteries.
Mayne's sign More than a 15 mmHg decrease in DBP with arm elevation from
the value obtained with the arm in the standard position.
Hill's sign Popliteal cuff systolic pressure exceeding brachial pressure by
more than 60 mmHg.
Rosenbach's
sign
Systolic pulsations of the liver.
Gerhard's sign Systolic pulsations of the spleen.

7. • The diastolic murmur of AR begins immediately after A2
.
• It is high pitched, often blowing in quality, and may be
sustained in intensity or decrescendo.
• It may be soft and barely audible, often appreciated only
when the patient is sitting up, leaning forward, and
holding his or her breath in expiration.

8. • Patients with a longer diastolic murmur, a displaced left
ventricular
peripheral
impulse, a wide pulse
findings of a wide pulse pressure
pressure, and the
are
considered to have severe AR.
Note: When the Diastolic murmur of AR is louder in the 3rd
/4th RICS than in the 3/4th LICS ,the AR is likely to result
of leaflets
from Aortic root dilatation than deformitiy
alone.

9. • In a review of the literature, the presence of an early
diastolic murmur, as heard by a cardiologist, was the
most useful finding for establishing the presence of AR
(positive likelihood ratio 8.8 [ie, the odds of AR are
increased 8.8 fold]) and its absence the most useful
finding for eliminating the presence of AR (negative
likelihood ratio 0.2 to 0.3 [ie, the odds of disease are
reduced by a factor of 0.2 to 0.3]) .

10. • Laboratory testing in patients with aortic regurgitation
should be guided by the clinical scenario.
• For example, in patients with AR
infective endocarditis, peripheral
due to suspected
blood counts and
cultures may help clarify the diagnosis and identify the
causative organism.
• Specific serologic tests may assist in the diagnosis of
rheumatological causes.

11. • Aortic valve structure and morphology (bileaflet versus trileaflet,
flail, thickening)
• Presence of vegetations
• Severity of AR
• Color Doppler jet width
• Vena contracta width
• Regurgitant volume, fraction, and orifice area
• Premature closure of the mitral valve (seen in severe AR)
• Associated lesions of the aorta, including dilation, aneurysm,
dissection
• LV structure and function
• LV hypertrophy and dilation
• EF and end-systolic dimension are key determinants of outcome

12. MILD MOD SEVERE
Structural parameters
Left ventricular size N N or dilated Dilated, except acute
AR
Aortic leaflets N or abnormal N or abnormal Abnormal/flail, or wide
coaptation defect
Doppler parameters
Color Doppler jet
width
Central jet, width <25
percent of LVOT
Central jet, width 25 to
65 percent of LVOT
Central jet width >65
percent of LVOT
Doppler vena
contracta width
<3 mm 3 to 6 mm >6 mm
Quantitative parameters
Regurgitant volume <30 mL/beat 30 to 59 mL/beat ≥60 mL/beat
Regurgitant fraction <30 percent 30 to 49 percent ≥50 percent
Regurgitant orifice
area
<0.10 cm2 0.10 to 0.29 cm2 ≥0.30 cm2
Severe chronic AR is typically a/w c/f including a longer diastolic
murmur, a displaced LVI, a wide PP, and the peripheral findings
of a wide PP.

17. • In acute severe AR, surgical intervention is usually
indicated, but the patient may be supported medically
with dobutamine to augment cardiac output and shorten
diastole and sodium nitroprusside to reduce afterload
in hypertensive patients.
• In chronic severe AR, vasodilator therapy may be used
in select conditions to reduce afterload in patients with
systolic hypertension to minimize wall stress and
optimize LV function; in normotensive patients,
vasodilator therapy is not likely to reduce regurgitant
volume (preload) significantly and thus may not be of
clinica
, l ben
rnef.it.

18. • The acute administration of Na Nitoprusside ,
hydralazine, nifedipine or felodipine ↓PVR and results in
an immediate augmentation in forward CO and a ↓ in
regurgitant volume.
• With nitroprusside and hydralazine ,these acute
hemodynamic changes lead to a consistent ↓in EDV
and an ↑in EF.

19. • Reduced EDV and ↑EF have also been observed in
small number of pts receiving long term oral therapy with
hydralazine and nifedipine for a period of 1-2 yrs. With
nifedipine these effects are A/W ↓ in LV mass.
• Reduced BP with enalapril and quinapril has been A/W
↓ in EDV and mass but no change in EF.

20. • Indicated for long-term therapy in patients with chronic,
severe AR and symptoms of LV dysfunction but who
are not candidates for surgery.( CLASS I: LOE-b)
• Is reasonable for short-term therapy in patients with
severe LV dysfunction and HF symptoms to improve
their hemodynamic profile before proceeding with
surgery.(CLASS IIa: LOE-c)
• Is acceptable for long-term therapy in asymptomatic
patients with severe AR and LV dilation with normal

21. • Surgical treatment of AR usually requires replacement
of the diseased valve with a prosthetic valve, although
valve-sparing repair is increasingly possible with
advances in surgical technique and technology.

22. Class I indications for CC under current ACC/AHA
guidelines include the following.
• Assessment of coronary anatomy prior to aortic valve
surgery in patients with risk factors for coronary artery
disease.

23. • Patient is symptomatic.
• Patient is asymptomatic, with a resting EF of ≤ 55%.
• Patient is asymptomatic, with LV dilation (LV end-systolic
dimension >55 mm).

24. • For patients undergoing AV replacement, careful
consideration should be given to the relative risks and
benefits of mechanical vs bioprosthetic valves.
• Mechanical valves : more durable but require long-term
anticoagulation due to increased risk of thrombosis.
• Bioprosthetic valves carry a greater risk of long-term
deterioration and risk of reoperation but avoid the need
for long-term warfarin.

25. The prognosis for patients with severe AR depends on the
presence or absence of LV dysfunction and symptoms, as
follows:
• In asymptomatic patients with normal EF
1. Rate of progression to symptoms &/or LVD = < 6% per yr
2. Rate of progression to asymptomatic LVD = < 3.5% per yr
3. Rate of sudden death = less than 0.2% per yr
• In asymptomatic patients with decreased EF, rate of
progression to symptoms = >25% per year.
• In symptomatic patients, mortality rate = >10% per yr.
The strongest predictors of outcome are echocardiographic
parameters (EF and LV end-systolic dimension).