BMJ Ar

Aortic regurgitation
The right clinical information, right where it's needed
Last updated: Nov 05, 2019

Table of Contents
Summary 3
Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 5
Classification 6
Prevention 8
Primary prevention 8
Secondary prevention 8
Diagnosis 9
Case history 9
Step-by-step diagnostic approach 9
Risk factors 13
History & examination factors 13
Diagnostic tests 18
Differential diagnosis 21
Diagnostic criteria 22
Treatment 24
Step-by-step treatment approach 24
Treatment details overview 26
Treatment options 28
Follow up 34
Recommendations 34
Complications 35
Prognosis 36
Guidelines 37
Diagnostic guidelines 37
Treatment guidelines 37
References 39
Images 43
Disclaimer 50
Summary
◊ The diastolic leakage of blood from the aorta into the left ventricle (LV).
◊ Chronic aortic regurgitation (AR) may be asymptomatic for years until overt symptoms of congestive
heart failure develop. Initial symptoms can include palpitations and uncomfortable awareness of the
pounding heart when lying on the left side.
◊ Acute AR is a medical emergency, presenting with sudden onset of pulmonary oedema and
hypotension or cardiogenic shock. May also present as myocardial ischaemia or aortic root
dissection.
◊ Echocardiography is the best non-invasive test to diagnose and grade the severity of AR.
◊ Vasodilator therapy improves haemodynamics and delays the need for aortic valve replacement/
repair (AVR) in asymptomatic patients with chronic severe AR.
◊ AVR is indicated in symptomatic patients or those with LV ejection fraction <50%, and asymptomatic
patients with severe AR if LV end-diastolic volume is >75 mm or LV end-systolic volume is > 55mm.
Aortic regurgitation Basics
Definition
Aortic regurgitation (AR) is the diastolic leakage of blood from the aorta into the left ventricle. It occurs due
to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic
BASICS
root. It can remain asymptomatic for decades before patients present with irreversible myocardial damage.
Epidemiology
AR is not as common as aortic stenosis and mitral regurgitation. One US study showed a prevalence of 13%
in men and 8.5% in women with most being trace or mild; a prevalence of 15.6% was reported in African-
Americans.[4] Prevalence increases with age in both genders.[5]
Of asymptomatic people >55 years of age, 13% have moderate or severe echocardiographic AR with a total
prevalence of 29% (including mild AR).[6] A prospective multicentre epidemiological study of healthy young
adults aged 23 to 35 years revealed a prevalence of AR of 1.3%. There was no difference in the prevalence
on the basis of gender or race.[7]
Aetiology
AR can be caused by primary disease of the aortic valve leaflets or dilation of the aortic root. In developing
countries rheumatic heart disease is the most common cause, but congenital bicuspid aortic valve and
aortic root dilation account for most of the cases in developed countries. Causes of aortic root dilation
include Marfan's syndrome, related connective tissue diseases, and aortitis secondary to syphilis, Behcet's,
Takayasu's, reactive arthritis, or ankylosing spondylitis. Endocarditis can lead to rupture of leaflets or even
paravalvular leaks. Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting
in leakage of blood.[8] Aortic root dissection is a cause of acute AR.
AR may develop acutely (acute AR) or over a period of many years in progressively increasing severity
(chronic AR). An analysis of the causes of AR in patients >20 years of age undergoing isolated aortic valve
replacement/repair (AVR) found non-valvular causes accounted for 54% of cases and valvular causes for
46%. Acute AR was responsible for only 18% of AVR, and, of these, 56% resulted from active infective
endocarditis and 44% from aortic dissection. Aortic enlargement from unclear aetiology was the most
common cause of chronic AR, accounting for 34% of the total, followed by bicuspid congenital malformation
(22% of total). Older patients most commonly had an unclear aetiology.[9]
The role of systemic hypertension in aortic root dilation leading to AR is a frequent source of debate. Aortic
root diameter at the supra-aortic ridge, which is the site of commissural attachment, is significantly greater in
hypertensive patients than in age and gender-matched normotensive patients.[10]
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 05, 2019.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2020. All rights reserved.
BASICS
Causes of AR
Dr Sanjeev Wasson and Dr Nishant Kalra; used with permission
Pathophysiology
AR can present acutely or over decades.
Acute AR is a medical emergency with high mortality and results in an acute rise in left atrial pressure,
pulmonary oedema, and cardiogenic shock.
During acute AR:
• End-diastolic pressure in the left ventricle rises sharply .

• The heart tries to compensate by increasing the heart rate and increasing the contractility (Starling's
law) to keep up with the increased preload, but this is insufficient to maintain the normal stroke volume
and fails.
Chronic progressive AR results in:
• Both left ventricular volume and pressure overload.

• An increase in left ventricular volume and pressure causes an increase in wall tension.
• According to Laplace's law, wall tension is directly proportional to the product of cavity pressure and
radius, and inversely proportional to wall thickness.
• To compensate for the increased wall tension, the heart wall undergoes hypertrophy. Both concentric
and eccentric hypertrophy can occur but most are eccentric. Eccentric hypertrophy, in which
sarcomeres are laid down in series, results from volume overload; concentric hypertrophy, in which
sarcomeres replicate in parallel, results from pressure overload from increased systolic pressure to
normalise the end-systolic stress.[11]
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 05, 2019.
5
• Systolic hypertension occurs secondary to increased stroke volume, which combines both regurgitant
and forwards stroke volume.
• The volume overload, which is directly related to the severity of the leak, results in an increase in left
ventricular end-diastolic volume.
BASICS
• End-diastolic pressure remains normal due to an increase in ventricular compliance resulting from
increased cavity size.
In chronic AR, most patients remain asymptomatic for decades, as the left ventricle maintains forwards
stroke volume with compensatory chamber enlargement and hypertrophy. Eventually, the left ventricular
systolic dysfunction supervenes and left ventricular end-diastolic pressure rises resulting in symptomatic
congestive heart failure. Timing AVR before irreversible myocardial dysfunction develops is of critical
importance.
Classification
Acute aortic regurgitation: clinically accepted criteria
A medical emergency where the left heart rapidly decompensates due to its inability to handle a sudden
increase in end-diastolic volume. Most commonly it results from aortic dissection or endocarditis and, in rare
cases, trauma.
Chronic aortic regurgitation: clinically accepted criteria

Chronic regurgitation has a prolonged course over a period of months to years. The left ventricle is able to
compensate for volume overload initially but then decompensates with the appearance of clinical symptoms
of congestive heart failure.
Classification of the severity of aortic regurgitation in adults (ACC/

AHA practice guidelines for the management of patients with
valvular heart disease)[1]
Mild AR
• Angiographic grade: 1+
• Colour Doppler jet width: central jet, width <25% of left ventricular outflow tract (LVOT)
• Doppler vena contracta width (cm): <0.3
• Regurgitant volume (mL/beat): <30
• Regurgitant fraction (%): <30
• Regurgitant orifice area (cm^2): <0.10.
Moderate AR
• Colour Doppler jet width: greater than mild but no signs of severe AR
• Doppler vena contracta width (cm): 0.3-0.6
• Regurgitant volume (mL/ beat): 30-59
• Regurgitant fraction (%): 30-49
• Regurgitant orifice area (cm^2): 0.10-0.29.
Severe AR
• Angiographic grade: 3-4+

• Colour Doppler jet width: central jet, width >65% of LVOT
• Doppler vena contracta width (cm): >0.6
• Regurgitant volume (mL/beat): ≥60
BASICS
• Regurgitant fraction (%): ≥50
• Regurgitant orifice area (cm^2): ≥0.30
• Left ventricular size: increased.
Stages of chronic aortic regurgitation assessed by echocardiogram

and cardiac catheterisation
Different criteria have been developed to diagnose patients based on Doppler echocardiographic and cardiac
catheterisation measurements, to help time the surgery and ensure the benefits outweigh the perioperative
risk (mortality 4%) and long-term complications of prosthetic valve.[1] [2] [3]
Compensated
• Ejection fraction >55%

• Fractional shortening >32%
• End-diastolic diameter <60 mm
• End-systolic diameter <45 mm
• End-diastolic volume <120 mL/m^2
• End-systolic volume <50 mL/m^2
Transitional
• Ejection fraction 51% to 55%

• Fractional shortening 30% to 31%
• End-diastolic diameter 60-70 mm
• End-systolic diameter 45-50 mm
• End-diastolic volume 130-160 mL/m^2
• End-systolic volume 50-60 mL/m^2
Decompensated
• Ejection fraction ≤50%

• Fractional shortening <29%
• End-diastolic diameter >75 mm
• End-systolic diameter > 55 mm
• End-diastolic volume >170 mL/m^2
• End-systolic volume >60 mL/m^2
7
Aortic regurgitation Prevention
Primary prevention
Streptococcal throat infection should be treated with antibiotics to avoid the development of rheumatic fever.
High blood pressure should be controlled to prevent damage to the aortic root. Intravenous drug abuse
should be avoided. Good dental hygiene should be maintained.
Secondary prevention
Antibiotic prophylaxis is recommended for patients with prosthetic valves during surgical or dental procedures
to prevent endocarditis.[38]
PREVENTION
Aortic regurgitation Diagnosis
Case history
Case history #1
A 55-year-old white man presents with weakness, palpitations, and dyspnoea on exertion. On physical
examination, his blood pressure is 148/50 mmHg with a bounding pulse and an early diastolic murmur
over the left sternal border. He denies any history of drug abuse, rheumatic fever, or connective tissue
disorder. The patient is taking hydrochlorothiazide for high blood pressure. Echocardiography reveals a
left ventricular ejection fraction (LVEF) of 55%, left ventricular end-diastolic diameter of 70 mm, and end-
systolic diameter of 50 mm.
Case history #2
A 31-year-old black man presents to clinic for the first time for a routine physical examination. He denies
any complaints. On physical examination the only abnormality is a systolic murmur best heard over
the second right intercostal space and an early diastolic murmur best heard over the third left sternal
border. LVEF is 55% to 60% with mild LVH. Left ventricular end-systolic diameter is 45 mm and aortic root
diameter is 3.5 cm.
Other presentations
In acute AR, patients can present with sudden onset of pulmonary oedema and hypotension or in
cardiogenic shock. Patients may also present with signs and symptoms of myocardial ischaemia or
aortic root dissection. Due to the acute nature of the aortic regurgitation, there may be no increase in left
ventricular size, and the diastolic murmur may be short and/or soft due to diastolic pressure equilibrium
between aorta and ventricle occurring before the end of diastole. An apical diastolic rumble may be
present. Pulse pressure may not be increased due to reduced systolic pressure.[1]
DIAGNOSIS
Step-by-step diagnostic approach
AR is usually detected on clinical examination with a diastolic murmur, or incidentally during
echocardiographical evaluation for other causes. ECG, CXR, and echocardiogram are routinely performed
for all patients with features of AR.
Acute AR: clinical presentation

The patient can present with sudden onset of pulmonary oedema and hypotension or in cardiogenic
shock. Patients may also present with signs and symptoms of myocardial ischaemia or aortic root
dissection. When valvular regurgitation is acute, many of the characteristic findings of chronic AR
are absent and the severity of the problem may be underestimated. For example, during the physical
examination, no increase in left ventricular (LV) size may be detected and the diastolic murmur may be
short and/or soft due to diastolic pressure equilibrium between aorta and ventricle occurring before the
end of diastole. An apical diastolic rumble may be present. Pulse pressure may not be increased due to
reduced systolic pressure.[1]
Signs and symptoms of pulmonary oedema
9
• Dyspnoea
• Pink frothy sputum
• Pale and sweaty
• Basal lung crepitations
• Wheeze (cardiac asthma).
Signs and symptoms of cardiogenic shock
• Pale and/or cyanotic, cool to touch with mottled extremities

• Evidence of hypoperfusion with altered mental status and decreased urine output
• Rapid and faint peripheral pulses
• Jugular venous distension
• Third and fourth heart sounds may be present
• Arrhythmias
• Dyspnoea.
Myocardial ischaemia, due to decreased perfusion pressure in acute severe AR, classically presents with
central crushing chest pain radiating to the jaw or left arm. Aortic root dissection classically presents with
chest pain radiating to the back.
Acute AR: investigation and imaging

ECG
• Determines any arrhythmias and the rate of tachycardia. It will also rule out or diagnose myocardial
ischaemia or infarction.
CXR
• May not show cardiomegaly, which is a characteristic finding for chronic AR. There may be
evidence of pulmonary oedema with bilateral basal shadowing, pleural effusions at costophrenic
angles, and fluid in the lung fissures.
DIAGNOSIS
Trans-thoracic echocardiogram
• One of the best non-invasive diagnostic tests to evaluate the valvular diseases.[16]
• Confirms the presence and severity of the valvular regurgitation, assesses LV size (which is usually
normal) and systolic function, and determines a cause.
Trans-oesophageal echocardiogram
• Performed if aortic root dissection is suspected: classically, patients have chest pain that radiates to
the back .[1]
Chronic AR: clinical symptoms

Patients have a protracted course and remain asymptomatic for decades. LV systolic dysfunction often
precedes the development of symptoms. Patients may remain asymptomatic with normal exercise
tolerance even with chronic severe AR due to LV compensation.
Initial symptoms may include uncomfortable awareness of the pounding heart when lying on the left side,
due to closer contact of the enlarged LV with the chest wall.[11] Palpitations occur frequently, secondary
to premature ventricular contractions. These symptoms may persist for years before exercise intolerance
occurs. With progressive systolic dysfunction, patients will complain of typical symptoms of CHF including
fatigue, weakness, orthopnoea, and paroxysmal nocturnal dyspnoea.[17]
Uncommonly, patients may complain of angina without CAD at rest or with exercise. Myocardial
ischaemia can result in interstitial fibrosis, which further deteriorates LV systolic function. Syncope and
sudden cardiac death are rare.
Chronic AR: clinical signs

Pulse
• Arterial pulse shows rapid rise and a quick collapse (Corrigan's pulse or water hammer pulse)
resulting in widened pulse pressure >50 mmHg.
• There are multiple eponymous peripheral haemodynamic signs associated with a bounding pulse
and systolic hypertension of chronic severe AR. The sensitivity and specificity of these signs in
diagnosing AR is low and should be used only as supportive evidence.[18]
Apical impulse
• Diffuse, hyperdynamic, and shifted inferiorly and leftwards.

• A systolic thrill may be palpable over the base of the heart or suprasternal notch due to increased
stroke volume.
Murmurs
• The murmur of AR is a high-pitched early diastolic, decrescendo blowing sound, which is heard
best with the diaphragm of the stethoscope just after A2.[19] The murmur is usually soft and can be
accentuated with the patient sitting up, leaning forwards, and holding his or her breath at the end of
expiration.
• The murmur due to valvular cause is best heard at the third and fourth intercostal space at the left
sternal border. Regurgitation due to aortic dilation resulting from dissection or aneurysm is best
heard at the second to third right intercostal space. Manoeuvres that increase arterial pressure,
DIAGNOSIS
such as squatting, accentuate the murmur, whilst inhalation of amyl nitrate or Valsalva, which lower
arterial pressure, decreases the intensity of the murmur.
• Moderate to severe AR is sometimes associated with an ejection systolic flow murmur after S1 due
to the flow of increased stroke volume across a non-stenotic aortic valve. The murmur is an early
peaking, crescendo-decrescendo systolic sound, best heard at the second right intercostal space,
and can be differentiated from an aortic stenosis murmur by the absence of an ejection click.
• Another murmur that is often associated with severe AR is the Austin Flint murmur. It is a soft,
rumbling, mid to late diastolic murmur heard best at the apex. It is produced by the abutment of an
aortic regurgitant jet against the LV endocardium.[20] An Austin Flint murmur is distinguished from
the murmur of mitral stenosis by the absence of an opening snap and loud S1.
Heart sounds
• Chronic AR is also associated with changes in heart sounds. S1 may be due to early coaptation of
the mitral valve leaflets from increased end-diastolic pressure. With increasing severity of AR, end-
diastolic pressure can rise steeply above left atrial pressure causing even diastolic closure of the
mitral valve.
11
• LV dysfunction can result in S3 gallop or occasionally S4 due to LVH. Inadequate closure of aortic
valve in severe AR may cause a soft A2 or even absent A2.
Chronic AR: imaging and investigations

Physical signs are not specific enough to judge the severity of the AR. Echocardiography should be
performed for evaluation of symptomatic and asymptomatic chronic AR. If the echocardiogram is of
insufficient quality, radionuclide angiography or MRI can be ordered to evaluate the valvular abnormality.
ECG
• Normal early in the disease but shows left axis deviation in chronic aortic regurgitation supporting
LV volume overload. May also show signs of conduction abnormalities.[1]
CXR
• Cardiomegaly is a characteristic finding in chronic AR.

Echocardiogram
• For asymptomatic patients with chronic AR, the diagnosis can be established using a good-quality
echocardiogram, and no further diagnostic testing is required.[1] This test allows visualisation of
the origin of the regurgitant jet and its width, and detection of the cause of aortic valve pathology. A
trans-thoracic echocardiogram is usually adequate, but a trans-oesophageal echocardiogram can
be used if the quality of the trans-thoracic echocardiogram is inadequate.[1]
• Two-dimensional echocardiography helps in evaluating the valvular anatomy and the impact of
volume overload on the ventricular size and function. M-mode imaging indirectly assesses the AR
by detecting premature closure of the mitral valve and diastolic fluttering of the anterior mitral leaflet
from the regurgitant aortic jet.
• Doppler echocardiography is the most specific technique used for detecting the severity
of regurgitation. Several indices are used to assess severity. Colour flow Doppler provides
visualisation of the origin of the regurgitant jet and its width. There are several pulsed and
DIAGNOSIS
continuous wave Doppler methods that give clues to the severity of AR. These include colour flow,
pulsed wave, and continuous wave Doppler.
Exercise testing
• In chronic severe AR, if the patient's physical activity is minimal or symptoms are equivocal,
exercise testing is helpful to assess the functional status and symptomatic response.[1]
Cardiac catheterisation, angiography, or MRI
• In asymptomatic patients with chronic AR, if the quality of the echocardiogram is inadequate to
assess LV function, radionuclide angiography or MRI can be used.[1]
• In cases of acute AR, right and left heart catheterisation shows severe elevations of LV end-
diastolic pressure and pulmonary capillary wedge pressure (PCWP) due to sudden volume
overloading of a normal sized LV. LV end-diastolic pressure is often much higher than PCWP
because of early closure of the mitral valve.
• Angiography is also used to evaluate coronary anatomy in patients with high risk for CAD and
who will be undergoing aortic valve replacement/repair. In this setting, men aged >35 years,
premenopausal women aged >35 years with risk factors for CAD, and postmenopausal women
should undergo coronary angiography.
Risk factors
Strong
bicuspid aortic valve
• This congenital abnormality accounts for most of the cases of AR in developed countries.
• Some pathological abnormalities of bicuspid aortic root occur, which lead to proximal aortic dilation
and worsening of aortic regurgitation.[9] [12]
rheumatic fever
• One of the most common causes of AR in developing countries.
endocarditis
• Can lead to rupture of leaflets or even paravalvular leaks.
• Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of
blood.[8]
Marfan's syndrome and related connective tissue disease

• 80% of Marfan's patients present at an early age with a diastolic murmur.[13]
• Disorders such as Marfan's syndrome often lead to progressive dilation of aortic root resulting in AR.
aortitis
• Inflammation of the aorta secondary to systemic diseases such as syphilis, Behcet's, Takayasu's,
reactive arthritis, and ankylosing spondylitis results in weakening of the aortic root and dilation.[15]
Weak
DIAGNOSIS
systemic hypertension
• Can lead to aortic root dilation and inadequate closure of aortic valve leaflets.[10] [14]
older age
• Older patients are more prone to develop aortic regurgitation along with aortic sclerosis.[6]
History & examination factors

Key diagnostic factors
presence of risk factors (common)
• Risk factors include bicuspid aortic valve, rheumatic fever, endocarditis, Marfan's syndrome and
related connective tissue disease, and aortitis.
diastolic murmur (common)

• The absence of diastolic murmur significantly reduces the likelihood of AR.[21]
13
• The severity of the AR correlates well with the duration of murmur, instead of the intensity of murmur.
In mild AR the murmur is early diastolic, and increases in duration to holodiastolic in severe AR.
• A diastolic murmur may be absent in acute AR.
Other diagnostic factors

dyspnoea (common)
• Caused by pulmonary oedema in acute AR, or progressive left ventricular dysfunction in chronic
severe AR.
fatigue (common)
• Symptom of chronic AR due to progressive left ventricular dysfunction.
weakness (common)
orthopnoea (common)
parox ysmal nocturnal dyspnoea (common)

pallor (common)
• Sign of cardiogenic shock.
mot tled extremities (common)

rapid and faint peripheral pulse (common)

DIAGNOSIS
jugular venous distension (common)

• Sign of cardiogenic shock and CHF.
basal lung crepitations (common)

• Sign of pulmonary oedema.
altered mental status (common)

urine output <30 mL/hour (common)

soft S1 (common)
• May be soft due to early coaptation of the mitral valve leaflets from increased end-diastolic pressure.
soft or absent A2 (common)

• Caused by inadequate closure of aortic valve in severe AR
collapsing (water hammer or Corrigan's) pulse (common)
• Arterial pulse shows rapid rise and a quick collapse resulting in widened pulse pressure >50 mmHg.
cyanosis (common)
• Sign of acute AR.
tachypnoea (common)
• Sign of acute AR with pulmonary oedema.
displaced, hyperdynamic apical impulse (common)

• Present on chronic AR with left ventricular enlargement.
chest pain (uncommon)

• Most common in chronic AR, although can be presenting symptom in acute AR. Acute severe central
crushing pain may indicate myocardial ischaemia, or, if referred to the back, aortic dissection.
pink frothy sputum (uncommon)

wheeze (cardiac asthma) (uncommon)

additional heart sounds (uncommon)

• Left ventricular dysfunction can result in S3 gallop or occasionally S4 due to LVH.
arrhythmias (uncommon)
• May be present in acute severe AR or chronic AR.
ejection systolic flow murmur (uncommon)

• Sometimes associated with moderate to severe AR. The murmur occurs after S1 due to the flow
DIAGNOSIS
of increased stroke volume across a non-stenotic aortic valve. It is an early peaking, crescendo-
decrescendo systolic sound, best heard at second right intercostal space, and can be differentiated
from an aortic stenosis murmur by the absence of an ejection click.
Austin Flint murmur (uncommon)

• A soft, rumbling, mid to late diastolic murmur heard best at the apex. It is produced by the abutment
of an aortic regurgitant jet against the left ventricular endocardium.[20] An Austin Flint murmur is
distinguished from the murmur of mitral stenosis by the absence of an opening snap and loud S1. It is
a specific finding for severe AR.
systolic thrill (uncommon)

• May be palpable over the base of the heart or suprasternal notch due to increased stroke volume.
Hill's sign (uncommon)

• Systolic pressure over popliteal artery exceeds brachial systolic blood pressure by >60 mmHg.
Peripheral haemodynamic sign associated with a bounding pulse and systolic hypertension of chronic
severe AR.
15
bisferiens pulse (uncommon)
• Double systolic arterial impulse.
de Musset's sign (uncommon)

• Patient's head may bob in time with each heart beat. Peripheral haemodynamic sign associated with a
bounding pulse and systolic hypertension of chronic severe AR.
Muller's sign (uncommon)

• Pulsations of the uvula.
Traube's sign (uncommon)

• Pistol shot sounds over the femoral artery with compression. Peripheral haemodynamic sign
associated with a bounding pulse and systolic hypertension of chronic severe AR.
Quincke's sign (uncommon)

• Subungual or lip capillary pulsations due to the large stroke volume. Peripheral haemodynamic sign
associated with a bounding pulse and systolic hypertension of chronic severe AR.
Duroziez's sign (uncommon)

• Systolic and diastolic murmurs heard over the femoral artery when compressed proximally and
distally, respectively. Peripheral haemodynamic sign associated with a bounding pulse and systolic
hypertension of chronic severe AR.
Mayen's sign (uncommon)

• Diastolic drop of blood pressure >15 mmHg with arm raised.
Lighthouse sign (uncommon)

• Blanching and flushing of forehead.
Becker's sign (uncommon)

DIAGNOSIS
• Pulsations of retinal vessels.
Landolfi's sign (uncommon)

• Alternating constriction and dilation of pupil.
Rosenbach's sign (uncommon)

• Systolic pulsations of liver.
Gerhardt's sign (uncommon)

• Pulsatile spleen.
Lincoln's sign (uncommon)

• Pulsatile popliteal artery.
Sherman's sign (uncommon)

• Dorsalis pedis pulse is unexpectedly prominent in age >75 years.
palmar click (uncommon)
• Palpable systolic flushing of palms.
syncope (uncommon)
• Rare presentation.
DIAGNOSIS
17
Diagnostic tests
1st test to order
Test Result
ECG may show non-specific
ST-T wave changes,
• Provides only supportive evidence. Echocardiography is required to
left axis deviation, or
confirm the presence of AR.
conduction abnormalities
• Chronic severe AR: may demonstrate non-specific ST-T wave
changes, LVH with left axis deviation due to compensatory left
ventricular (LV) chamber enlargement, or isolated premature
ventricular contraction. In later stages of LV dysfunction, LV
conduction delays may be seen.
• Acute AR: may reveal some non-specific ST-T wave changes and
sinus tachycardia or arrhythmias; evidence of myocardial ischaemia
may also be present.
• Conduction abnormalities can also be seen in active infective
endocarditis resulting from paravalvular abscess.
CXR may show cardiomegaly
• Chronic AR may produce cardiomegaly in the leftwards and inferior
direction due to compensatory eccentric hypertrophy from increased
end-diastolic volume. The aortic knob is typically prominent in severe
hypertensive patients and those with aortic root dilation.
• In chronic severe AR, the aortic root sometimes progressively
enlarges due to increased stroke volume and increased systolic blood
pressure; calcification of the aortic valve is uncommon in pure AR but
can be seen in patients with combined atrial stenosis and AR.
echocardiogram visualisation of the origin
• The preferred method for non-invasive detection and evaluation of the of regurgitant jet and its
width; detection of cause
severity and aetiology of aortic regurgitation.
of aortic valve pathology
M-mode and 2-dimensional imaging assessment of valvular

DIAGNOSIS
anatomy, aortic root

• Helps indirectly assess AR. Two-dimensional echocardiography is
dilation, and left
very important in evaluating the valvular anatomy, assessing aortic
ventricular response to
root dilation, and monitoring the left ventricular response to volume
volume overload
overload.
[Fig-2]
• Possible findings include premature closure of the mitral valve
(severe/acute AR), diastolic fluttering of the anterior mitral leaflet from
the regurgitant aortic jet, and hyperdynamic interventricular septal
motion.
colour flow Doppler detection and
quantification of
• One of the most specific and sensitive techniques used to judge the
regurgitant flow
severity of the regurgitant flow by using the ratio of proximal jet width
[Fig-3]
to left ventricular outflow tract

[Fig-4]
and ratio of cross-sectional area of jet to left ventricular outflow tract.

Vena contracta, which is the narrowest region of regurgitant jet just
below the aortic valve, may also be used.
Test Result
[Fig-5]
[22]
• The length of the jet column in the ventricle was previously used but
is no longer considered a measure of severity.
• Parasternal views are preferred over the apical view because of
better axial resolution.
pulsed wave Doppler detection and
quantification of
• As AR gets worse, a greater degree of flow reversal occurs and
holodiastolic flow reversal
holodiastolic flow reversal indicates severe AR; pulsed wave Doppler
can quantitate this effect by assessing the regurgitant stroke volume
and effective regurgitant orifice area.
• The diastolic flow reversal is measured in the descending aorta from
a suprasternal probe position.
[Fig-6]
Regurgitant stroke volume can be calculated by subtracting forwards

stroke volume, which can be determined at mitral valve, from total
stroke volume (aortic valve). Both regurgitant stroke volume and
regurgitant fraction can be calculated from this.
• Effective regurgitant orifice area is another measure to assess the
severity of AR, and can be calculated by dividing regurgitant stroke
volume by jet velocity time integral of the AR assessed by continuous
wave Doppler.[22]
continuous wave Doppler may show shorter
pressure half-time or
• As aortic regurgitation gets worse, left ventricular diastolic pressure
steeper slope of velocity
rapidly increases and aortic diastolic pressure rapidly falls, resulting
in shorter pressure half-time or steeper slope of velocity deceleration. deceleration in severe AR
These measures can be used as part of the assessment of AR
severity.
[Fig-7]
DIAGNOSIS
19
Other tests to consider
Test Result
radionuclide angiography measurement of ejection
fraction and regurgitation
• A useful non-invasive, accurate method of evaluating AR in patients
fraction; detection of
with sub-optimal echocardiogram. Serial measurements can be
relative ventricular
helpful in early detection of systolic dysfunction.[23]
enlargement
MRI measurement of
ventricular diameter
• Provides accurate assessment of ventricular diameters and volumes
and volume, regurgitant
both in systole and diastole. It also allows accurate measurement
volume, and orifice size
of regurgitant volume and orifice size. MRI is the most accurate
non-invasive technique for assessing AR, but is seldom used due
to its high cost. MRI can be used for initial and serial evaluation of
left ventricular function, volume, and AR severity in patients with an
inconclusive echocardiogram.
exercise stress testing assessment of
functional capacity and
• Not used as a diagnostic test, but can be used to assess the
symptomatic response in patients with history of equivocal symptoms symptomatic response
and chronic AR.[1]
cardiac catheterisation evaluation of the extent
and severity of CAD
• Used to evaluate coronary anatomy in patients with high risk for
and measurement of
CAD and who will be undergoing aortic valve replacement/repair.
associated left ventricular
Men aged >35 years, premenopausal women aged >35 years
with risk factors for CAD, and postmenopausal women should (LV) function
undergo coronary angiography. Although echocardiogram accurately
evaluates the severity of AR, if the results are inconclusive or
discordant with clinical findings, cardiac catheterisation should be
performed to assess the severity of AR and LV function.[1] With the
help of aortic root angiography, the severity of AR and aortic root size
can be assessed.
DIAGNOSIS
Differential diagnosis
Condition Differentiating signs / Differentiating tests

symptoms
Mitral regurgitation (MR) • Distinguishing signs are • CXR: pulmonary oedema,
right ventricular heave, soft enlarged left atrium and left
S1, split S2, and aloud P2. ventricle, and mitral valve
The classical murmur of MR calcification.
is pansystolic at the apex • ECG: can present with atrial
radiating to the axilla. fibrillation.
• Echocardiography: for MR
it is used to assess left
ventricular function.
Mitral stenosis • Distinguishing features • CXR: pulmonary oedema,

are a malar flush, low enlarged left atrium, and
volume pulse, a tapping and mitral valve calcification.
undisplaced apex beat, and • ECG: can present with atrial
loud S1 with an opening fibrillation. RVH may also be
snap. present.
• The murmur is a rumbling • Echocardiography:
mid-diastolic one, which diagnostic for mitral stenosis.
can be distinguished from
the Austin Flint murmur
sometimes heard in severe
AR by the absence of the
opening snap and loud S1.
Aortic stenosis • Presentation includes • CXR: LVH, calcified aortic

dyspnoea, dizziness, valve.
fainting, and congestive • ECG: P-mitrale, LVH with
cardiac failure. strain pattern, left bundle
• Characteristic signs are a branch block, or complete
slow rising pulse, heaving AV block.
DIAGNOSIS
but undisplaced apex bear, • Echocardiography:
left ventricular heave, and diagnostic for aortic stenosis.
an ejection systolic murmur
that radiates towards the
carotids and can have an
ejection click. This can
be distinguished from the
ejection systolic murmur that
is sometimes heard with
moderate or severe AR by
absence of an ejection click
and no radiation towards the
carotids.
Pulmonary regurgitation • Diamond-shaped diastolic • CXR: may show dilation of

murmur best heard in main pulmonary artery with
the second and third left right ventricular dilation.
intercostal spaces. The • ECG: right ventricular
murmur increases with hypertrophy is usually
inspiration, and P2 is loud in present.
the presence of pulmonary
artery hypertension.
21
Condition Differentiating signs / Differentiating tests

symptoms
• Echocardiography:
diagnostic for pulmonary
regurgitation.
Diagnostic criteria
Acute aortic regurgitation: clinically accepted criteria
A medical emergency where the left heart rapidly decompensates due to its inability to handle a sudden
increase in end-diastolic volume. Most commonly it results from aortic dissection or endocarditis and, in rare
cases, trauma.
Chronic aortic regurgitation: clinically accepted criteria

Chronic regurgitation has a prolonged course over a period of months to years. The left ventricle is able to
compensate for volume overload initially but then decompensates with the appearance of clinical symptoms
of congestive heart failure.
Classification of the severity of aortic regurgitation in adults (ACC/

AHA practice guidelines for the management of patients with
valvular heart disease)[1]
Mild AR
DIAGNOSIS

Moderate AR
Severe AR

Stages of chronic aortic regurgitation assessed by echocardiogram

and cardiac catheterisation
Different criteria have been developed to diagnose patients based on Doppler echocardiographic and cardiac
catheterisation measurements, to help time the surgery and ensure the benefits outweigh the perioperative
risk (mortality 4%) and long-term complications of prosthetic valve.[1] [2] [3]
Compensated
• Ejection fraction >55%

• Fractional shortening >32%
• End-diastolic diameter <60 mm
• End-systolic diameter <45 mm
• End-diastolic volume <120 mL/m^2
• End-systolic volume <50 mL/m^2
Transitional
• Ejection fraction 51% to 55%

• Fractional shortening 30% to 31%
• End-diastolic diameter 60-70 mm
• End-systolic diameter 45-50 mm
• End-diastolic volume 130-160 mL/m^2
• End-systolic volume 50-60 mL/m^2
Decompensated
• Ejection fraction ≤50%
DIAGNOSIS
• Fractional shortening <29%
• End-diastolic diameter >75 mm
• End-systolic diameter > 55 mm
• End-diastolic volume >170 mL/m^2
• End-systolic volume >60 mL/m^2
23
Aortic regurgitation Treatment
Step-by-step treatment approach

Acute AR is an emergency requiring urgent surgical intervention. Chronic AR has a protracted course and
the patient may remain asymptomatic for decades. Many of those who have mild or moderate AR remain
stable and may never require any corrective surgery. Surgery should be performed as soon as possible in
patients with chronic AR who develop haemodynamic instability or CHF.
The treatment of chronic AR depends on 5 factors:
• Whether the regurgitation is mild, moderate, or severe

• Whether the patient is asymptomatic or symptomatic
• Whether the patient has normal left ventricular (LV) function or LV dysfunction
• Whether the patient has LV dilation
• Whether the patient is a surgical candidate.
Assessment of disease severity

Aortic regurgitation is classified as mild, moderate, or severe based on defined echocardiographic,
Doppler, and angiographic features.[1]
Mild AR
Moderate AR
Severe AR

TREATMENT

Acute AR
Acute AR is a surgical emergency. Patients require assessment and management of the airway, with
intubation if necessary. Positive inotropic agents (e.g., dopamine and dobutamine) and a vasodilator
(e.g., sodium nitroprusside) are recommended for haemodynamic support. The definitive management
is with urgent surgery, especially for patients with AR resulting from infective endocarditis and aortic root
dissection.[1]
Mild to moderate chronic AR

Patients with mild to moderate disease who are asymptomatic with normal LV function do not require
treatment and can be reassured; the outcome in these patients is excellent . In patients with this degree
of AR severity, symptoms or LV dysfunction, if present, are unlikely to be due to AR. An alternative
underlying cause such as hypertension, CAD, or a cardiomyopathy is more likely and should be
investigated and treated.
Severe chronic AR
Patients who are asymptomatic are managed according to the stage of their disease, which is reflected
by the presence and severity of LV function, measured by the ejection fraction (EF), and LV dilation,
measured by the end-diastolic (EDD) and end-systolic (ESD) diameters.
• Compensated disease: if LV function is normal (EF >50%) and there is no LV dilation (EDD <60
mm or ESD <45 mm), no treatment is required and the patient can be reassured.
• Transitional disease: if LV function is normal but LV dilation in the range EDD 60-70 or ESD 45-50
mm is present, an exercise tolerance test should be performed. If the exercise test is normal,
no treatment is required. However, if an abnormal haemodynamic response occurs, vasodilator
therapy (hydralazine or nifedipine) is recommended.[24]
• Decompensated disease: surgery is required in patients with normal LV function but an EDD >70 or
ESD >50 mm or with abnormal LV function (EF ≤50%). Vasodilators may be used while the patient
is awaiting surgery.
All symptomatic patients require surgery, regardless of their LV function and dilation. If the patient is not
a surgical candidate due to comorbidities, long-term therapy with vasodilators or angiotensin converting-
enzyme inhibitors (e.g. enalapril) is recommended.[25] For high-risk surgical patients and non-surgical
candidates with severe AR, transcatheter aortic valve implantation (TAVI) may be considered as an off-
label indication.[26]
The surgical options are aortic valve replacement (AVR) or repair. There is no difference in the indications
for replacement or repair. AVR is performed in most patients requiring surgery. Aortic valve repair is
possible in selected patients but is only performed in specialist centres. Following surgery, most of
the patients show reversal of LV dilation and improvement in EF. Preoperative LV function is the best
predictor of long-term prognosis in patients undergoing AVR.[27] Patients with normal preoperative EF
or a brief duration of LV dysfunction (<14 months) have greater improvement in LV diameters and early
and late postoperative improvement in LV function.[28] Among patients with LV dysfunction, patients
with impaired preoperative LV function have a greater risk of developing CHF and are at a higher risk
TREATMENT
of death compared with patients with normal preoperative LV function.[29] Survival among patients
with preoperative severe LV dysfunction has improved dramatically since 1985 and has become almost
equivalent to that among patients with non-severe LV dysfunction.
25
Treatment details overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Acute ( summary )
acute AR
1st inotropes + vasodilators + urgent aortic

valve replacement/repair
TREATMENT
Ongoing ( summary )
mild to moderate chronic AR
asymptomatic with 1st reassurance

normal left ventricular
function
symptomatic or left 1st investigation and treatment of alternative

ventricular dysfunction underlying cause
severe chronic AR: asymptomatic

with ejection fraction >50%
compensated disease 1st reassurance
transitional disease: 1st reassurance

negative exercise test
transitional disease: 1st vasodilator therapy

positive exercise test
decompensated disease: 1st aortic valve replacement or transcatheter

surgical candidate aortic valve implantation
decompensated disease: 1st vasodilator or ACE inhibitor therapy or

non-surgical candidate transcatheter aortic valve implantation

with ejection fraction ≤50%
surgical candidate 1st aortic valve replacement or transcatheter

aortic valve implantation
non-surgical candidate 1st vasodilator or ACE inhibitor therapy or

transcatheter aortic valve implantation
severe chronic AR: symptomatic

adjunct vasodilator therapy
non-surgical candidate 1st vasodilator therapy or transcatheter aortic

valve implantation
TREATMENT
27
Treatment options
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Acute
acute AR
1st inotropes + vasodilators + urgent aortic

valve replacement/repair
Primary options
» dopamine: 2-5 micrograms/kg/min

intravenously initially, titrate to effect,
maximum 20 micrograms/kg/min
-or-
» dobutamine: 0.5 micrograms/kg/min
intravenously initially, titrate to effect,
maximum 20 micrograms/kg/min
--AND--
» nitroprusside: 0.3 to 0.5 micrograms/kg/min
intravenously, titrate to effect, maximum 10
micrograms/kg/min
--AND--
» aortic valve replacement
» Acute AR is a surgical emergency.

Haemodynamic support with inotropic agents
(dopamine and dobutamine) and vasodilators
may be necessary for stabilisation before
surgery.
» Aortic valve replacement or repair should be

performed as soon as possible. Aortic valve
repair is possible in selected patients but is only
performed in specialist centres.
» Prosthetic valve patients are at high risk for

thromboembolism and need antithrombotic
therapy. The risk of bleeding must be weighed
against the benefit of anticoagulation.
» Intravenous infusion rates >10 micrograms/

kg/min may lead to cyanide toxicity with
nitroprusside.
TREATMENT
Ongoing
mild to moderate chronic AR
asymptomatic with 1st reassurance

normal left ventricular
function » Patients with normal left ventricular function
(ejection fraction >50%) do not require treatment
and can be reassured. The outcome in these
patients with no therapy is excellent.
symptomatic or left 1st investigation and treatment of alternative
ventricular dysfunction underlying cause
» Medical therapy and surgery are not

recommended, as an alternative cause is likely.
Patient should be investigated for alternative
causes for the symptoms of left ventricular
dysfunction: for example, hypertension, CAD, or
a cardiomyopathy.
with ejection fraction >50%
compensated disease 1st reassurance
» Patients with normal left ventricular (LV)

function (ejection fraction >50%) and no LV
dilation as indicated by normal end-diastolic
and end-systolic diameters have compensated
disease. No treatment is required in these
patients.
transitional disease: 1st reassurance
negative exercise test
function (ejection fraction >50%) and either end-
diastolic diameter 60-70 mm or end-systolic
diameter 45-50 mm have transitional disease.
» These patients require an exercise tolerance

test. If the results are normal, no treatment is
required.
transitional disease: 1st vasodilator therapy
positive exercise test
Primary options
» nifedipine: 30-60 mg orally (extended-

release) once daily
OR
» hydralazine: 10-25 mg orally 2 to 4 times

TREATMENT
daily initially, titrate according to response,

maximum 300 mg/day

function (ejection fraction >50%) and either end-
29
Ongoing
diastolic diameter 60-70 mm or end-systolic
diameter 45-50 mm have transitional disease.
» These patients require an exercise tolerance

test. If there is an abnormal haemodynamic
response to an exercise test, vasodilator
therapy is recommended. Vasodilators include
hydralazine and nifedipine.
decompensated disease: 1st aortic valve replacement or transcatheter
surgical candidate aortic valve implantation

function but an end-diastolic diameter >70
mm or an end-systolic diameter >50 mm have
decompensated disease. These patients require
surgery.
» Aortic valve replacement with a mechanical

or a biological valve has a low rate of requiring
reoperation. This durability comes at the
expense of valve-related complications such
as thromboembolism, anticoagulant-related
bleeding, and infective endocarditis.
» For high-risk surgical patients, transcatheter

aortic valve implantation (TAVI) may be
considered as an off-label indication.[26]

decompensated disease: 1st vasodilator or ACE inhibitor therapy or
non-surgical candidate transcatheter aortic valve implantation
Primary options

release) once daily
OR

maximum 300 mg/day
OR
» enalapril: 5-20 mg orally twice daily

TREATMENT
function but an end-diastolic diameter >70

mm or an end-systolic diameter >50 mm have
decompensated disease.
» Surgery is contraindicated in patients with

severe comorbidities. Severe LV dysfunction
Ongoing
is not a contraindication. If contraindications
to surgery are present, these patients can be
managed with medical therapy.
» Vasodilator therapy may be considered for

long-term treatment in stable patients (class
IIb).[1] Long-term studies on the effects of
vasodilators on haemodynamics have shown
inconsistent results.[30] [31] [32] [33] [34] There
are no recommendations on the preference of
vasodilators.
» For non-surgical candidates, transcatheter

with ejection fraction ≤50%

» Patients with an ejection fraction ≤50% have

decompensated disease and require surgery.
» Aortic valve replacement with a mechanical

or a biological valve has a low rate of requiring
reoperation. This durability comes at the
expense of valve-related complications such
as thromboembolism, anticoagulant-related
bleeding, and infective endocarditis.


non-surgical candidate 1st vasodilator or ACE inhibitor therapy or
transcatheter aortic valve implantation
Primary options

release) once daily
OR

TREATMENT

maximum 300 mg/day
OR
» enalapril: 5-20 mg orally twice daily
31
Ongoing
» Patients with an ejection fraction ≤50% have
decompensated disease.

» Vasodilator therapy may be considered for

long-term treatment in stable patients (class
IIb).[1] Long-term studies on the effects of
vasodilators on haemodynamics have shown
inconsistent results.[30] [31] [32] [33] [34] There
are no recommendations on the preference of
vasodilators.

severe chronic AR: symptomatic

» Indicated for all symptomatic patients

regardless of left ventricular function or dilation.
Aortic valve replacement with a mechanical or
a biological valve has a low rate of reoperation.
This durability comes at the expense of valve-
related complications such as thromboembolism,
anticoagulant-related bleeding, and infective
endocarditis.


adjunct vasodilator therapy
Treatment recommended for SOME patients in
selected patient group
Primary options

release) once daily
TREATMENT
OR

maximum 300 mg/day
Ongoing
» Using vasodilator therapy should be
considered while awaiting surgery.
non-surgical candidate 1st vasodilator therapy or transcatheter aortic
valve implantation
Primary options

release) once daily
OR

maximum 300 mg/day

» Using vasodilator therapy should be

considered in symptomatic patients who have
contraindications to surgery.

TREATMENT
33
Aortic regurgitation Follow up
Recommendations
Monitoring
FOLLOW UP
Patients who present to their physician with AR on initial evaluation need to be followed up closely due
to the protracted course and potential complications of the disease. These patients need to be serially
monitored based on the severity of AR, left ventricular ejection fraction (LVEF), and left ventricular (LV)
diameters.
Asymptomatic patients with mild chronic AR and normal LVEF can be seen yearly, and routine
echocardiography can be done every 3 to 5 years. Asymptomatic patients with chronic severe AR and
normal LVEF are serially monitored based on LV diameters.[1]
Those with LV end-systolic diameter <45 mm and end-diastolic diameter <60 mm need clinical evaluation
every 6 to 12 months, and echocardiography every 12 months.[1]
In patients with LV end-systolic diameter 45-50 mm and end-diastolic diameter 60-70 mm, clinical
evaluation every 6 months and echocardiography every 12 months is required.[1]
Those with LV end-systolic diameter 50-55 mm and end-diastolic diameter 70-75 mm and normal
haemodynamic response to exercise need clinical evaluation every 6 months and echocardiography every
6 months.[1]
Patients with aortic root dilation and diameter >4 cm should undergo serial evaluations of aortic root and
ascending aorta by echocardiography, CT scan, or MRI yearly.[1]
Patients who undergo aortic valve replacement/repair need close follow-up during the early and late
postoperative course and need to be serially monitored. Asymptomatic patients need to be followed
up yearly for a complete history and physical examination.[1] Any change in clinical status demands
echocardiography.
Prosthetic valve patients are at high risk for thromboembolism and need antithrombotic therapy. The risk
of bleeding must be weighed against the benefit of anticoagulation.
Patient instructions
Patients are encouraged to do moderate exercise, but patients with severe AR and LV end-diastolic
diameter >65 mm should be advised to avoid active sport.[42] Those on anticoagulation are advised to
avoid contact sport.
Patients should be advised of the possible complications of having a prosthetic valve, such as
thromboembolism, infective endocarditis, haemolysis, structural valve failure, and arrhythmias. They
are advised to seek medical help if they become suddenly breathless, develop a fever, or experience
palpitations or sudden onset of weakness of a limb, or complete or partial loss of sight.
Patients should also be advised about the risks of being on anticoagulation, the main one being
haemorrhage. The patient should report unusual bruises, bleeding gums, coughing up blood, dark
urine, and black bowel movements. Ideally, they are advised to avoid any activity that may increase their
chances of bruising or bleeding, such as contact sport. They are also reminded that they should tell the
pharmacist, doctor, and dentist that they are taking warfarin, as some medications affect how the drug
works: for example, broad-spectrum antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs).
Patients are encouraged to attend every appointment to have their INR checked.
Complications
Complications Timeframe Likelihood
FOLLOW UP
operative mortality short term medium
There is a 4% risk of death with AVR, and the risk increases to 6.8% if performed along with CABG.[37]
[41]
CHF long term high
The most common complication of severe AR. Mild to moderate AR may remain asymptomatic throughout
patient's life or may progress to severe AR and then CHF.
Chronic severe AR patients should be referred for aortic valve replacement/repair (AVR) as soon as they
develop any symptoms, impaired exercise tolerance, or decreased ejection fraction.[35] [37]
Patients with severe left ventricular dysfunction and symptoms of CHF should be started on medical
therapy (inotropes and vasodilators) and referred for AVR.
arrhythmias long term low
Stretching and dilation of the left atrium results in atrial fibrillation, which leads to weakness, dyspnoea,
palpitations, and occasionally syncope.
The AV node, due to its proximity to the aortic valve, may be damaged secondary to stretching and
scarring, which sometime results in bradyarrhythmias and different degrees of block that are treated with
medications and/or a pacemaker.
infective endocarditis variable low
Bacteraemia with organisms likely to cause endocarditis results in this complication in patients with
underlying structural valvular defects.
Patients with AR are considered to be at low risk of developing endocarditis, and prophylactic antibiotics
are not required before bacteraemia-causing procedures.[38]
sudden death variable low
Sudden death is rare in patients with severe AR and normal ventricular function. Annual mortality is 0.4%.
One paper reported unexpected sudden deaths in patients with maintained systolic function but severe
ventricular dilation.[36]
myocardial ischaemia variable low
Patients with AR may complain of angina without CAD due to increased myocardial oxygen requirement
and decreased coronary flow reserve.[39] [40]
35
Prognosis
FOLLOW UP
Mortality is low (<0.4 % per year) in this group and therefore aortic valve replacement is not required, but
patients do need to be monitored closely for developing symptoms or LV dysfunction.[35] These patients are
at risk of progressing to symptoms and/or LV dysfunction at the rate of 5% per year with a mortality of 0.2%
per year.[36]
In patients with more severe LV dilation (end-systolic diameter >50 mm or end-diastolic diameter >70 mm),
there is an even higher risk of developing LV dysfunction (19%) or symptoms (10%).[1] [36]
The outcome and prognosis of patients depends on the magnitude of LV function and symptoms.[28] [29]
The 5-year survival in patients with normal LV function has been reported as 96% whereas that in patients
with reduced LV function is 62%.[29] Long-term improvement in LV function is related to the immediate and
short-term (first 6 months) response to surgery. Patients who have an immediate reduction in LV dilatation
following surgery are more likely to have short- and long-term improvements in the ejection fraction (EF).
Furthermore, patients who have an improvement in EF within the first 6 months following surgery are likely to
have further late improvements in LV function after this time. The EF is unlikely to improve in patients who do
not have an improvement in EF within the first 6 months of surgery.[28]
Aortic regurgitation Guidelines
Diagnostic guidelines
Europe
2017 ESC/EACTS guidelines for the management of valvular heart disease

Published by: European Society of Cardiology; European Association Last published: 2017
for Cardio-Thoracic Surgery
Assessment of valvular regurgitation. Part 1: aortic and pulmonary

regurgitation (native valve disease)
Published by: European Association of Echocardiography Last published: 2010
North America
2014 AHA/ACC guideline for the management of patients with valvular heart
GUIDELINES
disease
Published by: American College of Cardiology; American Heart Last published: 2014
Association
Treatment guidelines
Europe
2017 ESC/EACTS guidelines for the management of valvular heart disease

Published by: European Society of Cardiology; European Association Last published: 2017
for Cardio-Thoracic Surgery
Antithrombotics: indications and management

Published by: Scottish Intercollegiate Guidelines Network Last published: 2013
ESC guidelines for the management of grown-up congenital heart disease

Published by: European Society of Cardiology Last published: 2010
Recommendations for the management of individuals with acquired

valvular heart diseases who are involved in leisure-time physical activities or
competitive sports
Published by: Department of Cardiology, Ruhr University Bochum, Last published: 2008
Germany
37
Aortic regurgitation Guidelines
North America
2014 AHA/ACC guideline for the management of patients with valvular heart
disease
Published by: American College of Cardiology; American Heart Last published: 2014
Association
2018 AATS/ACC/SCAI/STS Expert Consensus Systems of Care Document:

Operator and Institutional Recommendations and Requirements for
Transcatheter Aortic Valve Replacement: A Joint Report of the American
Association for Thoracic Surgery, American College of Cardiology, Society
for Cardiovascular Angiography and Interventions, and Society of Thoracic
Surgeons
Published by: American Association for Thoracic Surgery; American Last published: 2019
College of Cardiology; Society for Cardiovascular Angiography and
Interventions; Society of Thoracic Surgeons
GUIDELINES
Aortic regurgitation References
Key articles
• Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of
REFERENCES
patients with valvular heart disease: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines. Circulation. 2014 Jun 10;129(23):e521-643. Full text
Abstract
• Lancellotti P, Tribouilloy C, Hagendorff A, et al. European Association of Echocardiography

recommendations for the assessment of valvular regurgitation. Part 1: aortic and pulmonary
regurgitation (native valve disease). Eur J Echocardiogr. 2010 Apr;11(3):223-44. Full text Abstract
• Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity
of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc
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in clinical practice: a long-term follow-up study. Circulation. 1999 Apr 13;99(14):1851-7. Full text
Abstract
References
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Abstract
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16. Lancellotti P, Tribouilloy C, Hagendorff A, et al. European Association of Echocardiography

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Aortic regurgitation Images
Images
IMAGES
Figure 1: Causes of AR
Dr Sanjeev Wasson and Dr Nishant Kalra; used with permission
43
IMAGES Aortic regurgitation Images
Figure 2: Parasternal long-axis view demonstrating aortic regurgitation jet

From the collections of Dr Sanjeev Wasson and Dr Nishant Kalra; used with permission
IMAGES
Figure 3: Parasternal long-axis view demonstrating aortic regurgitation jet width and height
45
Figure 4: Parasternal long-axis view demonstrating left ventricular outflow tract diameter
IMAGES
Figure 5: Parasternal long-axis view showing vena contracta of the aortic regurgitation jet
47
Figure 6: Pulsed wave Doppler of the regurgitant jet

IMAGES
Figure 7: Continuous wave Doppler of the regurgitant jet demonstrating pressure half-time of the aortic
regurgitant velocity
49
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Contributors:
// Authors:
Sanjeev Wasson, MD
Medical Director
Department of Cardiology, Skagit Valley Hospital, Mount Vernon, WA
DISCLOSURES: SW declares that he has no competing interests.
Nishant Kalra, MD
Associate Faculty Member
Department of Cardiology, University of Arizona, Tucson, AZ
DISCLOSURES: NK declares that he has no competing interests.
// Peer Reviewers:
Kul Aggarwal, MD, MRCP, FACC, FACP

Professor of Clinical Medicine
University of Missouri-Columbia, Chief, Cardiology Section, Harry S. Truman Veterans Hospital, Columbia,
MO
DISCLOSURES: KA declares that he has no competing interests.
Rajdeep Khat tar, DM, FRCP, FACC, FESC

Consultant Cardiologist and Honorary Senior Clinical Lecturer
Manchester Heart Centre, Central Manchester and Manchester Children's NHS Foundation Trust,
Manchester, UK
DISCLOSURES: RK declares that he has no competing interests.
John Pepper, MChir FRCS

Consultant Cardiac Surgeon
Department of Surgery, Royal Brompton Hospital, London, UK
DISCLOSURES: JP declares that he has no competing interests.

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Aortic regurgitation

The right clinical information, right where it's needed

Last updated: Nov 05, 2019

During acute AR:

• End-diastolic pressure in the left ventricle rises sharply .

• Both left ventricular volume and pressure overload.

Chronic aortic regurgitation: clinically accepted criteria

Classification of the severity of aortic regurgitation in adults (ACC/

• Angiographic grade: 3-4+

Stages of chronic aortic regurgitation assessed by echocardiogram

• Ejection fraction >55%

• Ejection fraction 51% to 55%

• Ejection fraction ≤50%

Acute AR: clinical presentation

Signs and symptoms of pulmonary oedema

• Pale and/or cyanotic, cool to touch with mottled extremities

Acute AR: investigation and imaging

Chronic AR: clinical symptoms

Chronic AR: clinical signs

• Diffuse, hyperdynamic, and shifted inferiorly and leftwards.

Chronic AR: imaging and investigations

• Cardiomegaly is a characteristic finding in chronic AR.

Marfan's syndrome and related connective tissue disease

History & examination factors

diastolic murmur (common)

Other diagnostic factors

parox ysmal nocturnal dyspnoea (common)

mot tled extremities (common)

rapid and faint peripheral pulse (common)

jugular venous distension (common)

basal lung crepitations (common)

altered mental status (common)

urine output <30 mL/hour (common)

soft or absent A2 (common)

displaced, hyperdynamic apical impulse (common)

chest pain (uncommon)

pink frothy sputum (uncommon)

wheeze (cardiac asthma) (uncommon)

additional heart sounds (uncommon)

ejection systolic flow murmur (uncommon)

Austin Flint murmur (uncommon)

systolic thrill (uncommon)

Hill's sign (uncommon)

de Musset's sign (uncommon)

Muller's sign (uncommon)

Traube's sign (uncommon)

Quincke's sign (uncommon)

Duroziez's sign (uncommon)

Mayen's sign (uncommon)

Lighthouse sign (uncommon)

Becker's sign (uncommon)

• Pulsations of retinal vessels.

Landolfi's sign (uncommon)

Rosenbach's sign (uncommon)

Gerhardt's sign (uncommon)

Lincoln's sign (uncommon)

Sherman's sign (uncommon)

palmar click (uncommon)

M-mode and 2-dimensional imaging assessment of valvular

anatomy, aortic root

to left ventricular outflow tract

and ratio of cross-sectional area of jet to left ventricular outflow tract.

Regurgitant stroke volume can be calculated by subtracting forwards