Aortic Regurgitation

Question 1

Summarise aortic regurgitation

Answer 1

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.

Question 2

Define aortic regurgitation

Answer 2

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 root. It can remain asymptomatic for decades before patients present with irreversible myocardial damage.

Question 3

Describe the epidemiology of aortic regurgitation

Answer 3

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

Question 4

Describe the main aetiology of aortic regurgitation

Answer 4

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.

Question 5

Describe how aortic regurgitation can either develop acutely or progressively over the years

Answer 5

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

Question 6

Describe the role of systemic HTN in aortic regurgitation

Answer 6

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.

Question 7

Describe the pathophysiology of acute aortic regurgitation

Answer 7

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.

Question 8

Describe the pathophysiology of chronic progressive aortic regurgitation

Answer 8

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]
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.
End-diastolic pressure remains normal due to an increase in ventricular compliance resulting from increased cavity size.

Question 9

What’s important to remember in patients with chronic aortic regurgitation

Answer 9

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.

Question 10

Describe the difference between the classification of acute and chronic aortic regurgitation

Answer 10

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.

Question 11

Describe the criteria for mild AR

Answer 11

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.

Question 12

Describe the criteria for moderate AR

Answer 12

Moderate AR

Angiographic grade: 2+
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.

Question 13

Describe the criteria for severe AR

Answer 13

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
Regurgitant fraction (%): ≥50
Regurgitant orifice area (cm^2): ≥0.30
Left ventricular size: increased.

Question 14

Describe the key echocardiographic features of compensated AR

Answer 14

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

Question 15

Describe the echocardiographic features of transitional AR

Answer 15

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

Question 16

Describe the echocardiographic features of decompensated AR

Answer 16

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

Question 17

Describe a case history for AR

Answer 17

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.

Question 18

Describe another case history for AR

Answer 18

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.

Question 19

Describe some other presentations of AR

Answer 19

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.

Question 20

How is AR normally detected

Answer 20

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.

Question 21

Describe the acute clinical presentation of AR

Answer 21

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

Question 22

What are the signs and symptoms of pulmonary oedema

Answer 22

Signs and symptoms of pulmonary oedema

Dyspnoea
Pink frothy sputum
Pale and sweaty
Basal lung crepitations
Wheeze (cardiac asthma).

Question 23

What are the signs and symptoms of cariogenic shock

Answer 23

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.

Question 24

Describe the presentations of myocardial ischeamia and aortic root dissection

Answer 24

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.

Question 25

Summarise the key investigations for acute AR

Answer 25

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.
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

Question 26

Describe the clinical symptoms of chronic AR

Answer 26

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.

Question 27

Describe the pulse signs of chronic AR

Answer 27

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

Question 28

Describe the apical impulse signs of chronic AR

Answer 28

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.

Question 29

Describe the murmurs in chronic AR

Answer 29

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, 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

Question 30

Describe the heart sounds in chronic AR

Answer 30

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.
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.

Question 31

Describe the ECG and CXR in chronic AR

Answer 31

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.

Question 32

Describe the echocardiogram in chronic AR

Answer 32

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 continuous wave Doppler methods that give clues to the severity of AR. These include colour flow, pulsed wave, and continuous wave Doppler.

Question 33

Describe exercise testing in chronic AR

Answer 33

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

Question 34

Describe some other tests that can be used in chronic AR

Answer 34

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.

Question 35

Describe the key diagnostic factors in AR

Answer 35

presence of risk factors
Risk factors include bicuspid aortic valve, rheumatic fever, endocarditis, Marfan’s syndrome and related connective tissue disease, and aortitis.

diastolic murmur
The absence of diastolic murmur significantly reduces the likelihood of AR.[21]

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.

Question 36

Describe some other common diagnostic factors in AR

Answer 36

dyspnoea
Caused by pulmonary oedema in acute AR, or progressive left ventricular dysfunction in chronic severe AR.

fatigue
Symptom of chronic AR due to progressive left ventricular dysfunction.

weakness
Symptom of chronic AR due to progressive left ventricular dysfunction.

orthopnoea
Symptom of chronic AR due to progressive left ventricular dysfunction.

paroxysmal nocturnal dyspnoea
Symptom of chronic AR due to progressive left ventricular dysfunction.

pallor
Sign of cardiogenic shock.

mottled extremities
Sign of cardiogenic shock.

rapid and faint peripheral pulse
Sign of cardiogenic shock.

jugular venous distension
Sign of cardiogenic shock and CHF.

basal lung crepitations
Sign of pulmonary oedema.

altered mental status
Sign of cardiogenic shock.

urine output <30 mL/hour
Sign of cardiogenic shock.

soft S1
May be soft due to early coaptation of the mitral valve leaflets from increased end-diastolic pressure.

soft or absent A2
Caused by inadequate closure of aortic valve in severe AR

collapsing (water hammer or Corrigan’s) pulse
Arterial pulse shows rapid rise and a quick collapse resulting in widened pulse pressure >50 mmHg.

cyanosis
Sign of acute AR.

tachypnoea
Sign of acute AR with pulmonary oedema.

displaced, hyperdynamic apical impulse
Present on chronic AR with left ventricular enlargement.

Question 37

Describe some uncommon diagnostic features of AR

Answer 37

chest pain
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
Sign of pulmonary oedema.

wheeze (cardiac asthma)
Sign of pulmonary oedema.

additional heart sounds
Left ventricular dysfunction can result in S3 gallop or occasionally S4 due to LVH.

arrhythmias
May be present in acute severe AR or chronic AR.

Question 38

Describe some uncommon murmurs that may be associated with AR

Answer 38

ejection systolic flow murmur
Sometimes associated with moderate to severe AR. The murmur occurs after S1 due to the flow 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
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
May be palpable over the base of the heart or suprasternal notch due to increased stroke volume.

Question 39

Name some uncommon signs that you may observe in a patient with AR

Answer 39

Hill’s sign
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.

bisferiens pulse
Double systolic arterial impulse.

de Musset’s sign
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
Pulsations of the uvula.

Traube’s sign
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
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
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
Diastolic drop of blood pressure >15 mmHg with arm raised.

Lighthouse sign
Blanching and flushing of forehead.

Becker’s sign
Pulsations of retinal vessels.

Landolfi’s sign
Alternating constriction and dilation of pupil.

Rosenbach’s sign
Systolic pulsations of liver.

Gerhardt’s sign
Pulsatile spleen.

Lincoln’s sign
Pulsatile popliteal artery.

Sherman’s sign
Dorsalis pedis pulse is unexpectedly prominent in age >75 years.

palmar click
Palpable systolic flushing of palms.

Syncope- rare

Question 40

List some strong risk factors for AR

Answer 40

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

Question 41

Describe some weak risk factors for AR

Answer 41

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.

Question 42

Describe the ECG in AR

Answer 42

Provides only supportive evidence. Echocardiography is required to confirm the presence of AR.

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.

Result:
may show non-specific ST-T wave changes, left axis deviation, or conduction abnormalities

Question 43

Describe the CXR in AR

Answer 43

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.

Result:
May show cardiomegaly

Question 44

Describe the echocardiogram in AR

Answer 44

The preferred method for non-invasive detection and evaluation of the severity and aetiology of aortic regurgitation.

Result:

visualisation of the origin of regurgitant jet and its width; detection of cause of aortic valve pathology

Question 45

Describe the use of M-mode US in AR

Answer 45

Helps indirectly assess AR. Two-dimensional echocardiography is very important in evaluating the valvular anatomy, assessing aortic root dilation, and monitoring the left ventricular response to volume overload

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.

Result:
assessment of valvular anatomy, aortic root dilation, and left ventricular response to volume overload

Question 46

Describe the use of colour flow doppler in AR

Answer 46

One of the most specific and sensitive techniques used to judge the severity of the regurgitant flow by using the ratio of proximal jet width to left ventricular outflow tract 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.
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.

Result:
detection and quantification of regurgitant flow

Question 47

Describe the use of pulsed wave doppler

Answer 47

As AR gets worse, a greater degree of flow reversal occurs and 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.

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

Result:
detection and quantification of holodiastolic flow reversal

Question 48

Describe the use of continuous wave doppler in AR

Answer 48

As aortic regurgitation gets worse, left ventricular diastolic pressure rapidly increases and aortic diastolic pressure rapidly falls, resulting in shorter pressure half-time or steeper slope of velocity deceleration. These measures can be used as part of the assessment of AR severity.

Result:
may show shorter pressure half-time or steeper slope of velocity deceleration in severe AR

Question 49

Describe interpretation of angiography in AR

Answer 49

A useful non-invasive, accurate method of evaluating AR in patients with sub-optimal echocardiogram. Serial measurements can be helpful in early detection of systolic dysfunction

Result:
measurement of ejection fraction and regurgitation fraction; detection of relative ventricular enlargement

Question 50

Describe interpretation of MRI in AR

Answer 50

Provides accurate assessment of ventricular diameters and volumes both in systole and diastole. It also allows accurate measurement 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.

Result:
measurement of ventricular diameter and volume, regurgitant volume, and orifice size

Question 51

Describe interpretation of exercise testing in AR

Answer 51

Not used as a diagnostic test, but can be used to assess the symptomatic response in patients with history of equivocal symptoms and chronic AR

Result:
assessment of functional capacity and symptomatic response

Question 52

Describe interpretation of cardiac catheterisation in AR

Answer 52

Used to evaluate coronary anatomy in patients with high risk for CAD and who will be undergoing aortic valve replacement/repair. Men aged >35 years, premenopausal women aged >35 years with risk factors for CAD, and postmenopausal women should 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.\

Result:
evaluation of the extent and severity of CAD and measurement of associated left ventricular (LV) function

Question 53

Describe the signs and symptoms of mitral regurgitation

Answer 53

Distinguishing signs are right ventricular heave, soft S1, split S2, and aloud P2. The classical murmur of MR is pansystolic at the apex radiating to the axilla.

CXR: pulmonary oedema, enlarged left atrium and left ventricle, and mitral valve calcification.

ECG: can present with atrial fibrillation.

Echocardiography: for MR it is used to assess left ventricular function.

Question 54

Describe the signs and symptoms of mitral stenosis

Answer 54

Distinguishing features are a malar flush, low volume pulse, a tapping and undisplaced apex beat, and loud S1 with an opening snap.

The murmur is a rumbling mid-diastolic one, which can be distinguished from the Austin Flint murmur sometimes heard in severe AR by the absence of the opening snap and loud S1

CXR: pulmonary oedema, enlarged left atrium, and mitral valve calcification.

ECG: can present with atrial fibrillation. RVH may also be present.

Echocardiography: diagnostic for mitral stenosis

Question 55

Describe the signs and symptoms of aortic stenosis

Answer 55

Presentation includes dyspnoea, dizziness, fainting, and congestive cardiac failure.

Characteristic signs are a slow rising pulse, heaving but undisplaced apex bear, left ventricular heave, and 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.

CXR: LVH, calcified aortic valve.

ECG: P-mitrale, LVH with strain pattern, left bundle branch block, or complete AV block.

Echocardiography: diagnostic for aortic stenosis.

Question 56

Describe the signs and symptoms of pulmonary regurgitation

Answer 56

Diamond-shaped diastolic murmur best heard in the second and third left intercostal spaces. The murmur increases with inspiration, and P2 is loud in the presence of pulmonary artery hypertension.

CXR: may show dilation of main pulmonary artery with right ventricular dilation.

ECG: right ventricular hypertrophy is usually present.

Echocardiography: diagnostic for pulmonary regurgitation.

Question 57

Describe the primary prevention of AR

Answer 57

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.

Question 58

Describe secondary prevention of AR

Answer 58

Antibiotic prophylaxis is recommended for patients with prosthetic valves during surgical or dental procedures to prevent endocarditis

Question 59

Describe patient discussions in AR

Answer 59

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.

Question 60

Summarise the key features of AR

Answer 60

Aortic regurgitation can result from infective endocarditis, dilatation of the aortic root (e.g. in Marfan’s syndrome) or rheumatic heart disease. The backflow of blood into the left ventricle causes ventricular dilatation and in order to maintain cardiac output, left ventricular hypertrophy occurs. If onset is acute, these compensatory structural changes cannot take place and the increase in left ventricular pressure causes premature closure of the mitral valve and prevents diastolic filling.