Chronic Aortic Regurgitation

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Aortic Regurgitation
2007
Chronic Aortic Regurgitation
Definition
• Failure of aortic leaflet cooptation in diastole
Chronic Aortic Regurgitation - Etiology
• Cusps Disease
• Aortic Root Disease
Chronic Aortic Regurgitation - Etiology
Cusps Disease
• Endocarditis
• Bicuspid AV (10% pure AR).
• Rheumatic Heart Disease (usually with MV
disease but sometimes can be the dominant
lesion).
• Calcification of cusps (Degenerative).
Chronic Aortic Regurgitation - BAV
Chronic Aortic Regurgitation - Etiology
Aortic Root Disease
• Atherosclerosis
• Marfan’s syndrome (dilatation of sinotubular ridge
lifts the cusps).
• Aortic dissection.
• Syphilitic aortitis.
• Ankylosis spondilitis.
• Systemic lupus.
Chronic Aortic Regurgitation
Aortic Regurgitation
Aortic Regurgitation - Pathophysiology
• Initially chronic AR leads to a small increase in
LV end diastolic volume and a small increase in
stroke volume.
• Large regurgitant volume increases LV end
diastolic pressure (pulmonary congestion).
• If developed slowly, AR enters a chronic phase of
eccentric hypertrophy and progressive LV
dilatation and increased stroke volume (pulse
pressure) a combined pressure and volume
overload), and may remain compensated for
many years till LV dysfunction eventually
develops.
Aortic Regurgitation - Pathophysiology
• In AR there is not only volume overload but also
an increase in afterload and systolic wall stress.
• This distinguishes AR from mitral regurgitation
where systolic wall stress is normal or even low,
since the regurgitant blood is ejected into the low
pressure left atrium.
• Thus valve surgery in MR usually results in an
increase in afterload and commonly in worsening
of the LV ejection fraction, correction of AR results
in a decrease in afterload and frequently an
improvement of the ejection fraction.
Post op, if performed on time remodeling occur and LV
dimensions become smaller, without LV dysfunction..
Aortic Regurgitation
Chronic Aortic Regurgitation – Clinical Symptoms
Congestive Heart Failure
• After a long compensated phase (many years), LV
decompensation proceeds symptoms of dyspnea,
orthopnea and peripheral edema .
Angina
• Diastolic hypotension can impair coronary flow.
• Increase demand on coronary flow d/t increased
LV mass.
• Less common than in aortic stenosis.
Chronic Aortic Regurgitation – Physical Findings
• Bounding pulses (chronic AR).
• Diastolic decrescendo murmur (length correlates
with severity when LV function is good) in left
sternal border.
• Systolic murmur due to relative aortic stenosis.
• Mitral rumble (Austin Flint murmur), jet
impinging the mitral valve.
• Systolic hypertension and wide pulse pressure
(mod-sev AR).
• Signs become less apparent with decompensation
and S3 appears.
Chronic Aortic Regurgitation - Signs
Signs of aortic insufficiency
Sign
Finding
Corrigan’s
pulse
Rapid forceful carotid upstroke followed by rapid decline
Quincke’s
sign
Systolic plethora and diastolic blanching in nail bed when nail is
slightly compressed
De Musset’s
sign
Bobbing of head
Duroziez’s
sign
Systolic and diastolic bruit heard over femoral artery when
compressed by bell of stethoscope
Hill’s sign
Augmentation of systolic blood pressure in the arm by 30 mmHg
compared to the leg
Chronic Aortic Regurgitation - Echocardiography
• LV size and function , aortic root and cusps motion.
• Typical cusps morphology in different etiologies.
• Color Doppler interrogation of regurgitant flow in
LVOT, jet width to estimate severity (semi
quantitative).
• Descending aortic flow reversal in the aorta in
diastole.
• Pressure half time of aortic regurgitant flow, more
rapid in severe cases.
• When echocardiography is not available or clear MRI
is an alternative for assessment of valve morphology
and flow, and LV function and nuclear angiography
can be used for serial assessment of LV function.
Chronic Aortic Regurgitation
Chronic Aortic Regurgitation
Chronic Aortic Regurgitation
Echocardiographic Criteria of Severity of Aortic
Regurgitation
(color flow jet width)
Severity
Jet / LVOT
Jet width
(vena contracta)
Mild
<25%
< 3 mm
Moderate
25%-65%
3-6 mm
Severe
>65%
> 6 mm
Chronic Aortic Regurgitation
Chronic Aortic Regurgitation –
Cardiac Catheterization
• For controversial cases and patients above 40
and those with risk factors with suspected
coronary artery disease.
• Aortography visualizes flow of contrast media
(not velocities like echocardiography), the
denser the ventricle opacification the worse is
the regurgitation.
Chronic Aortic Regurgitation - Management
Exercise Testing
• Assessment of functional capacity and
symptomatic response when with history of
equivocal symptoms.
• Before participation in athletic activities
• For prognostic assessment before AVR in patients
with LV dysfunction.
Chronic Aortic Regurgitation - Management
• A diminished LV ejection fraction (below 50–
55%) is associated with reduced prognosis
even in asymptomatic patients (A).
• LV enlargement in and of itself also
constitutes an indication for surgery (B).
Chronic Aortic Regurgitation - Management
Surgery Recomended
• After symptoms and before dysfunction is irreversible.
• With evidence of contractile dysfunction even if
asymptomatic.
Ecocardiographic Criteria for surgery with Severe AR
• Simple measures of contractility: shortening fraction
(<27%) and ejection fraction (<55%).
• LV end systolic diameter (>5.0 cm).
• LV end-systolic volume >55 mL/m2
• A window of 18 months is available once those limits are
crossed. Repeat measures (LVEDD <4.0 – 2 y, 4.0-5.0 1
y, >5.0 – 6 m).
Chronic Aortic Regurgitation - Management
• The overall operative mortality for isolated AVR is
about 4.3%.
• In patients with marked cardiac enlargement and
prolonged LV dysfunction experience an operative
mortality rate of approximately 10% and a late
mortality rate of approximately 5% per year due to LV
failure despite a technically satisfactory operation.
• Because of the very poor prognosis with medical
management, even patients with LV failure should be
considered for operation.
Chronic Aortic Regurgitation - Management
AV replacement (with/without root replacement)
AV repair: (annular dilatation, valve perforation, non
calcified leaflets with prolapse)
Medical Therapy
• Vasodilators; Nifedipine, hydralazine, ACE
inhibitors are used to delay progression of AR in
asymptomatic patients. (more compelling data is
available with nifedipine).
Chronic Aortic Regurgitation
Acute Aortic Regurgitation
Background
• Medical emergency (mortality 75% with medical
therapy, 25% with surgery).
Etiology
• Endocarditis
• Aortic dissection
• Trauma
Aortic Regurgitation - Diagnosis
Echocardiography
•
•
•
•
Early closure of mitral valve.
Diastolic mitral regurgitation.
Vegetation, intimal tear.
Consider TEE (for vegetations, abscess, aortic
dissection).
Management
• Blood culture, antibiotics, vasodilators
• AVR (10% risk of reinfection).
‫‪Aortic Regurgitation - Guidelines‬‬
‫‪AHA ACC‬‬
‫‪2006‬‬
‫‪European‬‬
‫‪2007‬‬
‫‪ AR‬קשה‪ ,‬חולים סימפטומטים דרגה‬
‫תפקודית ‪2-4‬‬
‫‪I‬‬
‫‪I‬‬
‫‪ AR‬קשה ופגיעה בחדר שמאל‬
‫)‪(LVEF<50%‬‬
‫‪I‬‬
‫‪I‬‬
‫‪ AR‬קשה‪ ,‬מתוכנן ניתוח ‪ /CABG‬מסתם‬
‫אחר‪/‬האורטה העולה‬
‫‪I‬‬
‫‪I‬‬
‫‪IIa‬‬
‫‪LV>75/55‬‬
‫‪IIb‬‬
‫‪IIa‬‬
‫‪LV>70/50‬‬
‫‪-‬‬
‫‪ AR‬קשה‪ ,‬חולים אסימפטומטים עם ‪LVEF‬‬
‫מעל ‪ ,50%‬חדר מאד מורחב‬
‫‪ AR‬קשה‪ ,‬חולים אסימפטומטים עם ‪LVEF‬‬
‫מעל ‪ ,50%‬חדר מורחב במידה בינונית‬
‫(‪ 70-75/50-55‬מ"מ)‬
‫‪Aortic Regurgitation - Guidelines‬‬
‫קוטר האורטה העולה‬
‫‪European AHA ACC‬‬
‫‪2007‬‬
‫‪2006‬‬
‫‪ AR‬בכל דרגה‪ ,‬האורטה מורחבת‪:‬‬
‫מרפאן ‪ 45‬מ"מ‬
‫מסתם דו‪-‬עלי ‪ 50‬מ"מ‬
‫שאר המסתמים <‪ 55‬מ"מ‬
‫מעל ‪ 50‬ממ‬
‫בכל‬
‫האטיולוגיות‬
‫‪I‬‬
‫‪IIa‬‬
‫‪IIa‬‬
NATURAL HISTORY OF AORTIC REGURGITATION
Asymptomatic patients with normal LV systolic
function:
• Progression to symptoms and/or LV dysfunction
<6%/yr
• Progression to asymptomatic LV dysfunction
<3.5%/yr
• Sudden death
<0.2%/yr
Asymptomatic patients with LV systolic
dysfunction:
• Progression to cardiac symptoms
>25%/yr
Symptomatic patients:
• Mortality rate
>10%/yr
LV = left ventricular.
From Bonow RO, Carabello B, de Leon AC Jr, et al: ACC/AHA
Guidelines for the management of patients with valvular heart disease.
J Am Coll Cardiol 32:1486, 1998.
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