Aortic Regurgitation: Old and New

Andrew D. Ferguson

UIC Cardiology

February 7, 2008

Agenda

• Acute AR followed by Chronic

• Etiology

• Pathophysiology

• Natural History

• Diagnostic Evaluation

• Treatment

• Special Considerations

Acute AR: Etiology

• Endocarditis– Valve destruction and

leaflet perforation

– Paravalvular abscess rupture into LV, LA or RVOT

• Aortic dissection– Incomplete coaptation

of leaflets

– Flail leaflets from extension of dissection

Acute AR: Etiology

• Rupture of a congenital fenestration

• Traumatic rupture of leaflets after either deceleration injury or blunt trauma

• Iatrogenic– Aortic balloon valvotomy– Failed surgical repair or replacement

Pathophysiology

• Sudden, large regurgitant volume

• Normal-sized ventricle unable to fully accommodate volume overload

• Frank-Starling mechanism increases SV, but forward stroke volume markedly diminished (FSV=SV-Regurg volume)

Pathophysiology

• Tachycardia is compensatory– Increase or decrease CO?

• Increased LVEDP leads to:– Early closure of mitral valve– Increased LA pressures, which then lead to

pulmonary edema– Myocardial ischemia

• Diminished myocardial perfusion pressure

Pathophysiology

• Pre-existing LVH (i.e. HTN, AS):– More susceptible to drastic hemodynamic

consequences– Smaller, non-compliant LVs with a reduced

preload reserve

• Examples:– Aortic dissection in longstanding HTN– IE in pre-existing AS– Iatrogenic (i.e. valvulotomy) for congenital AS

Acute AR: Hemodynamics

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Natural History

• Severe acute AR generally presents with cardiovascular collapse:– Weakness– Severe Dyspnea– Hypotension

• Other sxs, if present, related to etiology:– For example, chest/back pain related to

aortic dissection.

Evaluation: Physical

• Manifestations of cardiogenic shock:– Hypotension, pallor, diaphoresis, occasional

cyanosis, peripheral vasoconstriction

• Soft or absent S1 due to early closure of MV (increased LVEDP)

• Soft A2, loud P2• Frequently an S3, no S4• Early diastolic, low-pitched murmur MAY be

present after S2.• Systolic flow murmur (increased SV)

Evaluation: Imaging

• CXR: CHF and pulmonary edema

• CT can be used in evaluation for aortic dissection

• Ultimately, echocardiography is the diagnostic procedure

Acute AR: Echo

• Color doppler demonstrates the regurgitant flow and aids grading

• Severe acute AR:– Vena contracta width >6mm– Diastolic pressure half-time <200ms– Holodiastolic flow reversal in desc. aorta

• TTE/TEE to diagnose IE, dissection

Treatment

• Death without tx is common, due to:– EMD, ventricular arrhythmias, pulmonary edema,

or circulatory collapse.

• Any severity of acute AR:– Urgent aortic valve replacement– If surgery delayed, may stabilize in ICU:

• IV Vasodilators, i.e. nitroprusside• Possibly inotropic agents, i.e. dopamine• IABP contraindicated

• Exception: Mild acute AR due to endocarditis

Chronic AR: Etiology

• Leaflet Abnormalities:– Rheumatic fever– Endocarditis– Trauma– Bicuspid aortic valve– Rheumatoid arthritis– Myxomatous degeneration– Acromegaly– Fenfluramine-phentermine

Chronic AR: Etiology

• Ascending root or ascending aorta:– Systemic hypertension– Aortitis (e.g. syphilis)– Reiter’s syndrome– Ankylosing spondylitis– Trauma– Dissecting aneurysm– Marfan syndrome– Ehlers-Danlos syndrome– Pseudoxanthoma elasticum– Inflammatory bowel disease– Osteogenesis imperfecta– Annuloaortic ectasia

Chronic AR: Epidemiology

• Framingham Heart Study:– ≥trace AI found in 13% men, 8.5% women– Rarely more than trace younger than 50– Prevalence of ≥moderate AI:

Age (range) Men Women

50-59 3.7 0.2

60-69 12.1 0.8

70-83 12.2 2.3

Chronic AR: Pathophysiology

• Course of AR is insidious, often decades before clinically important

• Compensatory mechanisms aimed at:– Preservation of forward stroke volume and

hence cardiac output– Maintenance of normal wall stress

Chronic AR: Wall Stress

• Large regurgitant volume leads to increase in LV end-diastolc volume

• Creates elevation in wall stress

• Laplace’s law:

• Compensate by increasing LV thickness, both eccentric and concentric

Cavity Pressure x RadiusLV Wall Stress = --------------------------------

Wall Thickness x 2

Chronic AR: Cardiac Output

• AR leads to diminshed forward stroke volume, and hence CO

• FSV = SV - ARV

• Increase SV to maintain FSV (CO) by:– Increase ventricular compliance (dilatation)– Maintain efficiency (hypertrophy)

Chronic AR: Hemodynamics

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Clinical Manifestations

• May be asymptomatic for decades

• Symptoms due to enlarged LV:– Awareness of heartbeat, pounding– Atypical chest pain– Palpitations (ST, PACs, PVCs)

• Symptoms of LVH with LV dysfunction

• Angina

Chronic AR: Angina

• Uncommon in isolated AR due to dilation of coronary arteries

• Underlying CAD• Subendocardial ischemia

– Diminished perfusion pressure

• Nocturnal ischemia– Heart rate slows, arterial diastolic pressure falls.– Splanchnic ischemia may also occur, abd pain.

Chronic AR: Examination

• Physical examination remains important both for initial diagnosis and following progression of disease

• Many characteristic attributes which help grade severity/progression:– Surface exam– Auscultation– Peripheral exam

Chronic AR: Surface Exam

• Consistent with LV enlargement and forceful systolic function

• Apical impulse:– Displaced laterally and inferiorly– Diffuse and hyperdynamic

• Dilatation of ascending aorta:– Sternal notch pulsation and possibly thrill

Chronic AR: Auscultation

• Heart Sounds:– S1 soft, ?reflecting long PR interval– S2 variable; soft, absent, or single

• A2 often soft or absent• P2 may be normal, increased or obscured by

the diastolic murmur

– S3 occasionally present due to volume overload

– S4 usually absent

Chronic AR: Auscultation

• Murmurs:– Diastolic regurgitant murmur:

• Good positive and negative predictive values• Begins immediately after A2• High-pitched, blowing, sustained or decrescendo• Best appreciated with patient sitting up, leaning forward, and

holding breath in expiration• Guage severity

– Intensity does not correlate to severity (may be absent)– Murmur in early diastole and blowing ---> mild AI– As lesion becomes more severe, murmur extends through more of

diastole, become holodiastolic and rougher

• **Beware of transient murmur of AR:– E.g. HD patients in volume overload, resolves with HD

Chronic AR: Auscultation

• Murmurs, cont.:– Regurgitant murmur varies with squatting/Valsalva– Austin Flint murmur

• Mid to late diastolic apical rumble• Results from competing flows of the mitral inflow and the

regurgitant lesion• Distinguish from MS by lack of loud S1 & OS

– Systolic murmur• Mainly a result of functional stenosis (SV and rate)• Cresc-decresc harsh murmur beginning after S1

Chronic AR: Peripheral Exam

• Wide pulse pressure– Increased stroke volume

• Abrupt distention of peripheral arteries• Elevation of systolic pressure

– Regurgitation into LV• Quick collapse of arteries• Low diastolic pressure

• Many non-specific peripheral signs

Peripheral Signs of Severe AR

• Quincke’s sign: capillary pulsation

• Corrigan’s sign: water hammer pulse

• Bisferiens pulse (AS/AR > AR)

• De Musset’s sign: systolic head bobbing

• Mueller’s sign: systolic pulsation of uvula

• Durosier’s sign: femoral retrograde bruits

• Traube’s sign: pistol shot femorals (auscultation)

• Hill’s sign:BP Lower extremity >BP Upper extremity by

– > 20 mm Hg - mild AR

– > 40 mm Hg – mod AR

– > 60 mm Hg – severe AR

Chronic AR: ECG

• LVH• Evidence of LA hypertrophy• Leftward axis• ST segment depression

– One study showed 83% of patients with rest or exercise ST abnl had enlarged ventricle (>55mm) or low EF (<45%)

• Arrhythmias/conduction abnl uncommon

Chronic AR: Echo

Chronic AR: Echo

• Characteristic Findings:– If primary valvular, can see leaflet thickening,

vegetations, calcification, and prolapsed or flail leaflets

– Aortic root dilatation or evidence of aneurysm (either dissecting or saccular)

– High frequency, diastolic fluttering of anterior mitral leaflet from AR jet

– Doppler is highly sensitive for detecting AR jet– Increased LVESV and LVEDV

Chronic AR: Severity Assessment

• Severe AR present by echo with at least one of the following findings:– Regurgitant fraction ≥50%– Vena contracta width >6mm– Regurgitant volume ≥60mL– Central jet width ≥65% OF LVOT– ERO area ≥0.30cm2

Chronic AR: Echo Severity

• Other indirect measures:– Rate of decline in regurgitant slope

• The sharper the decline, the more severe

– Degree of reversal in pulse wave velocity in the descending aorta

– Magnitude of LV outflow tract velocity

Chronic AR: Severity

Chronic AR: Cath

• Goals: LV size and function, aortic root dimensions/disorders, quantitation of AR

Chronic AR: CT/MRI

• Especially important with suspected aortic disease

• AR due to bicuspid aortic valve may have concommitant aortic dilatation

Chronic AR: Natural HistoryAsymptomatic %/Y• Normal LV function (Good prognosis)

– Progression to symptoms &/or LV dysfunction < 6– Progression to asymptomatic LV dysfunction < 3.5– 75% 5-year survival– Sudden death < 0.2

• Abnormal LV function– Progression to cardiac symptoms

25

• Symptomatic (Poor prognosis)– Mortality > 10

Bonow RO, et al, JACC. 1998;32:1486. (593 patients, mean 6.6yrs)

Chronic AR: Treatment

• Management depends upon:– Severity

• Based on clinical and echo criteria

– Symptoms• If equivocal, consider exercise testing

– LV function (>50% or ≤50%)• If equivocal, consider RVG or MRI

– LV dimensions (LVSD, LVDD)

Chronic AR: Treatment

• Mild to moderate AR– Do not require treatment– Serial monitoring (symptoms, echo)

• Symptomatic with mild to moderate AR– Consider other etiologies of symptoms

• E.g. mitral stenosis

Severe AR: Management

• Asymptomatic with normal LV function– First question if truly asymptomatic???– Consider exercise testing if sedentary or

equivocal symptoms

• Medical therapy (i.e. vasodilators)– Not recommended

• Serial monitoring– Symptoms and LV dimensions and function

Severe AR: Medical Therapy

• Treat systemic arterial diastolic HTN– Cautious use of BB

• Treat afib and bradyarrhythmias– Poorly tolerated

• Treat LV dysfunction prior to surgery– Digoxin, salt restriction, diuretics, ACE/ARB

• Treat angina– Nitrates not as helpful than in +CAD

• Vasodilators - next slide

Severe AR: Theory of Vasodilators

• Improve stroke volume and reduce regurgitant volume hopefully reducing:– LVEDV– Wall stress– Afterload

• Results in preserved LVEF and reduction in LV mass

Severe AR: Vasodilators

• Conflicting results of efficacy in controlled randomized trials

• Most recent and only placebo-controlled– 95 consecutive patients, followed 7 years– Placebo, long-acting nifedipine, enalapril– No reduction in symptoms or LV dysfunction– No sig dif in LV dimension, EF, or mass

• If used, goal is to reduce systolic BP• Not indicated in normal BP or normal LV size

Severe AR: Vasodilators

Physical Activity

• Reduction in regurgitant volume from:– Decrease in PVR and resultant diastolic

blood pressure– Decreased diastolic filling period which

accompanies tachycardia

• Failure of increased EF

• Uncertain ultimate consequences

Physical Activity

• Also recommend Holter monitoring in those who wish to perform competitive athletics to detect ventricular arrhythmias

36th Bethesda Conference, JACC 2005

Chronic AR: Serial Testing

• Initial Presentation (mod to severe AR)– Establish stability and chronicity– If unknown, repeat exam and TTE in 2-3mos

• Once stability and chronicity established, frequency of reevaluation depends on:– Severity of AR– Degree of LV dilatation– Level of systolic function– The level of progression of dilatation and/or dysfxn

• Repeat eval with any hint of progression

Chronic AR: Surgery

Chronic AR: Surgical Caveats

• Symptomatic severe AR with Normal LVSF:– Surgery indicated for NYHA class III-IV and

Canadian class II-IV angina– NYHA class II, question etiology of

symptoms (deconditioning or aging?)• Consider exercise testing

Chronic AR: Surgical Caveats

• Symptomatic severe AR with LVSF:– AVR for 25%<EF<50%, NYHA II-IV

• NYHA IV have worse post-op survival and lower rates of recovery of systolic function

– EF<25% and/or LVESD >60mm• NYHA IV - surgical mortality nears 10%

– Cannot predict who may recover LV function

• NYHA II-III - AVR likely, especially if:– Recent onset of symptoms and evidence of LV dysfunction– Intensive short-term vasodilators result in sx improvement– IV inotropy improves hemodynamics or systoic function

Long-term AVR survival

Copyright ©2006 American College of Cardiology Foundation. Restrictions may apply.

Bonow, R. O. et al. J Am Coll Cardiol 2006;48:e1-e148

Management strategy for patients with chronic severe aortic regurgitation

Special Considerations

• Endocarditis Prophylaxis– No longer recommended in this population

• Elderly– Pure AR is uncommon (combined AS/AR)– Age >75 more likely to:

• Develop symptoms or LVSF earlier• Have persistent LVSF and CHF sxs post-operatively• Have worse post-operative survival rate

– Goal of therapy is to improve QOL• Therefore, symptoms guide therapy after risks are

balanced against expected long-term improvement

Special Considerations

• Pregnancy– AR with NYHA III-IV sxs or EF<40%

• Considered high maternal and/or fetal risk• Should receive AVR before surgery

– AR with NYHA I-II sxs and normal EF• Considered low maternal and/or fetal risk• Generally tolerate pregnancy without problems

– Symptoms can be treated with diuretics and vasodilators (nifedipine), if necessary

– Termination if presents with high risk as above– If refuse, only operate for refractory class III-IV

Advice

• Please read the guidelines if:– You feel my talk was incomplete– I didn’t make any sense– You fell asleep, or– If you’re like me and need to hear/read

things many times to ingrain the info.

Thank You