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Aortic Regurgitation: Old and New. Andrew D. Ferguson UIC Cardiology February 7, 2008. Acute AR followed by Chronic Etiology Pathophysiology Natural History Diagnostic Evaluation Treatment Special Considerations. Agenda. Endocarditis Valve destruction and leaflet perforation

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aortic regurgitation old and new

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

Agenda
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
acute ar etiology4
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
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)
pathophysiology6
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
pathophysiology7
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
natural history
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
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
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
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
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
Chronic AR: Etiology
  • Leaflet Abnormalities:
    • Rheumatic fever
    • Endocarditis
    • Trauma
    • Bicuspid aortic valve
    • Rheumatoid arthritis
    • Myxomatous degeneration
    • Acromegaly
    • Fenfluramine-phentermine
chronic ar etiology15
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
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:
chronic ar pathophysiology
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
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 Radius

LV Wall Stress = --------------------------------

Wall Thickness x 2

chronic ar cardiac output
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)
clinical manifestations
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
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
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
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
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 auscultation26
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 auscultation27
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
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

Peripheral Signs of Severe AR
chronic ar ecg
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 echo32
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
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
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 cath
Chronic AR: Cath
  • Goals: LV size and function, aortic root dimensions/disorders, quantitation of AR
chronic ar ct mri
Chronic AR: CT/MRI
  • Especially important with suspected aortic disease
  • AR due to bicuspid aortic valve may have concommitant aortic dilatation
chronic ar natural history
Chronic AR: Natural History

Asymptomatic %/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
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 treatment40
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
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
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
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
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
physical activity
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 activity47
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
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 surgical caveats
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 caveats51
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
slide53

Management strategy for patients with chronic severe aortic regurgitation

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

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

special considerations
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 considerations55
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
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.