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aortic regurgitation

Pathophysiology. Chronic AR: LV overload ? LV dilatation, eccentric hypertrophy, insidious prog to CHF (decades, typically)Acute AR: nl LV poorly tolerates sudden increase LVEDV ? massive increase LVEDP leading to pulm edema, hypotension /- cardiogenic shock. Epidemiology. Overall prevalence 4.9%; moderate or greater severity 0.5% (Framingham)No sex or racial predilectionAge: dependent on etiology.

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aortic regurgitation

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    1. Aortic Regurgitation Dave Fitzhugh, MD UNC Morning Report March 21, 2008

    2. Pathophysiology Chronic AR: LV overload ? LV dilatation, eccentric hypertrophy, insidious prog to CHF (decades, typically) Acute AR: nl LV poorly tolerates sudden increase LVEDV ? massive increase LVEDP leading to pulm edema, hypotension +/- cardiogenic shock

    3. Epidemiology Overall prevalence 4.9%; moderate or greater severity 0.5% (Framingham) No sex or racial predilection Age: dependent on etiology

    4. Etiology, Acute Infective endocarditis Ascending dissection (type A) Prosthetic valve dysfunction Chest trauma

    5. Etiology, Chronic Valvular RHD (no longer common in US) Bicuspid AoV Infective endocarditis Aortic root dz CT dz: Marfan, Ehlers-Danlos, syphilis Inflamm: Ankylosing spondylitis, Takayasu, RA, SLE

    6. AR and Ankylosing Spondylitis 2-10% prevalence of symptomatic AR in AS (subclinically as high as 82% in TEE study of AS pts) Similar prevalence in other HLA-B27 (Reiter’s, psoriatic arthritis, IBD-assoc arthritis) Path involves aortic root/valve cusp retraction Frequently have conduction disorders, including high grade AV block due to dz extension into septum

    7. Clinical Manifestations Typically, classic CHF symptoms: DOE, orthop, PND Often, palpitations 2/2 hyperdynamic LV. Rarely, syncope Acute AR: pulm edema, hypotension prog to cardiogenic shock

    8. Physical Exam Tachycardia, widened pulse pressure (though not in severe AR due to rapid equalization) Murmur: classically, decrescendo diastolic murmur at LUSB (often unimpressive). Often, SEM with overloaded LV in mod to severe AR. Diastolic “rumble” = Austin-Flint murmur, 2/2 regurg jet interacting with flow across mitral valve S3 gallop Murmur increased with sitting up, expiration (incr preload) and decreased with straining, valsalva

    9. Fun you can have with eponyms! Corrigan’s pulse – water hammer pulse de Musset sign - patient’s head bobs with each heartbeat Quincke sign – subungual capillary pulsations Müller sign is systolic pulsations of the uvula Traube sign – double sound over fem art with distal compression Final Jeopardy: Landolfi’s sign = alternating constriction/dilatation of pupils

    10. Differential Dx CHF Other valvular lesions: AS, MS Causes of AI as above: bicuspid valve, RHD, endocarditis, Marfan’s, HLA-B27, etc.

    11. Diagnosis EKG typically with LVH, LAD, often left atrial enlargement CXR: CM, sometimes root dilatation TTE: estimate severity based on color flow dopplers

    12. Severity Classification

    13. TTE Before AVR

    14. TTE After AVR

    15. Treatment Medical Afterload reduction: ACEI, nifedipine, hydralazine Use BB cautiously, if at all, given prolonged diastole and therefore ? regurg volume Surgical AVR – 4% mortality alone, 6.8% with CABG LV dysfunction often irreversible, despite AVR

    16. Indications for AVR

    17. Outcomes of AVR for AR 3/5/10 year survival regardless of EF: 82%, 76%, 67% Improved somewhat with nifedipine preop in low EF (<35%) pts Again, many times, LV dysfunction is irreversible despite AVR, so still need aggressive CHF regimen

    18. References Enriquez-Sarano et al. Aortic Regurgitation. NEJM: 2004: (15); 1539-1546. Huffer LL et al. Aortic root dilatation with sinus of valsalva and coronary artery aneurysms associated with ankylosing spondylitis. Tex Heart Inst J. 2006;33(1):70-3. Hupppertz et al. Cardiac manifestations in patients with HLA B27-associated juvenile arthritis. Pediatr Cardiol. 2000 Mar-Apr;21(2):141-7.

    19. The End

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