Aortic Stenosis Randall Harada Echo conference: 12 Sep 2007

Aortic StenosisAortic Stenosis

Randall Harada

Echo conference: 12 Sep 2007

Etiology


Other

Rheumatic

Bicuspid

Calcific

Other

Rheumatic

Bicuspid

Calcific

Age < 70 Age ≥ 70

Pathophysiology

• Congential AS: turbulent flow → fibrosis, calcification

• Rheumatic AS: vascularization of leaflets → retraction, stiffening, adhesions, fusion

• Calcific / degenerative AS:


• Similarities to atherosclerosis: lipid accumulation, inflammatory cell infiltration, calcification

• Clinical factors mirror CAD risk factors

(Dissimilarities: little SM cell proliferation, lack of neovascularization, and more prominent micro-calcification)

Otto CM. Circulation 90; 1994

Pathophysiology


Stewart BF, JACC 29(3) 1997

Stepwise multiple logistic regression

Pathophysiology


Aortic stenosis

Increased afterload

LVH

Increased preload Preserved wall stress

Normal systolic function

Atrial contraction

Pathophysiology


Aortic stenosis

Increased afterload

LVH LVH inadequate(afterload mismatch)

Reduced myocardial contractility

↓ CBF per unit of mass

↑ O2 demand ↓ coronary perfusion pressure

Compression of intramyocardial arteries

Myocardial ischemia

Natural history

• Long latent period:

• Mortality is low during the latent period; similar to age-matched• Progression to symptomatic or severe aortic stenosis has

marked individual variability– Average rate of progression 0.10 – 0.12 cm2 per year


10 years 20 years 25 years

Mild 88% 63% 38%

Moderate 4% 15% 25%

Severe 8% 22% 38%

Horstkotte D, Eur Heart J 9(suppE) 1988

Natural history

• Severe stenosis with symptoms:


Avg life expectancy (y)

Angina 5

Syncope 3

Heart failure <2

Ross J, Circ 36(supp IV) 1968

Clinical care of AS

• Assessment of symptoms; patient education

• Careful exercise testing for asymptomatic patients with unclear medical histories:

• Serum BNP – non-specific marker


ACC/AHA, Circ 114, 2006

• Echocardiography: eval AS severity, LV function

Medical therapy

• Antibiotic prophylaxis no longer recommended• No medical therapies proven to prevent or delay AS• In severe AS, atrial fibrillation is often poorly tolerated


Medical therapy


Rajamannan NM, Circ 110, 2004

SALTIRE trial (atorvastatin 80 vs placebo)


Cowell SJ, NEJM 352, 2005

RAAVE study

• 121 patients• Not randomized

– Active arm: patients who need statin due to hyperlipidemia• Mean LDL 160 mg/dL → at end of study: 93 mg/dL• Higher prevalence of HTN and diabetes

– Control arm: patients who do not meet guidelines for a statin• Mean LDL 119 mg/dL → at end of study: 118 mg/dL


Moura LM, JACC 49, 2007

RAAVE study


Moura LM, JACC 49, 2007

Ongoing Statin RCTs


• Stop Aortic Stenosis (STOP-AS) - U.S.• Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) -

Europe• Aortic Stenosis Progression Observation Measuring

Effects of Rosuvastatin (???) - Canada

ASTRONOMER

Evaluation of AS severity


• Maximum aortic velocity• Mean transvalvular gradient• Aortic valve area by continuity equation



• Maximum aortic velocity

← 4.2 m/s

↔ max instantaneous gradient

← 71 mmHg

http://www.grc.nasa.gov/WWW/K-12/airplane/bern.html



• Maximum aortic velocity ↔ max instantaneous gradient

• Modified Bernoulli equation:

∆P = 4 [(V2)2 – (V1)2]

• Simplified equation (assuming V2 >>> V1) :

∆P = 4 V2



• Maximum aortic velocity

• Most reproducible• Strongest predictor of clinical outcomes

• Mild: 2.6 – 3.0 m/s• Moderate: 3 – 4 m/s• Severe: >4 m/s






• Mean transvalvular gradient



• Mean transvalvular gradient

• Mild: < 25 mm Hg• Moderate: 25 – 40 mm Hg• Severe: > 40 mm Hg






• Aortic valve area by continuity equation

• Volume flow proximal to valve = volume flow thru orifice

• CSALVOT x VTILVOT = AVA x VTIAV

• CSALVOT x VLVOT = AVA x VAV

• AVA = (CSALVOT x VLVOT) / VAV

• Velocity ratio = VLVOT / VAV




• Severity by AHA criteria:– Mild: > 1.5 cm2

– Moderate: 1.0 – 1.5 cm2

– Severe: < 1.0 cm2

• Severity by BIDMC criteria:– Mild: > 1.2 cm2

– Moderate: 0.8 – 1.2 cm2

– Severe: < 0.8 cm2

• Dimensionless ratio < 0.25 corresponds to severe AS




• Assumes:– Geometry of the LVOT

is round

– Acquired imaging plane (PLAX) is parallel to the LVOT

• 3D-echo may improve measurements

Doddamani S. Echocardiography 24;2007



• 55 consecutive patients w/ nl AV

• Estimations of LVOT area:

a. 2D-echo PLAX: (π r2)

b. 3D-echo idealized PLAX: (π r2)

c. 3D-echo planimetry in the “transverse plane”

d. 3D-echo “ellipse”: (π x LVOTlong x LVOTshort)




• Eccentricity index = 1 – (LVOTshort / LVOTlong)


←Round Oblate →

median



• Comparison of LVOT area estimations




• Comparison of LVOT area estimations


Timing of valve replacement

Echo conference: 12 Sep 2007 Otto CM, JACC 47, 2006

Timing of valve replacement


Asymptomatic patients


• Risk of sudden death with AS < 1%• What is the risk of surgery?

In-hospital, post-op mortality

Echo conference: 12 Sep 2007 Ambler G, Circ 112, 2005

In-hospital, post-op mortality

Echo conference: 12 Sep 2007 Ambler G, Circ 112, 2005

Exceptions to the asymptomatic rule


Undergoing other cardiac sx

Problematic situations


• Hypertension– May mask the severity of AS

• For a given AVA, transaortic ∆P (velocity) decreases when systemic arterial compliance decreases.

Otto CM, JACC 47, 2006

Problematic situations


• LV dysfunction– Primary cardiomyopathy vs. secondary due to true AS– Low stroke volume may reduce leaflet motion in a

non-stenotic valve– Dobutamine stress echo to differentiate

• Flexible leaflets: increase in EF, leaflet excursion, and AVA• Severe AS: increase in EF, no change in AVA• “Lack of contractile reserve”: no increase in EF

Congenital AS


• Subvalvar• Supravalvar• Valvar

Subvalvar / Subaortic stenosis

• Dynamic stenosis:– HOCM

• Fixed stenosis:– Thin membrane– Thick fibromuscular ridge






Subaortic stenosis


• Pathophysiology

– Underlying abnormality of LVOT structure

– Turbulent flow → progressive LVOT fibrosis

→ AV leaflet thickening → AR 55%

– Infectious endocarditis 12%• Timing of surgery

– Children: gradient ≥ 30 mm Hg– Adults: gradient ≥ 50 mm Hg– AR

• Recurrence rate: 15 - 27% reoperation

Supravalvar stenosis


• Hourglass deformity (discrete constriction) 60-75%• Diffuse narrowing of variable length in ascending aorta

25-40%

Supravalvar stenosis


• Etiologies– Homozygous familial hypercholesterolemia– Familial autosomal dominant form – mutation of elastin gene– Sporadic mutation form– As a feature of Williams syndrome

• Gene deletions (including elastin)

• Short stature, facial abnormalities, visuospatial cognition defects, renovascular HTN, mental retardation

• Endocarditis prophylaxis• Indications for surgery uncertain

Valvar AS


• Unicuspid or unicommissural valve• Bicuspid or bicommissural valve• Aortic annular hypoplasia

Bicuspid AV


• Prevalence estimate: 0.5-2%• 3:1 male:female• Peak age of symptom onset:

40 – 60 years-old• Familial

– Present in ~9% 1st degree relatives

Huntington K, JACC 30, 1997

Bicuspid AV


Bicuspid AV


Bicuspid AV


• Aortic abnormalities– Coarctation: 6%– Dilatation of aortic root and/or ascending aorta: ~50%– Predictor of ascending aorta aneurysm or dissection– Presence is independent of the functional state of the AV– Defects in aortic media

Bicuspid AV – aortic media

Echo conference: 12 Sep 2007 de Sa M, J Thorac Cardiovasc Surg 118, 1999

Tricuspid valve

Bicuspid valve

Bicuspid AV – aortic media

Echo conference: 12 Sep 2007 Cotrufo M, J Thorac Cardiovasc Surg 130, 2005

Percutaneous AVR (CoreValve)


• 86 consecutive patients– 8/05-9/06: 2nd generation 21-F device (n=50)– 9/06-2/07: 3rd generation 18-F device (n=36)

• Required less access site surgical cut-down, lower procedural time, and less frequent hemodynamic support (i.e. ECMO, bypass, cardiac assist)

Grube E, JACC 50; 2007

Age 82 ± 6 yearsWomen 65%CAD 56%Prior CABG 19%Prior stroke 11%NYHA III/IV 83%LVEF 54 ± 16%EuroSCORE 22 ± 13%Peak grad 71 ± 13 mmHgAVA 0.60 ± 0.16 cm2


Echo conference: 12 Sep 2007 Grube E, JACC 50; 2007


Echo conference: 12 Sep 2007 Grube E, JACC 50; 2007

Acute device success 88%

Conversion to surgery 6%

Only valvuloplasty 2%

Valve in valve placement 2%

48-hour AE

Death 6%

Stroke 10%

MI 0%

Cardiac tamponade 9%

Coronary flow impairment 0%

30-day AE

Death 12%

Stroke 10%

MI 1%

Percutaneous AVR (Cribier Edwards)


• 50 consecutive patients

Webb JG, Circulation 116; 2007

Age 82 ± 7 yearsWomen 40%CAD 72%Prior stroke 12%NYHA III/IV 90%EuroSCORE 28%Mean grad 46 ± 17 mmHgAVA 0.6 ± 0.2 cm2


Echo conference: 12 Sep 2007 Webb JG, Circulation 116; 2007


Echo conference: 12 Sep 2007 Webb JG, Circulation 116; 2007

Procedural success 43 (86%)Inability to pass iliac artery 1Inability to cross AV 3Defect in prototype delivery catheter 1Malpositioning of the prosthesis 2

Procedural death (aortic injury) 1 (2%)Emergent cardiac surgery 030-day death 6 (12%)Stroke 2 (4%)MI 1 (2%)

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Aortic Stenosis Randall Harada Echo conference: 12 Sep 2007