Aortic Valve Disease questions Flashcards Preview

From Flashcardlet big > Aortic Valve Disease questions > Flashcards

Flashcards in Aortic Valve Disease questions Deck (64):

How is severity of aortic stenosis quantified

1) Planimetry--short axis view on 2D echo
2) Continuity equation--total flow of blood that passes through the LVOT is the same as the total flow passing through the aortic valve
3) Gorlin equation-- AVA = CO/44.3 x HR x LVET (left ventricle ejection time) x square root of mean gradient.


3 main causes of aortic stenosis and the pathological features of the disease

1) Rheumatic fever--- commissural fusion with leaflet thickening and fibrosis, resulting in triangular aortic valve orifice

2) Calcific degeneration--- begins at the base of the cusps and progresses toward the leaflet edges with the commissures remaining open

3) Bicuspid aortic valve--- cusps are prone to earlier progressive thickening and calcification with age


Describe pathological findings of calcific degeneration

Masses of lipocalcification lying on the aortic side of the valve consisting of
1) inflammatory cell infiltrate (macrophages, T lymphocytes
2) lipids (LDL and lipoprotein A)
3) Microscoptic calcification
4) other proteins


What are signs of aortic stenosis

Pulsus tardus (slow-rising pulse)
Palsus parvus (small amplitude pulse)
Single heart sound: A2 component is diminished due to calcification and stiffening
Paradoxical splitting of the second heart sound (delayed A2)
Fourth heart sound---pre-systolic thrust generated from atrial contraction into a hypertrophied and non-compliant left ventricle
Crescendo-decrescendo systolic murmur causes by turbulent flow-(not pansystolic)
Late peaking of AS murmur indicates its severity rather then intensity


What is low-flow, low gradient aortic stenosis? how is it managed

Patients with low ejection fraction of <40%, a mean gradient of < 30 mmHg, and a calculated aortic vavle area of < 1.0 cm2

Dobutamine stress echocardiography, 5 -20 ug/kg/min of dobutamine administered in increments of 5 ug every 5 minutes and assesses for increase peak pressure gradient and change in EOA.


What are physical signs of Aortic Regurgitation

Widened pulse pressure
Duroziez's sign-systolic and diastolic murmur audible over femoral arteries
Quinke's sign-pulsation in the capillary membranes of the fingertips
Traube's sign-pistol shot sound audible over the femoral artery
De Musset's sign-head bobbing with a collapsing pulse
Corrigans pulse--water-hammer collapsing pulse
Mueller's sign--pulsation of the uvula
Hills sign--SBP in the leg greater then SBP in the arm by at least 20 mmHg.
3rd heart sound loudest at apex
Decrescendo diastolic murmur hear best with patient exhaling
Austin Flint--low pitched diastolic murmur occurs because of turbulence across the mitral valve


List surgical options for patients with a small aortic root

Implanting a valve prosthesis with an improved EOA
stentless valve
small sewing ring valve (CE perimount magna)
Aortic root enlargement with bovine pericardial patch
Aortic annular enlargement
Aortic root replacement
Apico-Aortic valved conduit


What is Freedom from structural valve deterioration for the different aortic valve prostheses
For patients 70 years old at 15 years

1) Mechanical valve 97%
2) Aortic valve homograft 85%
3) Bovine pericardial valve 85%
4) Porcine bioprosthesis 80%
5) stentless bioprosthesis 80%
6) pulmonary autograft (Ross) 74% for the aortic valve and 80% for the pulmonary valve


Structural valve deterioration (SVD) in bioprosthetic valves based on age at 10 years

40% in patients aged 0 - 40 years
30% in patients aged 40 to 69
10% in patients aged > 70 years


Describe other lesions associated with BAV

Short left main stem coronary artery
A left dominant coronary artery circulation
An anomalous position of the coronary ostia
coarctation of the aorta
earlier onset of aortic stenosis

Histological analysis reveals cystic medial necrosis, reduced fibrilin-1 production and elastin fragmentation


List factors to consider when pregnant pt with a mechanical valve insitu

Warfarin crosses the placenta and increases risks of abortion, prematurity, and stillbirth
Warfarin associated with embryopathy in 5-10% of pts but is lower if dose <5mg/day.
Heparin dose not cross placenta but may induce bleeding at uteroplacental junction
warfarin during weeks 1-6
Unfractionated heparin during 6 -12 weeks
warfarin 12 to 36 weeks
UFH from week 36
stop heparin before delivery


How can atherosclerosis of aorta be classified

Type I: Circumferential calcification or "porcelain aorta" Easily palpable
Type II: Diffuse intimal thickening with ragged friable edges. Unreliable to manual palpation, easy to identify by the TEE or epiaortic scan.
Type III: intramural liquid debris. the most difficult to palpation on TEE.


What is natural history of untreated aortic stenosis

Angina --5 years
Syncope--3 years
dyspnea--2 years


What are two posterior root enlargement procedures

Nicks aortic annuloplasty: incision through the middle of non-coronary sinus

Manougian's aortic annuloplasty: incision pass through the commissure between the left and non-coronary sinuses and onto the anterior leaflet of the mitral valve


What is natural history of patients with untreated AI

6% of asymptomatic patients with good left ventricular function either become symptomatic develop left ventricular dysfunction per year

25% of asymptomatic patients with left ventricular dysfunction develop symptoms per year

symptomatic patients have a 10% mortality per year


How is aortic regurgitation quantified

mild mod Severe
Jet width <25 25-65 > 65
Vena contracta 0.6
Regurgitant fraction% <30 30-50 > 50
Regurgitant volume <30 30-60 >60
Effective regurgitant orifice <0.1 0.1-0.3 >0.3


What structures are at risk during aortic valve surgery

Anterior mitral valve leaflet (beneath the non-coronary and left coronary cusps)
Membranous septum: (beneath the non-coronary and right coronary cusps)
Bundle of HIS: (beneath the commissure between the non-coronary and right coronary cusps)
Left and right coronary ostia


What are the surgical approaches to the aortic valve

Oblique aortotomy (J-shaped)
transverse aortotomy
Greater curve aortotomy, which can be combined with an aortoplasty to reduce the size of a moderately enlarged ascending aorta


What are different methods of implanting an aortic valve prosthesis

Interrupted sutures technique, reduced risk of paravalvular leak
Everting suture--place the prosthetic valve in an intra-annular position thereby reducing the relative effective orifice area (EOA) of the annulus allowing a smaller valve to be implanted
Non-everting sutures-place the prosthetic valve in a supra-annular position, thereby increasing the effective orifice area of the annulus, allowing a larger valve to be implanted, relative to the everting suture technique.

Semi-continuous technique, which is faster, but has theoretical increased risk of PV leak.


What is Marfan syndrom

Autosomal dominant variably penetrant inherited disorder; prevalence is 1 in 5000

Mutation in the gene that endocodes fibrillin-1 on chromosome 15


What are the diagnostic (Ghent) criteria for marfan

Family history
Mutation of FBN1
Aortic root dilation
Dissection of ascending aorta
mitral valve prolapse
calcification of the mitral valve
dilation of the pulmonary artery
dilation or dissection of the descending aorta
ectopia lentis
flat cornea
elongated globe
pectus excavatum
pectus carinatum
pes plans
thumb sign
scoloisis. or spondyloisthesis
arm span > 1.05
apical bulla/spontaneous pneumothorax
unexplained stretch marks/recurrent incisional hernia


What is Loeys-Dietz syndrome

mutations in TGF beta receptors 1 and 2
similar to that of Marfan or more drastic associated with dissection in children.
characterized by the triad of
bifid uvula/cleft palate
generalized arterial tortuosity with wide spread vascular aneurysm and dissection


What is Vascular Ehlers-Danlos syndrome

rare autosomal dominant inherited disorder of the connective tissue resulting in COL3A1 gene encoding of type III collagen

spontaneous rupture without dissection of large and medium-caliber arteries accounts for most deaths

Aortic root dilation is common


Name other causes of aneusrym disease of aorta

Infectious (syphilitic)
giant cell
Ankylosing spondylitis
Reiters sydrome
psoriatic artheritis
polyarteritis nodosa
Behcet's disease


What is natural history of biscuspid aortic valve

Mayo clinic showed at 15 year follow up the 20 year survival was similar to that of the general population but the incidence of surgery on the aortic valve and/or ascending aorta was 27% and the total adverse cardiovascular events was 42%.


What are rates of rupture based on size of ascending aortic aneurysms

Median size of ascending aortic aneursym at time of rupture was 5.9 cm for all pt
incidence of rupture < 4cm was 8%
9.5% for 4 to 4.9cm
17.8% for 5 o 5.9
27.9% for >6 cm

This was over a 29.4 month period (Coady, total of 370 patients)


What are the differences of generations for stented prostheses valves

First generation: preserved in high-pressure and were placed in the annular position)

Second generation: treated with low or zero pressure fixation , several placed in supra-annuluar position

Third generation: zero or low pressure, antimineralization (reduce material fatigue and calcium), stent have a lower profile, flexible, thinner, and scalloped.


How does Glutaraldehyde work?

Cross-linking collagen fibers to reduce tissue antigenicity.

Ameliorates in vivo enzymatic degradation and causes the loss of cell viability, thereby preventing extracellular matrix turnover.


How is sizing of company valves determined

Label sizes refer to either the internal or the external diameter of the stent, the external diameter of the sewing cuff or the maximal opening diameter of the valve leaflets


Describe the anterior approach for root enlargement

Described by Konno in 1975
Used when you need more then 4 sizes of increase
Longitudinal incision in aorta and extended to the right coronary sinus of valsalva and then through the anterior wall of the right ventricle to open the right ventricular outflow tract
the ventricular septum is incised.


Indicate the current recommendations to the use of warfarin and target INR

AVR with mechanincal valve and NSR = 2.0 to 3.0
AVR biological with atrial fribrillation = 2.0
Mitral valve replacement with tissue valve 2.5 to 3.5
Mitral valve replacement with mechanical valve = 2.5 to 3.5


List seven complications of valvular substitutes

Strctural valve failure
periprosthetic leak
Anticoagulant-related hemorrhage
Prosthetic valve endocarditis
Hemodynamic valve failure


What is patient prosthesis mismatch

Defined as the EOA of an implanted prosthetic valve being too small relative to the patients body surface area. It is sub-classified by a prosthetic EOAI (EOA indexed)

a) mild > 0.85 cm2/m2
b) moderate 0.65 cm2/m2---0.85 cm2/m2/
c) severe < 0.65 cm2/m2

Leads to persistently high transvalvular pressure gradients, reduced left ventricular mass regression, reduced symptom improvement and reduced exercise tolerance, there is controversary regarding the effects of PPM on short and long-term mortality.


At what indexed effective orifice area can PPM mismatch theoretically occur?

< 0.85cm/m2


For pts with PPM what percentage will be expected to develop symptoms



What is clinical impact of PPM

worse hemodynamics
lesser regression of LV hypertrophy
more cardiac events
Debate of short and long term survival---especially if LV dysfunction is present


What is clinical impact of PPM in the aortic position

less improvement in symptoms and functional class
impaired exercise capacity
less regression of LV hypertropy
less improvement in coronary reserve
more adverse cardiac events

The impact on PPM is more pronouced in younger, those with poor LV function.


Describe the incision in the aorta and heart to perform a Nicks

An oblique incision in the anterior ascending aorta steers inferiorly and to the right and crosses the aortic annulus in the middle of the noncoronary sinus and extends for a variable distance into the base of the anterior mitral leaflet


How does a Manouguina root enlargement differ from the Nicks procedures

The incision crosses the annulus through the commissure between the left and the noncoronary sinus
Down onto the anterior leaflet of the mitral valve
May require a patch


How much can the aortic annulus diameter be enlarged with Nicks and Manougian

Nicks 2 mm

Manougian up to 4 mm


Echocardiographer tells you that the peak velocity of blood flow across the aortic valve of a pt is 4meters/second.

What is peak gradient?

How did you arrive at this estimated value

Estimated peak gradient = 64mmHg

estimated by the Gorlin equation: aortic valve gradient = 4v2 (v = peak velocity of blood flow across the aortic valve)


What are 3 indications for surgery in asymptomatic adults with chronic severe AI

Left ventricular systolic dysfunction (EF < 50%)

associated cardiovascular disease requiring surgery such as coronary artery disease

enlarging left ventricule (LVEDD 70-75mm and ESDD 50-55mm)


List 3 absolute contraindications to the Ross procedure

Marfan and other collagen disorders
Auto-immune or other systemic disorders (Libman-sacks, rheumatoid arthritis)
Anatomical abnormality on the pulmonic valve
Multiple valve disease
Poor LV function
Severe aortic annular dilation


List absolute contraindications to Ross procedure

Marfan's disease
Bicuspid or quadricuspid pulmonary valve
Immunological disorders
fenestrated pulmonary valve


List relative contraindications to Ross procedure

Aortic annulus > 30 mm
Bicuspid aortic valve
disparity between aortic annulus and pulmonary annulus (> 2mm in size)


55 year old male with stenotic bicuspid aortic valve. Ascending aorta is 6 cm. Coronary artery ostia appear to be displaced at least 2 cm from aortic annulus. What operation would recommend?

Replacement of aortic valve, replacement of ascending aorta and reimplantation of coronary ostia (ie, modified bentall procedure)


Describe Konno (Konno-Rastan Aortoventriculoplasty)

vertical aortotomy to the L of RCA, through annulus in RCC
Annulus of RVV incised to the L of the nadir and extended into interventricular septum
separate incision in infundibulus of RV to guide septal incision
posterior annulus sutures placed and valve tied down
patch of pericardium sewn into the IVS defect and brought up to anterior aspect of mechanical valve
Patch sewn to sewing ring of valve and then patch carried distally to enalrge and close the aorta
RVOT defect close with fixed pericardium


How do you calculate BSA

Mosteller formula = sqrt [ht (cm) x wt (kg)/3600]
average for women 1.6 to 1.6
men 1.9m2


What is long outcomes from AVR in Carpentier edwards pericardial valve

Freedom from structural valve degeneration at 15 year was
34.7% in patients < 65
89% in patients 65 to 75 years of age
99.5% in patients more than 75 years

Mccure and Cohn from Brigham and Womens hospital 2010, Annals of thoracic surgery 2010


What is pseudo aortic stenosis

A low calculated AVA, which is artificial because flow is too low (to open a mildly or moderatly diseased aortic valve) or an eorr in the calculated AVA

TTE can underestmate the LVOT by as much as 17% because of its shape.
Use 3D echo, CT or MRI obtain more accurate measure of aortic annulus.


What are potential reactions from Dobutamine stress Echo

True AS--increase in peak velocity, MPG, and no change in AVA
Pseduo-AS--increase in AVA by > 0.3cm2 with no significant change in MPG, and peak velocity
Absence of contractile reserve did not help distinguish between the two groups because there was no change in forward stroke volume.

Presence of contractile reserve is defined ass increase in peak velocity of 0.6m/s, stroke volume > 20% and MPG > 10 mmHg with Dobutamine.


What does contractile reserve infer about mortality post AVR for low flow low gradient AS

5% mortality if you have contractile reserve VS 32% mortality if you do not


If you have no contractile reserve in AS what is the relationship compared to medical therapy

Tibroiilloy showed 5 year survival of AVR on medical therapy to be 54% and 13% if you just stayed on meds...despite a 22% mortality

Therefore, absence of contractile reserve should not preclude AVR even though it clearly portends a higher operative mortality.


What is natural history of AS in terms of increase in gradient

The aortic valve gradient increases by 0 to 15 mmgHg per year

the AVA decreases by 0.12cm2/year


What are qualitative feature of AI

mild mod severe
Angiographic 1+ 2+ 3-4+ Color dopp jet width 65%
vena contracta 0.6


Name one component that contributes to anti-calcifification in bioprosthetic valves

alpha-amino acid (AOA)--a compound from oleic acid.


List indications for stentless valves

1) Aortic root disease when bioprosthesis is desired
2) Aortic dissection, (when valve need a replacement). Extensive dissection in the sinuses of valsalva is easily handled with a stentless bioprothetic
3) Endocarditis--allows maximal debridement


Describe durability outcomes of stentless AVR (Toronto SPV) ?

9 years the Freedom from SVG was 90% and there was actual improvement in survival.
12 years there was 69% freedom from SVG and only 52% in those < 65 years of age
Freedom from moderate to severe AI was 48%


What is rate of sudden death with severe AS (asymptomatic)



What are the physical findings of severe AS

Late-peaking creseendo-descresendo systolic murmour radiating to the carotids
Single A2 heart sound
delay and reduced amplitude of carotid pulse
*severe AS is very unlikley if you hear splitting of S2*


What addition test can be performed in a patient with severe asymptomatic AS

Exercise stress testing
Brain natriuretic peptide


What are important BNP cut off for severe AS

BNP and ANP are endogenous hormones with diuretic and peripheral regulatory actions
BNP is produced predominatly from stretched LV in response to wall stress
if the BNP level is around 100 the AVA is usually < 1.0
An NYHA class II pt would have a BNP around 100
if the BNP is 25 then AVA is usually > 1.0.
it's the 25 to 100 number which is interesting


What is natural history of AI

Symptomatic pts have a 10%/year mortality
Progression to cardiac symptoms in pts with LV systolic dysfunction 25%
Asymptomatic rate of sudden death is 0.2%
Asymptomatic progression to LV dysfunction in <3.5%
Asymptomatic if LVESD is >50 to LV systolic dysfunction is 19%


What is Laplace Law

Relates how left ventricular hypertrophy occurs as compensatory mechanism to reduce will stress

WS (wall stress) = P (pressure) x r (radius)/ 2 x Th (Left ventricular wall thickness)

Decks in From Flashcardlet big Class (79):