4. Aortic Valve Anatomy
• Aortic Valve is composed of three cusps of equal size, each of which is
surrounded by a sinus
• Cusps are separated by three commissures and supported by a fibrous annulus
• Each cusp is crescent shaped and capable of opening fully to allow unimpeded
forward flow, then closing tightly to prevent regurgitation
• Free edge of each cusp curves upward from the commissure and forms a slight
thickening at the tip or midpoint, called the Arantius nodule.
• When the valve closes, these three nodes meet in the centre.
5. Anatomy
• Overlap of Valve tissues along the lines of closure produces a tight seal and
prevents backflow during Diastole.
• Doesn’t have chordae tendinae, papillary muscles unlike mitral valve.
• More the number of cusps, more the chance for regurgitation (Quadricuspid aortic
valve-AR)
• Less the number of cusps, more the chance for stenosis (Bicuspid-AS)
6.
7. Function of Heart Valves
• Maintains the forward flow and prevents the
reversal of flow.
• Valves open and close in response to the
pressure differences (gradients) between
cardiac chambers.
8. Cardiac cycle
• 3 phases of SYSTOLE (ventricular) –
Total duration 0.3 sec
• Events during SYSTOLE:
Isovolumetric contraction
Rapid Ejection
Reduced Ejection
9. Cardiac Cycle
• 5 phases of DIASTOLE (ventricular) – total
duration 0.5 sec
• Events during DIASTOLE:
Proto diastole
Isovolumetric relaxation
Rapid Filling
Reduced Filling
Atrial Systole
10. Atrial systole is the
last part of
diastole which is
required for the
remaining 30%
blood to be
pushed to the
ventricle.
Mitral valve
closes
LV is
contracting
as a closed
chamber
At the end of IVC,
Aortic valve
opens.
11. Aortic Stenosis
• Occurs in one fourth of all patients with
chronic valvular heart disease.
• Common causes:
1. Congenital Aortic stenosis (bicuspid,
unicuspid)
2. Degenerative Calcific (Atherosclerotic)
3. Rheumatic Fever
4. Radiation
12. Epidemiology
80% patients are males
30% of elderly have valve
sclerosis, not severe to cause
obstruction.
MC valvular pathology
worldwide: Aortic Sclerosis
13. Etiology and pathogenesis
• Degenerative Calcification of Aortic cusps, most commonly on bicuspid aortic valve,
chronic (trileaflet) deterioration, or previous rheumatic inflammation.
• Associated with vascular atherosclerosis, lipid accumulation, inflammatory cell
activation, cytokine release, upregulation of several signaling pathways.
• Valvular myofibroblasts differentiate into osteoblasts and produce bone matrix
proteins that allow for the deposition of calcium hydroxyapatite crystals.
• Atherosclerotic risk factors like LDL, cholesterol, lipoprotein a, diabetes mellitus,
smoking, CKD, Metabolic syndrome.
• Angiogram in the patient is mandatory, as there will be ongoing atherosclerosis in
most patients.
14. Continues…
• Aortic Valve Sclerosis (focal thickening and calcification of the leaflets not severe
enough to cause obstruction)-excess risk for CVD and MI ->65 yrs of age.
• Rheumatic disease-commissural fusion-bicuspid appearing valve-susceptible to
trauma-fibrosis, calcification, further narrowing.
• AS in RHD is less common.
• MC combination in RHD: (MS+MR) > (MS+AR) > (AR+AS)
• Mediastinal radiation- late scarring, fibrosis, calcification of Aortic leaflets.
15.
16.
17. Bicuspid Aortic Valve Disease
• Most common congenital valve defect with 4: 1 male to female predominance.
• Autosomal Dominant
• Mutation in NOTCH 1 , GATA 5, GATA 4 gene.
• ENOS defect
• Medial degeneration with ascending aortic aneurysm formation occurs commonly.
Always rule out Aortopathy.
• Patients with BAV are at risk of Aneurysm formation and Coarctation
• Can be a component of complex congenital heart disease like Shone’s complex
18. Bicuspid Aortic valve
• Degeneration and clacification can occur
in young person, if he has bicuspid AV.
• It is the major cause of AS in young
population.
• BAV – Always look for aortopathies
• CT Angiogram is mandatory irrespective of
age.
19. Classification
3 types
• Valvular Stenosis (at the
level of valve)
• Subvalvular Stenosis (due to
HCM)
• Supravalvular Stenosis
(associated with William
Syndrome)
20. Pathophysiology and Hemodynamics
• LV pressure in systole: 120 mm Hg
• Aortic pressure in systole: 120 mm Hg
• Normally valve completely opens in systole – Absolutely no pressure gradient
between LV and Aorta
• In AS, as valve does not open completely, there will be pressure gradient b/w LV
and Aorta.
21. Severe Aortic Stenosis
• Mean Transvalvular Pressure gradient (Gradient b/w LV and Aorta); > 40 mmHg
• Peak Velocity across valve: >4m/sec
• Valve surface area:< 1cm^2
• Usually AS is asymptomatic, by the time AS producing symptoms, it is severe AS.
22. Grading of Aortic Stenosis
Severity Mean Gradient
(mmHg)
Aortic Valve area
(cm^2)
Mild <25 >1.5
Moderate 25-40 1-1.5
Severe >40 <1
Critical >80 <0.5
23. Compensatory mechanism of AS: Concentric
LVH to increase the left ventricular pressure
by increasing the wall thickness.
Increase in thickness is at the expense of
the cavity size (decreases). LVH can be
associated with strain.
In very severe AS: Diastolic Dysfunction
and LV filling pressure will be high. Later
contractile function deteriorates CO
24. During Diastole
• Normal Diastolic pressure in LV: 8-12
mmHg
• Normal Diastolic pressure in Aorta: 80
mmHg
• LA pressure; 8-12 mmHg
• LVEDP= LA Pressure= Pulmonary
Capillary Wedge pressure
26. • Atrial Fibrillation can be fatal in AS ( Patient can go into shock)
• Systemic Hypertension can mask AS as gradient decreases due to higher Aortic
pressures.
• LV failure – LV pressure drastically reduces – Low flow low gradient AS
• HEYDES syndrome – AS + Angiodysplasia of Colon, patient will be having Lower
GI bleed.
27. Symptoms
• Angina
i. LVH increases O2 demand
ii. Decreased diastolic perfusion time
iii. Decreased capillary density with respect to wall thickness
iv. Atherosclerosis
• Syncope due to low cardiac output
• Dyspnoea due to increased left ventricular filling pressure.
28. Mean Survival Based on Symptoms
• Angina: < 5 years
• Syncope: < 3 years
• Dyspnoea: < 2 years
• Sudden cardiac death may occur in asymptomatic individuals = 4%
29. Signs of Aortic Stenosis
• Pulse:
• In severe AS – Pulsus tardus pattern
• In Very severe AS- Pulsus parvus et tardus
• Carotids:
• Associated carotid artery thrill or shudder
30. Signs of Aortic Stenosis
• Blood Pressure:
• LVH disproportionate to degree of hypertension.
• HTN can mask AS. HTN can increase aortic pressure and reduce gradient and
mask AS.
• Very severe AS – low cardiac ouput – decrease in systolic BP – Narrow Pulse
pressure
31. Signs of Aortic Stenosis
Apex:
Slightly displaced laterally (due to LVH)
High Amplitude + Sustained Apex ->
Haeving Apex
32. Signs of Aortic Stenosis
• Heart Sounds:
• S1- Normal. Loud S1 may be due to Aortic ejection click in Bicuspid Aortic Valve
• S2 – Single heart sound A2. Degenerative sclerosed valve – softer A2, Bicuspid
valve – Louder A2. Severe AS- due to LVH, paradoxical split S2 will be heard.
• S3 only in very severe AS due to Increased ventricular filling, and increased
LVESV
• S4 – criteria for S4 – Healthy atria in sinus rhythm have to contract vigorously to
pump blood across a non stenotic valve into a hypertrophic non dilated, non
compliant ventricle.
• S4 is heard in AS only, not in MS/MR/AR
33. Signs of Aortic Stenosis
• Murmur:
• Medium Pitched Murmur.
• Best heard at sitting and leaning forward position.
• Best heard at end expiration in aortic area (2nd right I/C
space)
• Heard with diaphragm of stethoscope.
• Called as ROUGH RASPING MURMUR.
• MID SYSTOLIC MURMUR with late systolic peaking (Marker
of severity)
34. Signs of Aortic Stenosis
• Medium pitched murmur has 2 components:
Low pitched component going into carotids
High pitched musical quality murmur going into apex – GALLAVARDIN
Phenomenon
• Asymptomatic at mild to moderate level AS
• Hence patient usually present as Severe AS
• The patient long term survival depends a lot on whether surgery is done with
normal or low systolic function ->severe to very severe matters.
35. ECG in Aortic Stenosis
• Severe LVH will be seen
• V1Sor V2S + V5R or V6R
• > 35 mm, LVH present
• Sokolow-Lyon Criteria
• ST depression and T wave inversion
In I, avL (LV strain) may be seen.
36. X Ray in Aortic
Stenosis
• The Ascending aorta leading to arch is dilated,
• whereas the distal arch and descending aorta are
normal in size.
• Aortic valve calcification may be seen.
37. Echocardiogram
• Key findings – Thickening, calcification, reduced systolic opening of the valve
leaflets, LV hypertrophy.
• Eccentric closure of Aortic valves in congenital BAV.
• The valve gradient and aortic valve area can be estimated by Doppler.
• Useful in identifying coexisting valvular abnormalities, differentiating valvular AS
from other forms of LV outflow obstruction
• Dobutamine stress ECHO – useful in evaluation of pts with AS (low flow low
gradient severe AS with reduced EF) and Severe LV systolic dysfunction.
38. Cardiac Cathetarization
• Patients with multivalvular disease, in whom the role played by each valvular
deformity should be defined ton plan for operative treatment.
• Young, asymptomatic patients with non calcific congenital AS to define its severity,
because operation or PABV may be indicated, if severe AS is present.
• Patients in whom it is suspected that the obstruction may not be at the level of the
Aortic valve, but at the sub- or supravalvular level.
• To screen for CAD in patients with severe AS, considered for surgery for which
bypass grafting is indicated at the time of AVR
39. Medical Management
• Sternuous Physical activity and competitive sports should be avoided.
• Avoid dehydration and Hypovolumia to protect against significant reduction in CO
• Medications to treat hypertension or CAD include Beta blockers and ACE
inhibitors.
• Nitroglycerin - Helpful in relieving angina.
• HMG CoA reductase inhibitors (statins) exhibit slower progression of leaflet
calcification.
40. Surgical Management of Aortic Stenosis
• Aortic Valve replacement (preferably Bioprosthetic) is preferred in
Symptomatic AS
Asymptomatic with LVEF < 50%, Vmax > 5m/s
Those with BAV disease and an aneurysmal root or ascending aorta
Rapid Progression on Treadmill exercise and on yearly ECHO
Symptomatic on Dobutamine stress test
Undergoing any other procedure
41. Percutaneous Aortic Balloon Valvuloplasty (PABV)
• Preferable to operation in many children and young adults with congenital,
noncalcific AS.
• Not commonly used as definite therapy in adults with severe calcific AS because
of very high restenosis rate.
• But used successfully as a “bridge to operation” in patients with severe LV
dysfunction and shock who are too ill to tolerate surgery.
• It is performed routinely as a part of TAVR procedure.
42. Transcatheter
Aortic Valve
Replacement
(TAVR)
TAVR for treatment of AS has been performed worldwide using
either a balloon- expandable valve or a self expanding valve,
both of which incorporate a pericardial prosthesis.
Most frequently performed via the transfemoral route, although
trans-LV apical, subclavian, carotid, ascending aortic routes
have been used.
Aortic balloon valvuloplasty under rapid RV pacing is
performed as a 1st step to create an orifice of sufficient size for
prosthesis. Procedural success rates exceed 90%
Among elderly patients with severe AS who are considered
inoperable, 1- and 2- year survival rates are significantly higher
with TAVR than medical therapy.
43. Transcatheter Aortic Valve Replacement (TAVR)
• TAVR is associated with an early hazard for stroke and a higher incidence of
postprocedural, paravalvular AR, a risk factor for morboiodity over the next 2 years.
• Postprocedural heart block requiring permanent pacemaker therapy is observed
significantly with self-expanding valve.
• Overall outcomes with this transformative technology has been very favourable.
• The use of these devices for the treatment of patients at intermediate operative risk
and for those with structural deterioration of bioprosthetic aortic and mitral
valves(“valve-in-valve”) as an alternative to reoperative valve replacement, is under
active study.
