Download Aortic valve stenosis

Valvular
Heart
Disease
Krzysztof Jankowski
CAUSES OF VALVE DYSFUNCTION
1. Congenital heart defects
2. Ischemic heart disease
3. Cardiac hypertrophy or dilation as occurs in heart failure
4. Ruptured chordae tendineae
5. Bacterial inflammation
Valve stenosis
• valve doesn't open fully
• valve may have become hardened or stiff with calcium
deposits or scarring
• blood has to flow through a smaller opening
• less blood gets through the valve into the next chamber or
big vessels
Stenosis occurs in both the aortic and mitral valves:
• Aortic valve stenosis
• Mitral valve stenosis
Valve insufficiency
(also called regurgitation)
• valve doesn't close tightly
• valve's supportive structures may be loose or torn
• valve itself may have stretched or thinned
Insufficiency occurs in both the aortic and mitral valves:
• Aortic insufficiency
• Mitral insufficiency
VALVULAR STENOSIS
MITRAL VALVE STENOSIS
Mitral Stenosis
• Normal MVA 4 -5 cm2
• Symptoms not apparent until area < 2.5 cm2
Mild
Moderate
Severe
valve area
(cm2)
mean gradient
(mm Hg)*
> 1.5
<5
1.0 - 1.5
5 - 10
< 1.0
> 10
* assumes normal cardiac output
MITRAL VALVE STENOSIS
• results from a narrowing of the opened mitral valve orifice
• it is more difficult for blood to flow from the left atrium (LA) into the
left ventricle (LV) during ventricular diastole
increasing LA pressure
(normally ~10 mmHg).
MITRAL STENOSIS
1. increasing LA pressure
(normally ~10 mmHg).
left atrium enlarges
(hypertrophies) over time
2. left ventricular maximal filled
volume (end-diastolic volume) is
reduced despite the elevated left
atrial pressure
3. left ventricular end-diastolic
pressure is reduced (6 mmHg in
this example vs 10 mmHg in the
normal heart)
4. reduced ventricular filling (decreased preload) decreases ventricular
stroke volume (Frank-Starling mechanism)
A
5. If stroke volume falls significantly, the reduced cardiac
output may result in a reduction in aortic pressure (Ao 115/80 mmHg in
this example)
MITRAL VALVE STENOSIS
is associated with a diastolic murmur because of turbulence
that occurs as blood flows across the stenotic valve.
MITRAL STENOSIS
Clinical symptoms
• decrease in exercise tolerance
• exertional dyspnoea
• fatigue
• palpitations
• chest pain
• productive cough with blood-streaked sputum
• recurrent respiratory infections
• hoarseness due to compression of the recurrent
laryngeal nerve by an enlarged left atrium – Ortner syndrom
• reccurent pulmonary oedema (severe MS)
Mitral Stenosis
Natural History
• Latent (subclinical) phase
• 10 years of symptoms before disabling
•
•
•
•
When physically limiting symptoms
mean survival
< 3 years
10-year survival
0-15%
systemic embolism
10-20%
atrial fibrillation
30-40%
Mitral Stenosis
Diagnostics
•
•
•
•
•
•
History
Physical exam.
ECG
CXR
Echocardiography
± Exercise echocardiogram
Mitral Stenosis
Medical Therapy
• Infective endocarditis prophylaxis
• Limitation of strenuous physical activities
• Control of heart rate (negative chronotropes)
+
• Na restriction, diuretic use
• Management of AF (digoxin)
• Angiotensin converting enzyme inhibitors
• Anticoagulants (warfarin)
Mitral Stenosis
Interventional and Surgical Options
• Percutaneous mitral balloon valvotomy
(PMBV)
• Closed commissurotomy (obselete)
• Open commissurotomy
• Mitral valve replacement
Classification of Recommendations
Class I:
Conditions for which there is evidence and/or general agreement that a
given procedure or treatment is useful and effective.
Class II:
Conditions for which there is conflicting evidence and/or a divergence of
opinion about the usefulness/efficacy of a procedure or treatment.
IIa. Weight of evidence/opinion is in favor of usefulness/efficacy
IIb. Usefulness/efficacy is less well established by evidence/opinion.
Class III:
Conditions for which there is evidence and/or general agreement that the
procedure/treatment is not useful/effective, and in some cases may be
harmful.
Mitral Stenosis
Management Guidelines
Indications for PMBV (class I and IIa)
• Suitable anatomy, no LA clot, ≤ mild MR
• Symptomatic pts (NYHA class II-IV) with MVA
<1.5 cm2
• Asymptomatic pts with MVA <1.5 cm2 and
PASP 50 mmHg at rest, 60 mmHg - exercise
Mitral Stenosis
Management
Indications for MVR (class I and IIa)
• Symptomatic pts (NYHA class III and IV) with
MVA < 1.5 cm2 unsuitable for PMBV
• NYHA class I and II pts with MVA < 1.0 cm2 and
PASP >60 at rest unsuitable for PMBV
AORTIC VALVE STENOSIS
Aortic Stenosis
• Normal aortic valve area - 3.0 - 4.0 cm2
• Circulation affected when valve area reduced
by ca. 75% (i.e. 0.75 - 1.0 cm2)
valve area (cm2)
Mild
Moderate
Severe
mean gradient (mm Hg)*
> 1.5
< 25
1.0 - 1.5
25 - 50
< 0.75
> 50
* assumes normal cardiac output
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AORTIC VALVE STENOSIS
• is characterized by the left ventricular pressure being much
greater than aortic pressure during left ventricular (LV) ejection
Stenotic valve
A
•
In this example, LV peak systolic pressure during
ejection is 200 mmHg (normally ~120 mmHg)
•
Normally, the pressure gradient across the aortic valve
during ejection is very small (a few mmHg)
•
The high pressure gradient across the stenotic valve
results from both increased resistance (related to
narrowing of the valve opening) and turbulence distal
to the valve.
•
left ventricle is required to generate greater pressures
•
this leads to ventricular hypertrophy (thickening of the
muscular walls)
•
this leads to diastolic dysfunction (impaired filling)
The hypertrophied ventricle
• has less compliance (A)
• has a higher filling pressure at any given end-diastolic
volume (the end-diastolic pressure is 25 mmHg in this
example).
•
Elevated left ventricular end-diastolic pressure causes
blood to back up into the left atrium and pulmonary
veins
•
this increases left atrial pressure, enlarges the left
atrium and results in hypertrophy of the atrial wall
Thick
Thin
RUBBER BALLON
RUBBER BALL
What do you inflate easier?
CLINICAL SYMPTOMS OF AORTIC STENOSIS
• chest pain
• exercise syncope
• palpitations
• dizziness
• blurred vision
• exertional and rest dyspnea
• other symptoms of heart failure (less)
• the first symptom can be sudden cardiac death
caused by ventricular fibrillation, or pulmonary
edema
AORTIC VALVE STENOSIS
• is associated with a mid-systolic systolic murmur
because of turbulence that occurs as blood flows
across the stenotic valve.
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Aortic Stenosis
Natural History
• Latent phase: usually lasts decades
– Risk of sudden death: very low during this phase
• Rate of progression ranges from 0 - 0.3 cm2/yr.
(average rate is 0.12 cm2/yr)
• 50% of patients with severe AS do not progress
• We can not predict, who will progress
Aortic Stenosis
Natural History
• Once symptoms develop, avg. survival 2-3 yrs
• With LV systolic dysfunction, there may be increased
risk of sudden death and permanent LV dysfunction
Aortic Stenosis
Initial Diagnostic Testing
– Lipids, renal function, Ca, P in all patients
– CXR, ECG, Echocardiography in all patients
– Cardiac catheterization with angiography
• If clinical and echo data are discordant
• To assess coronary circulation prior to surgery
Aortic Stenosis
Initial Diagnostic Testing (cont.)
– Treadmill stress testing
• Dangerous in symptomatic pts
• Not useful for diagnosis of CAD
• May be used to assess functional significance of severe
AS in pts who deny symptoms (e.g. BP response)
Aortic Stenosis
Recommendations for Aortic Valve Replacement (AVR)
Class I
– Severe AS and symptoms
– Severe AS and need for CABG, other valve replacement or
aortic surgery
Class IIa
– Moderate AS and need for other cardiac surgery
– Asymptomatic severe AS and diminished LVEF or
hypotensive response to exercise
Aortic Stenosis
Management Guidelines
Recommendations for AVR (cont.)
Class IIb
– Asymptomatic AS and VT, severe LVH (>15mm)
or valve area <0.6 cm2
Class III
– Asymptomatic AS with none of the above
Transcatheter Aortic Valve Implantation (TAVI)
• catheter-based procedure
• implantation of an artificial aortic valve without openheart surgery
TAVI
• the procedure:
o is done in a hybrid cath lab/OR
o is performed by the invasive cardiologist
•
a wire with the artificial valve at the tip is threaded
through aorta to the aortic valve
•
the artificial valve is placed in the diseased natural
aortic valve and seated on top of it
•
the wires are then pulled back through the blood
vessels
•
this procedure is much less invasive than surgery
•
it is typically reserved for those patients who have
aortic stenosis but who are not good candidates for
open-heart surgery.
AORTIC REGURGITATION
• occurs when the aortic valve fails to close completely
• blood flows back from the aorta (Ao) into the left ventricle (LV)
•
Because the ventricle is being filled from two
sources (aorta and LA), this leads to much greater LV
filling
•
LV end-diastolic volume is increased as well as LV
end-diastolic pressure (20 mmHg in this example).
•
The increased ventricular end-diastolic volume
(preload) leads to an increase in the force of
contraction through the Frank-Starling mechanism
•
It causes a greater than normal stroke volume into the
aorta.
•
This elevates aortic systolic pressure (160 mmHg in
this example)
• The aortic diastolic pressure (60 mmHg in this example) is much lower than normal because
blood more rapidly leaves the aorta due to regurgitation back into the ventricle.
pulmonary veins
secondary: mitral regurgitation
1.
The elevation in LV end-diastolic pressure causes blood to back up into the
left atrium and pulmonary veins.
2.
It leads to an increase in left atrial pressure and pulmonary capillary wedge
pressure.
3.
It can result in pulmonary congestion and edema.
AORTIC REGURGITATION
The backward flow of blood into the ventricular chamber
during diastole results in a diastolic murmur.
Aortic Regurgitation
Natural history
• LV faces combined pressure and volume load
• Primary adaptation is dilatation (eccentric
hypertrophy)
• Since this adaptation takes time, AR classified as
acute or chronic
• Acute AR results in sudden increase in left
ventricular end-diastolic pressure pulmonary
edema and cardiogenic shock
Aortic Regurgitation
• Latent phase of AR may last decades
• In asymptomatic pts with severe AS and nl LV
systolic function, progression is slow
– 4.3% pts. develop symptoms of LV systolic
dysfunction (1 year)
– 1.3% pts progress to LV dysfunction without
symptoms† (1 year)
† pooled data from 7 series. 490 pts with mean follow-up of 6.4 yrs
Aortic Regurgitation
Initial Evaluation
•
•
•
•
ECG
CXR
Echocardiography
ETT (if pt asymptomatic but sedentary or if
symptoms are equivocal)
Aortic Regurgitation
Recommendations for AVR (chronic severe AR)
Class I
• NYHA functional class III or IV
• NYHA functional class II and progressive LV
dilatation or declining LVEF on serial studies
• CCS class II angina
• Mild or moderate reduction in EF (25-50%)
• Need for CABG or surgery on other valves
Aortic Regurgitation
Recommendations for AVR (chronic severe AR)
Class IIa
• NYHA class II with normal LVEF (>50%) with stable
EF, LV size and exercise tolerance
• Asymptomatic pts with normall LVEF but severe
LV dilatation (ESD > 55 mm or EDD > 75 mm)
Class IIb
• LVEF < 25%
• Asymptomatic pts with nl LVEF and progressive LV
dilatation with ESD 50-55 mm or ESD 70-75 mm
MITRAL VALVE REGURGITATION
• occurs when the mitral valve fails to close completely during
ventricular systole
• blood flows back (regurgitate) into the left
atrium (LA) as the left ventricle (LV) contracts
This causes LA pressure to increase (25 mmHg
in this example).
• during LV filling, the higher pressure and volume of the LA leads to an increase in LV
end-diastolic pressure (25 mmHg in this example) and LV end-diastolic volume.
• blood flows back (regurgitate) into the left
atrium (LA) as the left ventricle (LV) contracts
This causes LA pressure to increase (25 mmHg
in this example).
• during LV filling, the higher pressure and volume of the LA leads to an increase in LV
end-diastolic pressure (25 mmHg in this example) and LV end-diastolic volume.
• This increase in LV preload causes the LV to contract more forcefully
(Frank-Starling mechanism), which enables it to increase its stroke volume.
• blood flows back (regurgitate) into the left
atrium (LA) as the left ventricle (LV) contracts
This causes LA pressure to increase (25 mmHg
in this example).
• during LV filling, the higher pressure and volume of the LA leads to an increase in LV
end-diastolic pressure (25 mmHg in this example) and LV end-diastolic volume.
• This increase in LV preload causes the LV to contract more forcefully (Frank-Starling
mechanism), which enables it to increase its stroke volume.
• Although the LV stroke volume is increased, the net amount of blood ejected into the
aorta is reduced because part of the LV stroke volume (regurgitant fraction) is also
ejected into the LA.
• blood flows back (regurgitate) into the left
atrium (LA) as the left ventricle (LV) contracts
This causes LA pressure to increase (25 mmHg
in this example).
• during LV filling, the higher pressure and volume of the LA leads to an increase in LV
end-diastolic pressure (25 mmHg in this example) and LV end-diastolic volume.
• This increase in LV preload causes the LV to contract more forcefully (Frank-Starling
mechanism), which enables it to increase its stroke volume.
• Although the LV stroke volume is increased, the net amount of blood ejected into the
aorta is reduced because part of the LV stroke volume (regurgitant fraction) is also
ejected into the LA.
• Volume of blood ejected into the aorta is reduced, then aortic pressure may fall (110/75
mmHg in this example).
Mitral Regurgitation – Clinical Symptoms
• fatigue
• dyspnoea
• palpitations
• symptoms of right heart failure (in severe
regurgitation).
Acute Mitral Regurgitation
Physiology and Natural History
• Abrupt volume load---no time for adaptation
• Sudden  in forward stroke volume
• Sudden  in LA volume/pressure   PV
pressure
• Rapidly fatal
• Pulmonary oedema
Chronic Mitral Regurgitation
Natural History
• Gradual development allows adaptation
• LA dilatation and increase in compliance
• LV dilatation and  EF (via  preload and 
afterload)  maintenance of forward SV
• Compensation often adequate for vigorous
exercise
• May last many years
Chronic Mitral Regurgitation
DIAGNOSTICS
Initial evaluation
• History
• Physical Exam
• ECG
• CXR
• ECHOCARDIOGRAPHY
• ± Exercise echo
Chronic Mitral Regurgitation
Medical Therapy
• No generally accepted in asymptomatic pts
• No long term studies suggesting benefit of
afterload reduction in absence of
hypertension
• ACE-I if hypertensive
• AF requires rate control, anticoagulation
Chronic Mitral Regurgitation
Management Guidelines
Surgical Options
• Mitral valve repair
• Mitral valve replacement with preservation of
subvalvular apparatus
• Mitral valve replacement with excision of
subvalvular apparatus
• MVR with CABG (in ischemic MR)
Chronic Mitral Regurgitation
Indications for Surgery (class I and IIa)
• Symptomatic pts with severe MR and an LV
appearing “less than hopeless” (EF > 30, ESD <
55 mm)*
• Asymptomatic pts with moderate or severe
MR and any of the following: EF 30-60%, ESD >
45 mm, AF, PASP > 50 at rest, PASP > 60 with
exercise
*consider if chordal preservation appears very likely
RISK OF ENDOCARDITIS
RECOMMENDATIONS
Antibiotic prophylaxis should be considered for PATIENTS AT HIGHEST RISK for IE:
Class /
Level
IIa C
• Patients with any prosthetic valve, including a transcatheter valve,
or those in whom any prosthetic material was used for cardiac valve repair.
• Patients with a previous episode of IE.
• Patients with congenital heart disease (CHD):
o any type of cyanotic CHD.
o any type of CHD repaired with a prosthetic material, whether placed
surgically or by percutaneous techniques, up to 6 months after the
procedure or lifelong if residual shunt or valvular regurgitation
remains.
Antibiotic prophylaxis is not recommended in other forms of valvular or CHD.
CHD - congenital heart disease
III C
ESC 2015
Recommendations for prophylaxis of infective endocarditis IN THE HIGHEST-RISK PATIENTS
DENTAL PROCEDURES
RECOMMENDATIONS
Class/
level
A. Dental procedures
Antibiotic prophylaxis should only be considered for dental procedures requiring
manipulation of :
• the gingival
• peri-apical region of the teeth
• perforation of the oral mucosa
IIa C
Antibiotic prophylaxis is not recommended for
• local anaesthetic injections in non-infected tissues
• treatment of superficial caries
• removal of sutures
• dental X-rays
• placement or adjustment of removable prosthodontic or orthodontic
appliances or braces
• following the shedding of deciduous teeth or trauma to the lips and
oral mucosa
III C
B. Respiratory tract procedures
…………………………………………………………………………………………
ESC 2015
Recommended prophylaxis for high-risk dental procedures in high-risk patients
aAlternatively,
cephalexin 2 g i.v. for adults or 50 mg/kg i.v. for children, cefazolin or
ceftriaxone 1 g i.v. for adults or 50 mg/kg i.v. for children.
Cephalosporins should not be used in patients with anaphylaxis, angio-oedema, or
urticaria after intake of penicillin or ampicillin due to cross-sensitivity.
ESC 2015