Download Valvular Heart Disease

Valvular Heart Disease
Basic Science
March 22, 2006
1. Information on valves may be
accurately obtained by:
A. CXR
B. Transthoracic echocardiography (TTE)
C. Transesophageal echocardiography
(TEE)
D. CT scan
E. Cardiac catheterization
1. Information on valves may be
accurately obtained by:
A. CXR
B. Transthoracic echocardiography (TTE)
C. Transesophageal echocardiography
(TEE)
D. CT scan
E. Cardiac catheterization
TEE is more sensitive than TTE,
especially for aortic and mitral valve
lesions; even more so for mitral
regurgitation.
Cardiac catheterization can give detail on
mitral/aortic valve areas, calculated by the
Gorlin formula.
2. What is true concerning the
anatomy of the mitral valve?
A. The normal mitral valve has two
leaflets; the lateral and medial leaflets.
B. The chordae tendineae attach the
leaflets to two papillary muscles.
C. The two leaflets are identical mirror
images of each other, forming a tight
closure.
D. There is a fibrous continuity between
the mitral and aortic valves.
2. What is true concerning the
anatomy of the mitral valve?
A. The normal mitral valve has two
leaflets; the lateral and medial leaflets.
B. The chordae tendineae attach the
leaflets to two papillary muscles.
C. The two leaflets are identical mirror
images of each other, forming a tight
closure.
D. There is a fibrous continuity between
the mitral and aortic valves.
The two leaflets are anterior and posterior.
The two leaflets have the same surface
area but very different shapes. The base
of the anterior leaflet accounts for 1/3 of
the circumference of the mitral annulus
and the posterior leaflet accounts for 2/3.
3. What is true concerning mitral
stenosis?
A. Principal cause is rheumatic fever.
B. The normal cross-sectional area of the mitral
valve is 4-6 cm2, and moderate stenosis occurs
at 2 cm2 and severe stenosis occurs at 1 cm2.
C. There is normally a 5 mm Hg pressure
gradient across a normal valve, with symptoms
occurring once the gradient increases to greater
than 10 mm Hg.
D. Symptoms usually occur with bradycardia
and the heart’s inability to supply adequate
cardiac output to overcome the pressure
gradient across the valve.
3. What is true concerning mitral
stenosis?
A. Principal cause is rheumatic fever.
B. The normal cross-sectional area of the mitral
valve is 4-6 cm2, and moderate stenosis occurs
at 2 cm2 and severe stenosis occurs at 1 cm2.
C. There is normally a 5 mm Hg pressure
gradient across a normal valve, with symptoms
occurring once the gradient increases to greater
than 10 mm Hg.
D. Symptoms usually occur with bradycardia
and the heart’s inability to supply adequate
cardiac output to overcome the pressure
gradient across the valve.
There is normally no pressure gradient
across the mitral valve. A pressure
gradient of 20 mm Hg is needed to
maintain adequate left ventricular filling
across a 1 cm2 stenotic valve.
Contribution of an adequate left atrial
“kick” is important in mitral stenosis, and
loss of this contraction (with exertion or
atrial fibrillation) often leads to symptoms.
4. Mechanical relief of mitral
stenosis should be considered
when:
A. The valve size is 2 cm2 or smaller.
B. The patient becomes symptomatic.
C. Pulmonary hypertension develops.
D. With worsening Left ventricular
hypertrophy and dilatation.
E. Endocarditis develops in the valves.
4. Mechanical relief of mitral
stenosis should be considered
when:
A. The valve size is 2 cm2 or smaller.
B. The patient becomes symptomatic.
C. Pulmonary hypertension develops.
D. With worsening Left ventricular
hypertrophy and dilatation.
E. Endocarditis develops in the valves.
Mechanical correction should be
considered when the valve is 1 cm2 or less
in area.
Left ventricular hypertrophy is not
expected with isolated mitral stenosis.
Other causes for repair include systemic
embolization (usually from a-fib).
5. What is true concerning balloon
mitral valvuloplasty?
A. Treatment of choice in patients with pliable
valves, without calcification or deformation of the
chordae tendineae.
B. Contraindications include thickened, calcified
mitral leaflets and absence of any mitral
regurgitation.
C. Balloon inflation should increase the valve
area to greater than 4 cm2.
D. Mortality rate is 0.5-2% with total
complication rate of 3-6%.
E. Results compare favorably with surgical
valvuloplasty in appropriately selected patients.
5. What is true concerning balloon
mitral valvuloplasty?
A. Treatment of choice in patients with pliable
valves, without calcification or deformation of the
chordae tendineae.
B. Contraindications include thickened, calcified
mitral leaflets and absence of any mitral
regurgitation.
C. Balloon inflation should increase the valve
area to greater than 4 cm2.
D. Mortality rate is 0.5-2% with total
complication rate of 3-6%.
E. Results compare favorably with surgical
valvuloplasty in appropriately selected patients.
Moderate mitral regurgitation is a
contraindication for valvuloplasty.
An area of 2 cm2 should be achieved,
resulting in a significant decline in left atrial
pressure with 20% increase in CO.
Complications include systemic embolism,
cardiac perforation, and creation of mitral
regurgitation (1-2% complication rate for
each).
6. What is true concerning mitral
valve replacement?
A. The mitral valve should be replaced if dense
calcification precludes balloon valvuloplasty or
open commissurotomy.
B. Should be openly replaced if there is
concomitant mitral regurgitation.
C. The chordae tendineae should be divided,
especially when excessively shortened or
scarred.
D. Operative mortality is 1-2%.
E. The 5 year survival rate is 50-60%.
6. What is true concerning mitral
valve replacement?
A. The mitral valve should be replaced if dense
calcification precludes balloon valvuloplasty or
open commissurotomy.
B. Should be openly replaced if there is
concomitant mitral regurgitation.
C. The chordae tendineae should be divided,
especially when excessively shortened or
scarred.
D. Operative mortality is 1-2%.
E. The 5 year survival rate is 50-60%.
Efforts should be made to preserve the
posterior, and in some cases the anterior
leaflets and chordae tendineae; studies
have shown an advantage to left
ventricular function with preservation.
Operative mortality is 2-10%.
Five year survival rate is 70-90%.
7. Mitral regurgitation may be
caused by:
A.
B.
C.
D.
E.
F.
Rheumatic fever.
Trauma.
Myocardial infarction.
Endocarditis.
Hypertension.
Diseases of collagen formation.
7. Mitral regurgitation may be
caused by:
A.
B.
C.
D.
E.
F.
Rheumatic fever.
Trauma.
Myocardial infarction.
Endocarditis.
Hypertension.
Diseases of collagen formation.
Rheumatic fever remains the #1 cause
worldwide.
Chordal rupture can occur with trauma, MI,
endocarditis and collagen disorders.
Hypertension is not a known etiology of
mitral regurgitation.
8. Left ventricular ejection fraction
typically:
A. Increases with mitral regurgitation.
B. Decreases.
C. Remains the same.
8. Left ventricular ejection fraction
typically:
A. Increases with mitral regurgitation.
B. Decreases.
C. Remains the same.
Because the left ventricle is ejecting into
the aorta and left atrium, the EF is
increased, but the left ventricle ultimately
fails from chronic volume overload. Thus
relatively normal parameters of systolic
function (i.e. 40% EF) could indicate
significant contractile dysfunction.
9. Management of mitral
regurgitation includes:
A. Diuretics to decrease volume.
B. Inotropes to increase cardiac output.
C. ACE inhibitors to decrease afterload.
D. Nitroprusside in the setting of heart
failure from acute regurgitation.
E. Tylenol for the fevers.
9. Management of mitral
regurgitation includes:
A. Diuretics to decrease volume.
B. Inotropes to increase cardiac output.
C. ACE inhibitors to decrease afterload.
D. Nitroprusside in the setting of heart
failure from acute regurgitation.
E. Tylenol for the fevers.
The mainstay of medical treatment is
diuretics and ACE inhibitors.
Afterload reduction is key, since the blood
will flow down the path of least resistance.
There is no role for inotropes or tylenol in
mitral regurgitation (although tylenol is still
ok for fevers).
10. Indications for surgery in mitral
regurgitation include:
A. Ongoing symptoms despite medical
management.
B. An identified structural abnormality,
such as a ruptured chorda tendinea.
C. An EF of 20% or less.
D. An end-systolic diameter (ESD) of 60
mm or greater.
E. Development of pulmonary
hypertension.
10. Indications for surgery in mitral
regurgitation include:
A. Ongoing symptoms despite medical
management.
B. An identified structural abnormality,
such as a ruptured chorda tendinea.
C. An EF of 20% or less.
D. An end-systolic diameter (ESD) of 60
mm or greater.
E. Development of pulmonary
hypertension.
An EF of less than 60% suggests
myocardial dysfunction and operative
mortality increases. An ESD of 45 mm or
more makes for a worse prognosis after
surgery.
Thus even in the absence of symptoms
patients should be referred for surgery if
the EF is <60% or ESD is >45mm.
11. What is true regarding the
anatomy of the aortic valve?
A. The valve consists of three cusps.
B. Coronary arteries arise from each of the
three sinuses of Valsalva.
C. The coronary leaflets form commissures
over the anterior leaflet of the mitral valve
and the bundle of His.
D. The leaflets are divided into the left,
right, and posterior coronary leaflets.
E. The normal area of the valve is 1-2 cm2.
11. What is true regarding the
anatomy of the aortic valve?
A. The valve consists of three cusps.
B. Coronary arteries arise from each of the
three sinuses of Valsalva.
C. The coronary leaflets form commissures
over the anterior leaflet of the mitral valve
and the bundle of His.
D. The leaflets are divided into the left,
right, and posterior coronary leaflets.
E. The normal area of the valve is 1-2 cm2.
There are two coronary arteries that arise from
the sinuses: the left and right.
Thus the aortic leaflets are named after the
coronary arteries: the left coronary leaflet, the
right coronary leaflet, and the noncoronary leaflet.
The commissure between the left and
noncoronary leaflets sits over the anterior leaflet
of the mitral valve, while the commissure between
the right and noncoronary leaflets sits on the left
bundle of His.
Normal valve size is 3-4 cm2. Symptoms usually
arise at 1 cm2 with critical stenosis at 0.7 cm2.
12. Aortic stenosis may be caused
by:
A. Hypertension and the resultant left
ventricular hypertrophy.
B. Rheumatic fever.
C. Idiopathic.
D. Congenital valvular deformities.
E. Chronic steroid use.
12. Aortic stenosis may be caused
by:
A. Hypertension and the resultant left
ventricular hypertrophy.
B. Rheumatic fever.
C. Idiopathic.
D. Congenital valvular deformities.
E. Chronic steroid use.
Left ventricular hypertrophy is a result of aortic
stenosis, as the body compensates for the
increased pressure gradient across the valve.
There are unfortunately detrimental effects
including increased myocardial mass, increasing
oxygen demand, decreased ventricular
compliance leading to increased wall tension,
and thus decreased coronary artery flow. This all
leads to chronic ischemia, cell death, and
fibrosis.
Steroids have no known role in causing aortic
stenosis (and if there is I apologize, as I just
made this up).
13. The principle symptoms of
aortic stenosis are:
A.
B.
C.
D.
E.
F.
Headache.
Angina.
Palpitations.
Syncope.
Nightmares.
Dyspnea.
13. The principle symptoms of
aortic stenosis are:
A.
B.
C.
D.
E.
F.
Headache.
Angina.
Palpitations.
Syncope.
Nightmares.
Dyspnea.
The three principal symptoms are angina,
syncope, and congestive heart failure,
usually seen as dyspnea.
14. Viable treatment options for
symptomatic aortic stenosis in a
relatively healthy patient are:
A.
B.
C.
D.
E.
Balloon angioplasty of the valve.
Open valvuloplasty (commissurotomy).
Minimally invasive laser valvulotomy.
Replacement of the valve.
Medical management.
14. Viable treatment options for
symptomatic aortic stenosis in a
relatively healthy patient are:
A.
B.
C.
D.
E.
Balloon angioplasty of the valve.
Open valvuloplasty (commissurotomy).
Minimally invasive laser valvulotomy.
Replacement of the valve.
Medical management.
Surgical replacement of the valve is the
only solution with an acceptable long term
outcome.
“The only potential role of aortic balloon
valvuloplasty may be in aged, frail, and
possibly senile patients whose long-term
survival is poor.”
Answer C is complete nonsense.
15. Aortic insufficiency may be
caused by:
A.
B.
C.
D.
E.
Mixoid degeneration of the aortic root.
Trauma.
Rheumatic fever.
Endocarditis.
Annuloaortic ectasia.
15. Aortic insufficiency may be
caused by:
A.
B.
C.
D.
E.
Mixoid degeneration of the aortic root.
Trauma.
Rheumatic fever.
Endocarditis.
Annuloaortic ectasia.
Mixoid degeneration in Marfan’s, EhlersDanlos, and cystic medial necrosis.
Annuloaortic ectasia is an idiopathic
dilatation of the aortic root and annulus,
and is the most reason for aortic
insufficiency despite normal leaflet
morphology.
16. Treatment options for aortic
insufficiency include:
A. Observation and close monitoring for
patients with mild to moderate regurgitation who
are asymptomatic.
B. Medical treatment with diuretics and
afterload reduction agents in symptomatic
patients.
C. Valve replacement before the left ventricle
reaches 55 mm Hg in end-systolic volume.
D. Valve replacement once the end systolic
volumes have reached 90 mL/m2 or greater.
E. Valve replacement in symptomatic patients.
16. Treatment options for aortic
insufficiency include:
A. Observation and close monitoring for
patients with mild to moderate regurgitation who
are asymptomatic.
B. Medical treatment with diuretics and
afterload reduction agents in symptomatic
patients.
C. Valve replacement before the left ventricle
reaches 55 mm Hg in end-systolic volume.
D. Valve replacement once the end systolic
volumes have reached 90 mL/m2 or greater.
E. Valve replacement in symptomatic patients.
Pts with mild to moderate regurgitation have a
10 yr survival rate of 85-95%. These pts can be
followed with serial echocadiography or nuclear
studies.
They should be maintained on diuretics and
afterload reducers, but once symptoms develop,
it means that the multiple compensatory
mechanisms have failed and medical
management is not enough.
To achieve optimal results valve replacement
should take place before the left ventricle has
undergone irreversible dilitation.
End