3. Valvular heart disease accounts for 10% to 20% of all
cardiac surgical procedures in the United States.
Mitral stenosis- clinical observation in our set up.
About two thirds of all heart valve operations are for
aortic valve replacement (AVR), most often for aortic
stenosis (AS).
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5. Which of the following lesions are most
common in females?
A. MR
B. MS
C. AS
D. PS
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6. The most common cause of mitral stenosis is ?
A. Rheumatic valve disease
B. degenerative valve disease
C. Infective endocarditis
D. connective tissue disease
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7. 1. Rheumatic heart disease:
Leading cause of mitral stenosis
50 to 70 %of patients report a
history of rheumatic fever.
Rare in developed but ……..
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8. isolated MS : ~25 %
combined MS and MR: ~40 %
Multivalve involvement ~ 38 % of MS
patients
(AV = 35 % and the TV in 6 %, PV =
rarely)
Two thirds ….female
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9. Evidences – majority due to RHD
Mayo clinic- 452 MS patients 99% has
post inflammatory disease on surgical
pathology.
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11. Rheumatic fever affects all layers of
the heart? T/F
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12. classic pattern of "doming" of the leaflets
obliteration of the normal leaflet architecture
inflammation and edema of the leaflets
ARF
Disease progression results in a number of pathologic changes
affecting the mitral valve apparatus, which are diagnostic for
rheumatic valve disease :
Fusion of the leaflet commissures
Thickening, fusion and shortening of the
chordae tendineae
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13. continues about whether ?
1.Recurrent episodes of rheumatic fever or
2. From a chronic autoimmune process caused by
cross-reactivity between a streptococcal protein and
valve tissue or
3.whether calcific valve disease is superimposed.
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14. Evidence supporting recurrent infection as an
important factor in disease progression .
- Correlation between the geographic variability in
the prevalence of rheumatic heart disease and
- The age at which patients present with severe MS.
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20. 32 years old female came with dyspnea of 1
week duration .on exam has accetauted P2,
soft s1 and holo diastolic rumbling murmur at
the apex. which of the clinical findings
showes severity ?
A. P2 accentaution
B. Holodiastolic murmur
C. Soft S1
D. All
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22. 20 years old female patient who has been
complaining of hemoptysis and dyspnea for
the last 6 months. On further history she gave
dysphagia and change of voice the last 2
months. On exam has mid diastolic murmur at
the apex ?which symptoms are most common
in such mitral stenosis patients?
A. hemoptysis
B. Dyspena
C. Dysphasia
D. chanage of voice
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23. VARIABEL IN DIFFERENT GEOGRAPHIC AREAS- A) TIME TO
PRESENTATION
In a prospective study of 159 patients with MS from Germany, the
following observations were noted : AFTER 25 YRS OF ARF
The mean interval - rheumatic fever and the onset of
symptoms was 16.3 year
Sales
NYHA-IV
NYHA-III
NYHA-III
ASSY
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24. DYSPNEA -70% + cough and wheezing:
May be caused by a reduced ability to increase cardiac
output normally with exercise or elevated pulmonary
venous pressures and reduced pulmonary compliance
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26. OTHER SYMPTOMS:
hoarseness - Ortner's syndrome or
cardiovocal syndrome
Systemic Venous hypertension,
hepatomegaly, edema, ascites, and
hydrothorax (signs of right-sided heart
failure).
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27. 41 years of old man presented with fever and
joint pain of three days duration .up on exam
has macular lesions at the palms with
yellowish to brownish discoloration at the nail
beds of both hands. he was seen at the
emergency was given ant pain and go home
.one day later he came with un able to speak
with facial deviation and high grade fever. Ecg
–NSR, echo showed mild to moderate MS ,
mild MR and AR vegetation on AORIC VALVE.
How do you manage this patient.
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28. Clinical predictors of embolic events ?
The predictors of embolic events in
(MS,MVA,2cm and NSR) in 132 pts.
There were three major clinical and
echocardiographic predictors of embolism:
Left atrial thrombus
The degree of reduction in mitral valve area
Significant aortic regurgitation
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29. NB.
Transient AF and infective
endocarditis should also be
considered when embolization
occurs in patients with mitral
stenosis who are in sinus rhythm
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30. Other than auscultator findings
mitral facies (pinkish-purple patches on the
cheeks)
The arterial pulses are reduced in volume due
to ↓stroke volume
a prominent "a" wave (atrial contraction or
systole) in JVP.
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31. PRECORIAL EXAMINATION
API - generally normal, although it may
be reduced in intensity due to ↓ LV- filling.
Heart sounds (s1↑) , s3-never => s4
possible
Opening snap - best heard at the apex
and lower left sternal border (abrupt halt
in leaflet motion in early diastole, after
rapid initial rapid opening).
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32. A short A2-OS interval : is a reliable indicator of
severe MS
Murmur of MS : a low-pitched, rumbling, diastolic
murmur
In severe MS the murmur is holodiastolic, with
presystolic accentuation (duration of murmur
correlates with the severity of the stenosis but not
the intesity)
In so-called “silent” MS, there is usually marked RV
enlargement. Consequently, not audible at all or can
be heard only in the MAL or posterior axillary line.
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33. Maneuvers
The diastolic murmur and OS are ↓ inspiration,
↑ with expiration (in contrast to tricuspid
stenosis).
With inspiration, the A2-OS interval widens and
a distinct P2 may be heard.
=>Increasing venous return - ↑ but os-A2-
shortens
murmurs MS & PHN …Graham Steell
murmur(PR), murmur of TR (+ve carvallo’s sign)
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34. ECG-
The QRS amplitude and morphology are normal
unless there is mitral regurgitation or coexistent
aortic valve disease.
Left atrial hypertrophy and enlargement results in a P
wave that becomes broader (duration in lead II >0.12
sec), is of increased amplitude, and is notched (due to
the delay in left atrial activation). This is termed "
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36. P-mitrale."
The left atrial changes also produce a prominent
negative terminal portion of the P wave in lead
V1.
The P waves changes are not seen in patients
with atrial fibrillation.
The fibrillatory waves are coarse, generally >0.1
mV in amplitude, reflecting LAE
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38. Other radiologic findings
Interstitial edema (lung), an indication of
severe obstruction, is manifested as Kerley B
lines (dense, short, horizontal lines most
commonly seen in the costophrenic angles).
Severe, longstanding mitral obstruction often
results in Kerley A lines (straight, dense lines
up to 4 cm in length running toward the
hilum),
pulmonary hemosiderosis and rarely of
parenchymal ossification
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41. 1. Provides determination of the etiology of stenosis.
2. Evaluation of the detailed morphology of the valve
apparatus.
3. Measurement of valve orifice, and evaluation of
subvalvular structures, particularly the chordae
and papillary muscles.
4. Doppler echocardiography provides accurate
assessment of the trans valvular gradient and
MVA
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45. The two largest series followed a combined
total of 153 adults, with a mean age of
approximately 60 years, for an average of
slightly more than 3 years.
As in most series of MS patients, 75% to 80%
were women.
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46. From153 patients:
The initial valve area was 1.7 ± 0.6 cm2 and the
overall rate of progression was a decrease in
valve area of 0.09 cm2/yr.
Approximately one third of patients showed
rapid progression, defined as a decrease in valve
area greater than 0.1 cm2/yr.
Data in developing countries is not known
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48. AGE IN
YRS
% AF in
MS
21-30 17
31-40 45
41-50 60
>50 80
Even when MS is severe,
the prevalence of AF is
related to age.
In more recent BMV
studies,
4% in a series of 600
patients from India, with a
mean age of 27 yrs
27% in a series of 4832
patients from China, with a
mean age of 37 years
40% in a series of 1024
patients from France, with a
mean age of 49 yrs
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49. Systemic embolism - (80% -AF & 20% NSR)
45% MS pts with NSR have – SEC on TEE
50%-in brain…..HEART….RENAL
25%----Recurrence
IE- rare <1%
0.17/1000 patient-years, which is much lower
than the risk in patients with MR or AVD
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51. Objective
1.Monitoring disease progression to allow
intervention at the optimal time point (Echo yearly if
severe MS or as indicated)
2.prevention and treatment of complications of MS:
congestion, systolic dysfunction, arrhythmia or AF,
infection, Thromboembolism
3.prevention of recurrent rheumatic fever
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52. Evaluation and follow up of
Asymptomatic MS pts
SEVERITY OF
MS
CLINICAL ECHO
MILD ANNUALLY 3-5 YRE
MODERATE ANNAULLY 1-2 YRS
SEVER ANNAULLY ANNUALLY
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53. Exercise should be decreased.
Diuretics.
Beta blockers. (In pts with FC II and III
HF) , not in asymptomatic pts.
Digoxin. ( In pts with AF )
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56. BMV is recommended for
symptomatic patients with moderate to severe MS
(i.e., a mitral valve area < 1 cm2/m2 body
surface area [BSA] or <1.5 cm2 in normal-sized
adults)
with favorable valve morphology, no or mild MR,
and no evidence of left atrial thrombus .
SYMPTOMATIC WITH HIGH RISK FOR SURGERY
EG. restenosis after a previous BMV or previous
commissurotomy who are unsuitable for surgery .
PREGNANT WOMEN
SYMPTOMATIC WITH NEW ONSET AF
ASSYMPTOMATIC PTS WITH SEVER PHT
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57. ◦ Indicated in:
Combined MS & moderate or severe MR
Extensive commisural calcification, severe
fibrosis and subvalvuar fusion
in those who have undergone previous
valvotomy
-Disadv:
structural deterioration of biprosthetic
valves
Hazards of life long anticoagulation
-Operative mortality ~6.4%
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63. Left ventricular outflow obstruction is often due to
Valvular aortic stenosis ( most common cause )
Subvalvular aortic stenosis eg …. due to HOCMP
Supravalvular aortic stenosis
Valvular Aortic Stenosis
Rheumatic AS ( most common worldwide)
AS is found in ¼ of patients with RHD.
Degenerative calcific AS (most common in the
developed countries)
Congenital AS ( unicuspid or Bicuspid)
approximately 80% of adult patients with
symptomatic valvular AS are males.
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64. About 30% of persons
>65 years exhibit aortic
valve sclerosis
while 2% exhibit frank
stenosis..
It appears to be a marker
for an ↑ed risk of CHD
events.
risk factors for
atherosclerosis
such as age, male sex,
smoking
diabetes mellitus,
hypertension chronic
kidney disease, increased
LDL, reduced HDL
cholesterol, and elevated
C-reactive protein are all
risk factors for aortic
valve calcification. 9/1/2023 64
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67. there is growing consensus that
“degenerative” calcific AS shares
many pathophysiological features
with atherosclerosis and that
specific pathways might be
targeted to prevent or retard
disease progression.
Hence more evidences needed to prove benefit!
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68. more prevalent in men (70 to 80%)
~20 %: develop severe AR requiring AVR
between 10 and 40 years of age
often associated with dilatation of the
ascending aorta
risk of aortic dissection in patients with a
bicuspid AV is five to nine times higher than
the general population
most patients develop calcific AV stenosis later
in life (after 50 yrs of age)
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70. common in developing countries
Results from adhesions and fusions of the commissures and
cusps and vascularization of the leaflets of the valve ring,
leading to retraction and stiffening of the free borders of the
cusps
Calcific nodules develop on both surfaces, and the orifice is
reduced to a small round or triangular opening
As a consequence, the rheumatic valve is often regurgitant,
as well as stenotic
NB. Patients with rheumatic AS invariability have rheumatic
involvement of the mitral valve
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71. over the course of many years, LV output is maintained
by the presence of concentric LVH.
Initially, this serves as an adaptive mechanism because it
reduces toward normal the systolic stress developed by
the myocardium, as predicted by the Laplace relation:
pressure(P) X radius (r) = systolic wall stress (S )
wall thickness (h).
A large transaortic valvular pressure gradient may exist
for many years without a reduction in CO or LV dilatation;
ultimately, however, excessive hypertrophy becomes
maladaptive, and LV function declines.
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73. cardinal manifestations:
exertional dyspnea, angina pectoris, syncope,
and ultimately heart failure
Symptoms typically occur at age 50 to 70 years
with bicuspid aortic valve stenosis and at older
than age 70 years with calcific stenosis of a
trileaflet valve.
Syncope
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74. severe AS: “parvus and tardus” carotid
impulse
cardiac impulse is sustained and becomes
displaced inf. and later.
A hyperdynamic left ventricle suggests
concomitant AR and/or MR
In patients with calcified aortic valves, the systolic murmur
is loudest at the base of the heart, but high-frequency
components may radiate to the apex called Gallavardin
phenomenon
With severe AS, S2 may be single. Paradoxical
splitting
S1 is normal or soft and S4 is prominent
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75. DYNAMIC AUSCULTATION:
The murmur is augmented by squatting,
which increases stroke volume.
It is reduced in intensity during the strain of
the Valsalva maneuver and when standing,
which reduce transvalvular flow.
AR (which coexists in about 75% of patients
with predominant AS)
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76. slow↑ in carotid pulse
Mild to late peak of the
mermur
Decrease intensity of
S2
Max intensity at 2nd ICS
patients with 3 out of 4 were very likely to have
AS
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77. ECG
LVH ( 85% of patients with severe AS)
correlation between the absolute ECG voltages in precordial leads and the
severity of obstruction is poor in adults
left atrial enlargement
atrioventricular and intraventricular block
Evaluation of cause of AS and the severity of
valve calcification
evaluation of LVH and systolic function,
measurement of the transaortic jet velocity
Effective orifice area
Echocardiograp
hY
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78. CHEST RADIOGRAPHY:
the heart is usually of normal size or slightly enlarged, with a rounding of the LV border and apex
Dilatation of the ascending aorta
The left atrium may be slightly enlarged
signs of pulmonary venous hypertension
CARDIAC CATHETERIZATION AND ANGIOGRAPHY:
CHEST COMPUTED TOMOGRAPHY:
To asses AV calcification, & aortic dilation
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79. ASYMPTOMATIC PATIENTS:
long latent period (mild to mod stenosis)
Once moderate to severe stenosis is present, prognosis
remains excellent as long as the patient remains
asymptomatic.
SYMPTOMATIC PATIENTS:
poor prognosis with an average survival of only 1 to 3 years
after symptom onset
(angina pectoris, 3 years; syncope, 3 years; dyspnea, 2 years;
congestive heart failure, 1.5–2 years).
HEMODYNAMIC PROGRESSION :
annual decrease in AVA of 0.12 cm2/year, and an increase in
mean gradient of 7 mm Hg per year
factors associated with more rapid hemodynamic progression: older age, more
severe leaflet calcification, renal insufficiency, hypertension, smoking and
hyperlipidemia.
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81. In patients with severe AS (<1.0 cm2),
strenuous physical activity should be
avoided, even in the asymptomatic stage.
Care must be taken to avoid dehydration
and hypovolemia to protect against a
significant reduction in CO
PREVENTION OF DISEASE PROGRESSION:
◦ RHD: rheumatic fever prophylaxis
◦ Degenerative: ? statin therapy
CORONARY ARTERY DISEASE:
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82. severe symptomatic AS AVR
However, medical therapy may be necessary in
patients who are considered to be inoperable.
diuretics
ACE inhibitors should be used with caution but are
beneficial in treating patients with symptomatic LV
systolic dysfunction who are not candidates for
surgery
Beta-adrenergic blockers can depress myocardial
function and induce LV failure and should be avoided
in patients with AS.
AF-10 %
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83. AORTIC STENOSIS WITH LEFT VENTRICULAR DYSFUNCTION.
Surgical risk is higher in patients with impaired LV function (EF <
35%)
prognosis is extremely poor without operation, OS is improved
with AVR
The role of TAVI for severe AS with significant LV systolic
dysfunction has not been studied
AVR
Operation should, if possible, be carried out before frank LV failure
develops
Operative risk- 2% to 5% in <70yrs…<1%
If late stage:
high operative risk (15 to 20%)
Furthermore, long-term postoperative survival also correlates inversely
with preoperative LV dysfunction .
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The ensuing acute inflammatory process can lead to commissural adhesion prior to the more common degenerative sequelae
Dyspnea initially occurs with any condition that requires an increase in blood flow across the mitral valve or that reduces the time for such blood flow to occur (ie, diminishes the duration of diastole.
Lv f
Calcific aortic valve disease without a significant gradient (defined as an aortic jet velocity ≤ 2.5 m/sec) is called aortic valve sclerosis