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PRESSURE OVERLOAD
LESIONS
• Pressure overload to the Ventricle
– AS, PS
– HCM, Subaortic AS and Infundibular PS
– Supra-aortic and Supra-pulmonic PS
• Pressure Overload to the Atria
– Mitral Stenosis
– Tricuspid Stenosis
AORTIC STENOSIS
VOLUME OVERLOAD
LESIONS
• Ventricular Volume Overload
– AR and PR
• Atrial Volume Overload
– Mitral and tricuspid regurgitation
MITRAL REGURGITATION
PRESSURE OVERLOAD
LESIONS-VENTRICULAR
• Ventricular hypertrophy in response to AS or PS
• Dilatation may occur if hypertrophy is inadequate,
apoptosis occurs, or fibrous tissue replacement
• Atrial dilatation occurs in response to ventricular
hypertrophy with systemic or pulmonary venous
hypertension often related to reduced relaxation
and compliance from ventricular hypertrophy and
increases interstitial myocardial fibrous tissue
PRESSURE OVERLOAD
LESIONS-VENTRICULAR
• Symptoms are of LVOT or RVOT
obstruction
• AS: DOE, angina, syncope on effort
• PS: fatigue, angina, syncope on effort
PRESSURE OVERLOAD
LESIONS-VENTRICULAR
• LVOT or RVOT murmur
– SEM: AS-2nd RICS to carotid
PS-3rd LICS
– PMI heave and S4
VOLUME OVERLOAD
LESIONS
• Both AR and MR affect the LV as a volume
overload
• AR is a direct volume overload and MR is due to
excessive atrial filling
• The LV dilates and hypertrophies eccentrically;
atrial dilatation ensues with LA hypertension*,
and pulmonary venous congestion*
• Right heart dilatation then ensues*
• *The rate at which these effects occur on the
atrium and right heart depend on whether the
volume overload is directly to the atria or not.
VOLUME OVERLOAD
LESIONS
•
•
•
•
•
Displaced PMI
S3
Diastolic filling murmur across mitral valve
Regurgitant murmur
Right heart findings:
– JVD
– Enlarged and pulsatile liver
– edema
VOLUME OVERLOAD
LESIONS
•
•
•
•
Dyspnea on exertion
Palpitations
Angina
Syncope-Arrthymogenic
Patient presents with 3/6 systolic murmur
difficult to determine if holosystolic or not at
the LLSB.
• Which of the following diagnostic tests is
most appropriate and will provide you and
with the most useful information?
–
–
–
–
CT angiography
Cardiac catheterization and angiography
Comprehensive cardiac MR imaging
Transthoracic echocardiography
Diagnostic Testing
• Echocardiography: (repeat 6 months to 1 year, 1-2
years, or >3 years for mild, moderate or severe disease)
–
–
–
–
Severity of the valve lesion-Doppler
Presence of pulmonary hypertension
Co-existent lesions
Alterations of chamber size and function
• Exercise testing: functional capacity, changes in
gradients and degree of regurgitation
• B Natiuretic peptide-prognostic in AR, AS, and MR
• Cardiac Catheterization-hemodynamics if echo data
questionable and coronary arteriography
ETIOLOGY OF VALVAR AS
EXCISED AS VALVE
VALVULAR AS
• Calcific or senile degenerative-shares feature with
CAD and other vascular disease
– Active process
– Inflammatory
– Calcium deposition
• Bicuspid-manifests in 50’s
• Rheumatic-with mitral disease
• Congenital-younger
BICUSPID AV
PHYSIOLOGIC RESPONSE TO AS
• LV response to AS
– LVH to normalize wall stress Stress=R/WT*P
• Generate sufficient force to overcome valve narrowing
(occurs at 50% of valve area ie 1.5 cm2)
– Concentric hypertrophy: Radius/Wall Thickness is low;
increased interstitial fibrosis-leading to dyspnea
– Late: LV dilatation and dysfunction (> in men)
• Left atrial enlargement
• Right side normal unless RHD or late
76 year old male
• Patient with known systolic murmur though
to be AS and determined as moderate to
severe by echo 1 year ago presents with
angina. How would you evaluate the
angina?
–
–
–
–
Stress echo
Exercise Nuclear stress testing
PET imaging with adenosine stress
Coronary Angiography
HISTORY
• Angina: Thick muscle difficult to perfuse
especially with increased fibrosis and CAD also
present in >50% of patients; need coronary
angiography
• Syncope on effort: can not increase cardiac output
due to orifice obstruction and peripheral
vasodilatation from high LV wall stress
• DOE: LV dysfunction, dilatation and reduced
relaxation and elevated LV filling pressures
• 5 yr survival: 50%, 30%, 20%
• Survival is not impaired if no symptoms but
symptoms related to severity
81 year old female
• Patient with history of mild AS 10 years
ago presents with increasing dyspnea. She
has been found to have peak velocity across
the aortic valve of 4.2 m/s
• Why does she have dyspnea?
– Coronary ischemia due to LVH and inability to
perfuse the subendocardium
– LV dysfunction
– Impaired relaxation and increased myocardial
LV stiffness (reduced LV chamber compliance)
– Increased fraility with age
HISTORY
• Angina: Thick muscle difficult to perfuse especially with
increased fibrosis and CAD also present in >50% of
patients; need coronary angiography
• Syncope on effort: can not increase cardiac output due to
orifice obstruction and peripheral vasodilatation from high
LV wall stress
• DOE: LV dysfunction, dilatation and reduced relaxation
and reduced LV compliance and elevated LV filling
pressures
• 5 yr survival: 50%, 50%, 20%
• Survival is not impaired if no symptoms but symptoms
related to severity
Physical Exam
• Carotid upstroke : reduced and a shudder on
upstroke; transmitted murmur
• SEM upper LSB and RSB radiating to the neck
and carotid (R)
– May be heard at LLSB
– Thrill; A2 reduced, paradoxical splitting
• Congestion and edema are late findings unless
rheumatic
• Rhythm is sinus unless late or RHD
IMAGING THE VALVE IN AS
• 2D:
– SAX: 3 chunks of calcium that barely
move: works better with TEE where AVA
can be planimetered
– LAX: 2 chunks of calcium that barely move
Peak gradient overestimates gradient
Mean gradient agrees well with
invasive gradients.
LVOT/AV VELOCITY
Stages of Valvular Aortic Stenosis
Stage
A
Definition
At risk of AS
Valve Anatomy
●
●
B
Progressive
AS
●
●
Bicuspid aortic
valve (or other
congenital valve
anomaly)
Aortic valve
sclerosis
Mild-to-moderate
leaflet calcification
of a bicuspid or
trileaflet valve with
some reduction in
systolic motion or
Rheumatic valve
changes with
commissural fusion
Valve
Hemodynamics
● Aortic
Vmax <2 m/s
●
●
Mild AS: Aortic
Vmax 2.0–2.9
m/s or mean
P <20 mm Hg
Moderate AS:
Aortic Vmax
3.0–3.9 m/s or
mean P 20–
39 mm Hg
Hemodynamic
Consequences
● None
●
●
Early LV
diastolic
dysfunction
may be
present
Normal LVEF
Symptoms
●
None
●
None
Stages of Valvular Aortic Stenosis
Stage
Definition
Valve Anatomy
C - Asymptomatic severe AS
C1
Asymptomatic ● Severe leaflet
severe AS
calcification or
congenital
stenosis with
severely
reduced leaflet
opening
C2
Asymptomatic
severe AS with
LV
dysfunction
●
Severe leaflet
calcification or
congenital
stenosis with
severely
reduced leaflet
opening
●
●
●
●
●
Valve
Hemodynamics
Hemodynamic
Consequences
Aortic Vmax 4 m/s
or mean P ≥40
mm Hg
AVA typically is
≤1 cm2 (or AVAi
0.6 cm2/m2)
Very severe AS is
an aortic Vmax
≥5 m/s, or mean
P ≥60 mm Hg
Aortic Vmax ≥4 m/s
or mean P ≥40
mm Hg
AVA typically is
≤1 cm2 (or AVAi
0.6 cm2/m2)
●
Symptoms
●
●
LV diastolic
dysfunction
Mild LV
hypertrophy
Normal LVEF
None–
exercise
testing is
reasonable
to confirm
symptom
status
●
LVEF <50%
●
None
●
Stages of Valvular Aortic Stenosis
Stage
Definition
Valve Anatomy
D - Symptomatic severe AS
D1
Symptomatic ● Severe leaflet
severe highcalcification or
gradient AS
congenital
stenosis with
severely
reduced
leaflet opening
D2
Symptomatic
severe lowflow/lowgradient AS
with reduced
LVEF
● Severe
leaflet
calcification
with severely
reduced
leaflet motion
Valve Hemodynamics
● Aortic
Hemodynamic
Consequences
Vmax ≥4 m/s, or
mean P ≥40 mm Hg
● AVA typically is 1 cm2 (or
AVAi 0.6 cm2/m2), but
may be larger with mixed
AS/AR
● LV
● AVA 1
● LV
cm2 with resting
aortic Vmax <4 m/s or mean
P <40 mm Hg
● Dobutamine stress echo
shows AVA 1 cm2 with
Vmax 4 m/s at any flow
rate
diastolic
dysfunction
● LV hypertrophy
● Pulmonary
hypertension may
be present
diastolic
dysfunction
● LV hypertrophy
● LVEF <50%
Symptoms
● Exertional
dyspnea or
decreased
exercise
tolerance
● Exertional
angina
● Exertional
syncope or
presyncope
● HF,
● Angina,
● Syncope or
presyncope
Stages of Valvular Aortic Stenosis
Stage
Definition
Valve Anatomy
D - Symptomatic severe AS
D3
Symptomatic ● Severe leaflet
severe lowcalcification
gradient AS
with severely
with normal
reduced leaflet
LVEF or
motion
paradoxical
low-flow
severe AS
Valve
Hemodynamics
● AVA 1
cm2 with
aortic Vmax <4 m/s,
or mean P <40
mm Hg
● Indexed AVA 0.6
cm2/m2 and
● Stroke volume
index <35 mL/m2
● Measured when
the patient is
normotensive
(systolic BP <140
mm Hg)
Hemodynamic
Consequences
● Increased
LV
relative wall
thickness
● Small LV chamber
with low-stroke
volume.
● Restrictive diastolic
filling
● LVEF ≥50%
Symptoms
● HF,
● Angina,
● Syncope
or
presyncope
AVA by TEE
NATURAL PROGRESSION OF AS
• Yearly progression
– 0.32 m/s/yr
– 7 mm Hg/yr (mean gradient)
– 0.12 cm2/yr loss of AVA
• If peak velocity > 4m/s, 21% 2yr survival
without AVR
• If mild, moderate, or severe AS, repeat
studies in 3-5, 1-2, 6 months-1 year
MEDICAL THERAPY OF AS
• Treat hypertension and increased lipids
– Benefit to treating hypertension as it reduces total hemodynamic
load
– Benefit for hyperlipidemia relates more to concomitant CAD and
not progression of AS
•
•
•
•
Angina: none
Syncope: limit activity
CHF: diuresis, digoxin??
Valvuloplasty: works for 6 months
– Bridge for noncardiac surgery
– Short term symptom relief
Indications for Aortic Valve Replacement in Patients With Aortic Stenosis
Aortic Stenosis: Choice of Surgical or
Transcatheter Intervention
Recommendations
COR LOE
Surgical AVR is recommended in patients who meet
an indication for AVR (listed in Section 3.4) with low
I
A
or intermediate surgical risk
For patients in whom TAVR or high-risk surgical AVR
is being considered, members of a Heart Valve Team
I
C
should collaborate closely to provide optimal patient
care
TAVR is recommended in patients who meet an
indication for AVR for AS who have a prohibitive
I
B
surgical risk and a predicted post-TAVR survival >12
months
Aortic Stenosis: Choice of Surgical or
Transcatheter Intervention (cont.)
Recommendations
COR LOE
TAVR is a reasonable alternative to surgical AVR for
AS in patients who meet an indication for AVR and
IIa
B
who have high surgical risk
Percutaneous aortic balloon dilation may be
considered as a bridge to surgical or transcatheter
IIb
C
AVR in severely symptomatic patients with severe
AS
TAVR is not recommended in patients in whom the
III: No
B
existing comorbidities would preclude the expected
Benefit
benefit from correction of AS
Etiology of Chronic Aortic Regurgitation
• 9-14% of all valve disease with a male predominance
• Valvular
– Usual Causes of AS (including bicuspid due to prolapse and
incomplete closure)
– Rheumatic
– VSD
– Myxomatous degeneration of leaflets
– SLE, RA, Ankylosing Spondylititis
– Endocarditis
• Aortic Root (increasing in past few years and >50%)
Etiology of Chronic Aortic Regurgitation
• Valvular
• Aortic Root-dilatation of the root pulling leaflets apart
and may lead to changes in valve cusps from the stress
and additional AR
–
–
–
–
–
–
–
Age related and hypertension
Cystic medial necrosis-including Marfans’ Disease
Associated with bicuspid valve disease
Subaortic stenosis
Aortitis
Giant Cell arteritis
Aortic Dissection
PATHOPHYSIOLOGY
• LV response to AR: Both preload and afterload response
– Entire stroke volume ejected into high pressure
chamber. Compensation provided by increased end
diastolic volume. LV dilates to >6cm for EDD
– Eccentric LVH to normalize wall stress but results in
increased collagen content; PWT usually < 13 mm
• Adaptation results in the LV acting as a high
compliance pump with little change in LVEDP
• Over time, wall thickening does not keep pace with
end diastolic wall stress resulting in afterload
mismatch and EF falls, LV volume and LVEDP
rises.
Pathophysiology of Acute AR
• Large regurgitant volume reenters a small noncompensated LV
• Acute volume overload dilates the LV leading to high
LVEDP
• Early mitral valve closure as LVEDP exceeds LAP-may
get diastolic MR
• Pulmonary edema
• Increase demand, shortened diastolic filling time, low
diastolic pressures reducing coronary perfusion pressure
resulting in reduced coronary blood flow and ischemia
• Reduced LV function may ensue
Pathophysiology of Acute AR
CHRONIC AORTIC REGURGITATION:
History has similarities to AS
• Asymptomatic for long periods of time-symptoms
develop with myocardial ischemia or reduced cardiac
reserve
• Angina-difficult to perfuse thickened myocardium;
especially with a dilated cavity with increased wall
stress and low diastolic pressures
• Dyspnea on exertion: hypertrophy and fibrosis result in
elevated LV filling pressures with exertion. Often LVEF
still preserved
• Palpitations can be troublesome due to ventricular
ectopy and a sense of pounding in the chest due to
volume overload. Syncope is arrhythmia related.
PHYSICAL EXAM
• Carotid upstrokes are increased and are bisfierens (bifid)
• Displaced and diffuse PMI - thrill may be felt at the base
• A2 is variable based on valve (soft) or root disease
(normal)
• Diastolic decrescendo murmur at the 3rd LICS or RICS.
– Longer duration correlated with greater severity. Harsh systolic flow murmur
is also heard at the base.
– S3 may be heard at LV apex and early diastolic rumble (Austin Flint)
• Peripheral pulses bounding and high pulse pressures
(160/60); other peripheral signs of AR
• Congestion and edema are late findings
CHEST X-RAY and EKG
Cardiomegaly is common finding
Assessment by Echocardiography
•
•
•
•
•
Valve anatomy
Root anatomy
Demonstration of AR
Quantification of AR
Effect on chamber size
Aortic Regurgitation
Aortic Root Dilatation with Noncoronary
Cusp Malcoaptation
Natural History of Chronic Aortic Regurgitation
• Normal LV function: 45% are asymptomatic at 10
years
– 3.5% yearly rate of development of LV systolic
dysfunction
– 6% yearly rate of the development of LV systolic
dysfunction or symptoms
– Low sudden death rate if asymptomatic
•
•
•
•
•
If LV dysfunction-25% yearly rate to symptoms
If symptoms 10% yearly mortality
Angina-4 year survival
Heart failure- 2 year survival
Dujardin: 4 year survival with CHF=30%
Survival in Chronic AR: NYHA
Survival in Chronic AR: EF
Management of Chronic AR
• No endocarditis prophylaxis
• Follow-up echocardiography for mild to moderate AR
12-24 months
• Follow-up for severe AR with normal function every 6
months
• Limit vigorous activity in patients with LV dysfunction
and limited cardiac reserve
• Treat hypertension to reduce regurgitant flow with
nifedipine and ACEI
• Treat rapid tachyarrhythmias vigorously as they are
poorly tolerated
Symptomatic AR
• Treat heart failure in the standard fashion to
stabilize patients and improve surgical risk
– Digoxin may be more useful
– Beta blockers may be less useful
• Nitrates for angina may help (reduced LV
filling pressures)
• AVR is the preferred therapy
Stages of Chronic Aortic Regurgitation (cont.)
Stage
C
Definition
Asymptomatic
severe AR
Valve Anatomy Valve Hemodynamics
●
●
●
●
●
Calcific aortic
valve disease
Bicuspid valve
(or other
congenital
abnormality)
Dilated aortic
sinuses or
ascending aorta
Rheumatic
valve changes
IE with
abnormal leaflet
closure or
perforation
●
o
o
o
o
o
o
o
o
Severe AR:
Jet width ≥65% of
LVOT
Vena contracta
>0.6 cm
Holodiastolic flow
reversal in the
proximal abdominal
aorta
RVol ≥60 mL/beat
RF ≥50%
ERO ≥0.3 cm2
Angiography grade
3+ to 4+
In addition, diagnosis
of chronic severe AR
requires evidence of
LV dilation
Hemodynamic
Consequences
C1: Normal LVEF
(50%) and mild-tomoderate LV dilation
(LVESD 50 mm)
C2: Abnormal LV
systolic function with
depressed LVEF
(<50%) or severe LV
dilatation (LVESD >50
mm or indexed LVESD
>25 mm/m2)
Symptoms
●
None;
exercise
testing is
reasonable
to confirm
symptom
status
Stages of Chronic Aortic Regurgitation (cont.)
Stage
D
Definition
Symptomatic
severe AR
Valve Anatomy
●
●
●
●
●
Calcific valve
disease
Bicuspid valve
(or other
congenital
abnormality)
Dilated aortic
sinuses or
ascending aorta
Rheumatic valve
changes
Previous IE with
abnormal leaflet
closure or
perforation
Valve Hemodynamics
●
o
o
o
o
o
o
o
o
Severe AR:
Doppler jet width ≥65%
of LVOT;
Vena contracta >0.6
cm,
Holodiastolic flow
reversal in the proximal
abdominal aorta,
RVol ≥60 mL/beat;
RF ≥50%;
ERO ≥0.3 cm2;
Angiography grade 3+
to 4+
In addition, diagnosis
of chronic severe AR
requires evidence of
LV dilation
●
●
Hemodynamic
Symptoms
Consequences
Symptomatic severe ● Exertional
AR may occur with
dyspnea or
normal systolic
angina, or
function (LVEF
more
severe HF
50%), mild-tomoderate LV
symptoms
dysfunction (LVEF
40% to 50%) or
severe LV
dysfunction (LVEF
<40%);
Moderate-to-severe
LV dilation is
present.
Indications for Aortic Valve Replacement for Chronic Aortic Regurgitation
Bicuspid Aortic Valve
• Bicuspid aortic valve disease is the most common congenital
heart lesion, occurring in approximately 1% of persons.
• Bicuspid aortic valve is associated with coarctation of the aorta,
interrupted aortic arch, and Turner syndrome.
• More than 70% of patients with a bicuspid valve will require
AVR for AS or AR.
• Progressive degenerative changes with premature calcification of
the bicuspid valve generally lead to AS rather than AR occurring
at an earlier age. 50% of AVR’s performed have bicuspid
pathology.
• Have a higher rate of valve-related complications with
approximately 2% annually developing symptoms or needing
cardiac surgery. Endocarditis may occur in 2% of patients
Bicuspid Aortic Valve
• Ascending aortic dilation may occur in persons with a
bicuspid aortic valve, in combination with aortic valve
disease independently. The aortopathy results from
intrinsically abnormal connective tissue.
• Serial evaluation of ascending aortic diameter should be
performed by transthoracic echocardiography (or by CT
or MR if not adequately visualized by echo).
• Balloon valvotomy in patients <30 years without
significant valvular calcification may offer
intermediate-term benefit, thus delaying eventual AVR
Bicuspid Aortic Valve
• Surgery to replace the ascending aorta is indicated
if diameter >4.5 cm due to progressive dilation.
• Surgery to replace the ascending aorta is
recommended in patients with a bicuspid aortic
valve if the diameter of the aortic root or
ascending aorta is >5.0 cm
• After aortic valve replacement for bicuspid aortic
valve disease, serial evaluation of the ascending
aorta is still warranted.
ETIOLOGY OF MITRAL STENOSIS
• Rheumatic disease most common cause by far
–
–
–
–
Leaflet thickening beginning at the edges of the leaflets
Fusion of the commissures
Produces significant narrowing of orifice
Subvalvular involvement
• Non-rheumatic - annular calcification extending
down leaflets may also cause restricted motion
• Congenital-single papillary muscle-parachute MV
SAX-MITRAL VALVE
Anatomic features of rheumatic mitral
stenosis
1. Diffuse fibrous thickening of the margins of closure
2. Fibrous thickening involving the entire anterior and
posterior leaflets producing leaflet rigidity
3. One or both valve commissures fuse reducing the
size of the mitral orifice
4. Shortened, thickened, and fused chordae
tendineae leading to subvalvular stenosis
5. Calcific deposits in one or both leaflets
6. Presence of Aschoff nodules in the myocardium
PATHOPHYSIOLOGY
• Restricted egress of blood out of LA
• Increased LAP and pressure gradient
through diastole with increased LA size
– Increased with increased HR
– Increased with increased venous return
– Atrial fibrillation decreases LAP
but increases rate
•
•
•
•
Pulmonary venous hypertension and congestion
RV dilatation due to pulmonary hypertension
TV ring dilatation and TR
Systemic venous hypertension
History
• Dyspnea on exertion progressing to
orthopnea
• Palpitations with dyspnea
• Leg swelling
• Abdominal swelling
• Rare chest pain
Cardiac Exam in Mitral Stenosis
Inspection
Malar flush
Peripheral cyanosis (severe MS)
Jugular venous distension (right ventricular failure)
Palpation
Parasternal right ventricular impulse
Palpable pulmonary arterial impulse
Palpable S1, P2, and occasionally, the diastolic rumble
Auscultation
Increased intensity of the first heart sound
Opening snap
Low-pitched diastolic rumbling murmur
Mitral regurgitant murmur and TR
Stages of Mitral Stenosis
Stage
C
Definition
Valve Anatomy
Asymptomatic  Rheumatic valve
severe MS
changes with
commissural
fusion and
diastolic doming
of the mitral valve
leaflets
 Planimetered
MVA ≤1.5 cm2
 (MVA ≤1 cm2 with
very severe MS)
Valve Hemodynamics




Hemodynamic
Consequences
MVA ≤1.5 cm2
 Severe LA
(MVA ≤1 cm2 with very
enlargement
severe MS)
 Elevated PASP
Diastolic pressure
>30 mm Hg
half-time ≥150 msec
(Diastolic pressure
half-time ≥220 msec
with very severe MS)
Symptoms
 None
Stages of Mitral Stenosis
Stage
D
Definition
Valve Anatomy
Symptomatic  Rheumatic
severe MS
valve changes
with
commissural
fusion and
diastolic doming
of the mitral
valve leaflets
 Planimetered
MVA ≤1.5 cm2




Valve
Hemodynamics
MVA≤1.5 cm2
(MVA ≤1 cm2 with
very severe MS)
Diastolic pressure
half-time ≥150
msec
(Diastolic pressure
half-time ≥220
msec with very
severe MS)
Hemodynamic
Consequences
 Severe LA
enlargement
 Elevated PASP
>30 mm Hg
Symptoms
 Decreased
exercise
tolerance
 Exertional
dyspnea
Indications for Intervention for Rheumatic Mitral Stenosis
Mitral Regurgitation
• Organic Causes
– Mitral valve prolapse, rheumatic heart disease, infective
endocarditis, collagen vascular disease
• Functional (resulting from left ventricular systolic
dysfunction causing mitral annular dilation or
restricted leaflet mobility).
– Mitral regurgitation due to coronary artery
disease
• Ischemia
• Papillary Muscle dysfunction or rupture
• Focal or general LV dilatation causing mitral leaflet tethering
and malcoaptation).
MR-Pathophysiology
• MRis generally progressive with increased preload with reduced
or unchanged afterload due to low impedance to flow in LA
• Eccentric hypertrophy accommodates the increased left
ventricular filling volume and maintains forward stroke volume.
• Increased left atrial pressure results in dyspnea and pulmonary
hypertension, and progressive left atrial dilation with AF.
• Progressive LV dilation may lead to systolic dysfunction.
• In asymptomatic patients with chronic severe MR, either
symptoms or LVdysfunction develops within 6 to 10 years.
• In patients with acute severe MR, the lack of compensatory
eccentric hypertrophy commonly results in fulminant symptoms
of heart failure and possible cardiogenic shock.
Pulmonary hypertension----Right heart dilatation and TR
Mitral Valve Prolapse
• Patients with MR due to MVP, present in 1%-2.5% of the population,
are heterogeneous regarding spectrum of disease and associated
manifestations.
• Mitral valve prolapse is diagnosed by echocardiography with
visualization of a displaced coaptation level of the anterior and
posterior mitral leaflets >2 mm above the mitral annulus.
• Patients with MVP generally have a benign prognosis, but some
patients have symptoms of “mitral valve prolapse syndrome,” which
include palpitations, nonanginal chest pain, fatigue, and dyspnea;
• Patients with thickened mitral leaflets (≥5 mm) are at higher risk for
progressive severe MR and complications.
• In patients with flail mitral leaflets (lack of coaptation), the annual
mortality rate is significantly higher than that for MVP with
regurgitation, and earlier intervention should be considered.
Doppler Echo
SYMPTOMS
• DOE
• Other pulmonary congestive symptoms
• Symptoms suggesting right heart failure
– Leg swelling
– Fatigue (RV dysfunction)
• Palpitations (Arrhythmias)-atrial and
ventricular
PHYSICAL EXAM
•
•
•
•
BP a bit low, irregular pulse
JVD*, low volume carotids
Crackles
Displaced PMI, S3, filling murmur at apex, HSM
radiating to axilla and occasionally LSB; RV tap*,
Increased P2*
• Liver enlarged*
• Edema*
*=Right heart failure
LAB INVESTIGATIONS
• EKG: LVH, LAA, MI, NASTT abn
• CXR: cardiomegaly, LA enlargement,
pulmonary congestion, increased PA size
• Echo:
–
–
–
–
Dilated LV, LA
Right heart variable
Valvular abnormality: Mitral valve competence
Doppler: MR; TR
Management of MR
• Medical therapy has a limited role in organic MR.
Symptomatic patients with acute severe MR should be
promptly referred for cardiac surgery. In this situation,
afterload reduction or IABP and stroke volume enhancement
with inotropic agents may stabilize the patient before urgent
cardiac surgery.
• In patients with asymptomatic severe MR, no studies have
demonstrated a clinical benefit with medical therapy.
• In patients with functional or chronic ischemic mitral
regurgitation with LV systolic dysfunction, treatment of the
underlying heart failure with an ACE inhibitor or β-blocker
may reduce severity of regurgitation, improve left ventricular
function, and reduce cardiovascular events
Stages of Primary Mitral Regurgitation (cont.)
Stage
C
Definition
Valve Anatomy
Asymptomatic  Severe mitral valve
severe MR
prolapse with loss
of coaptation or
flail leaflet
 Rheumatic valve
changes with
leaflet restriction
and loss of central
coaptation
 Prior IE
 Thickening of
leaflets with
radiation heart
disease






Valve
Hemodynamics
Central jet MR
>40% LA or
holosystolic
eccentric jet MR
Vena contracta
≥0.7 cm
Regurgitant volume
≥60 cc
Regurgitant fraction
≥50%
ERO ≥0.40 cm2
Angiographic grade
3–4+





Hemodynamic
Symptoms
Consequences
● None
Moderate or
severe LA
enlargement
LV enlargement
Pulmonary
hypertension may
be present at rest
or with exercise
C1: LVEF >60%
and LVESD
<40 mm
C2: LVEF ≤60%
and LVESD
≥40 mm
Stages of Primary Mitral Regurgitation (cont.)
Stage
D
Definition
Valve Anatomy
Symptomatic  Severe mitral valve
severe MR
prolapse with loss
of coaptation or flail
leaflet
 Rheumatic valve
changes with leaflet
restriction and loss
of central
coaptation
 Prior IE
 Thickening of
leaflets with
radiation heart
disease






Valve
Hemodynamic
Hemodynamics
Consequences
 Moderate or
Central jet MR
>40% LA or
severe LA
holosystolic
enlargement
eccentric jet MR
 LV enlargement
Vena contracta
 Pulmonary
≥0.7 cm
hypertension
Regurgitant volume
present
≥60 cc
Regurgitant fraction
≥50%
ERO ≥0.40 cm2
Angiographic grade
3–4+
Symptoms
 Decreased
exercise
tolerance
 Exertional
dyspnea
Stages of Secondary Mitral Regurgitation (cont.)
Grade
C
Definition
Valve Anatomy
Valve
Associated
Hemodynamics Cardiac Findings
Asymptomatic  Regional wall
 Regional wall
 ERO ≥0.20
severe MR
motion
motion
cm2
abnormalities
 Regurgitant
abnormalities
and/or LV
volume ≥30 cc
with reduced LV
dilation with
systolic function
 LV dilation and
severe tethering
systolic
of mitral leaflet
 Annular dilation
dysfunction due
to primary
with severe loss
myocardial
of central
coaptation of
disease
the mitral
leaflets
Symptoms
●
Symptoms due
to coronary
ischemia or HF
may be present
that respond to
revascularization
and appropriate
medical therapy
Stages of Secondary Mitral Regurgitation (cont.)
Grade
D
Definition
Valve Anatomy
Symptomatic  Regional wall
severe MR
motion
abnormalities
and/or LV
dilation with
severe
tethering of
mitral leaflet
 Annular
dilation with
severe loss of
central
coaptation of
the mitral
leaflets
Valve
Hemodynamics
 ERO ≥0.20 cm2
 Regurgitant
volume ≥30 cc
Associated
Symptoms
Cardiac Findings
 Regional wall
 HF symptoms
motion
due to MR
abnormalities
persist even after
with reduced LV
revascularization
systolic function
and optimization
 LV dilation and
of medical
systolic
therapy
dysfunction due  Decreased
to primary
exercise
myocardial
tolerance
disease.
 Exertional
dyspnea
Indications for Surgery for Mitral Regurgitation
Tricuspid Valve Disease
• Tricuspid stenosis is uncommon caused predominantly by
rheumatic heart disease. Severe stenosis leads to RAP
elevation, atrial flutter, and systemic venous congestion
(edema, hepatomegaly, ascites).
• Tricuspid regurgitation associated with abnormal leaflets
include
–
–
–
–
–
–
–
–
Rheumatic heart disease
Infective endocarditis
Carcinoid tumor,
Ebstein’s anomaly
Radiation therapy
Connective tissue disease
Prolapse
Trauma and pacer and defibrillator leads
Tricuspid Valve Disease
• Functional tricuspid regurgitation commonly is present in
patients with pulmonary hypertension, due to the increased
right ventricular systolic pressure and right ventricular
dilatation.
– Valve disease
– CAD and LV dysfunction with MR
– HFPEF
• The appropriate timing of surgical intervention (repair or
replacement) for severe tricuspid regurgitation is
controversial, but is generally considered for patients with
right-sided heart failure symptoms refractory to medical
therapy or is performed concomitantly with mitral valve
surgery
Endocarditis
• Infective endocarditis is a bacterial or fungal infection of
the endocardium, including native or prosthetic valves, the
endocardial surface, or an implanted cardiac device.
• Endocarditis generally is caused by bacteremia with
adherence of bacteria to a preexisting endocardial,
particularly valvular, lesion.
– Streptococcal infection was the predominant cause in earlier eras,
staphylococcal infection is now the leading cause owing to the
increase in health care–related invasive procedures and
intravascular access.
– As a result, duration of symptoms before presentation is shorter.
Despite advancements in the diagnosis and therapy for
endocarditis, the in-hospital mortality rate remains high, at nearly
20%.
Endocarditis
• Infective endocarditis should be suspected with a new or increased
regurgitant heart murmur along with signs or symptoms of infection
or bacteremia. Blood cultures may be negative if antibiotics are
started before cultures are taken or if fastidious organisms.
• Echocardiography has a primary role in the diagnosis of endocarditis.
The modified Duke criteria for diagnosis of endocarditis include
typical bacteriologic evidence in blood cultures or valve specimens,
clinical findings, and echocardiographic evidence of endocardial
involvement (new or worsening valve regurgitation, vegetation,
paravalvular abscess, or leaflet perforation).
– TTE has less sensitivity than TEE for the detection of endocardial involvement.
– TEE has very high sensitivity and specificity for these diagnostic findings and
complications of endocarditis (intracardiac abscess, fistula).
– It may be an acceptable primary diagnostic test without previous TTE in certain
clinical situations: intermediate or high pretest probability of endocarditis;
patients with prosthetic heart valves; and evaluation for complications of
endocarditis, such as intracardiac abscess, valve perforation, or fistula formation.
Endocarditis
• Empiric antibiotic therapy is appropriate after multiple blood cultures
have been drawn when clinical suspicion for endocarditis is
intermediate or high.
• Tailored antibiotic therapy is guided by the causative organism and
its susceptibilities.
• Surgery during the index hospitalization is performed in nearly 50%
of patients with valvular infective endocarditis and a higher
percentage of those with cardiac device infective endocarditis.
• Indications for surgery include:
– (1) Severe hemodynamic perturbation, p related to severe left-sided valvular
regurgitation or fistula formation and resultant heart failure;
– (2) Evidence or likelihood of persistent infection despite appropriate antibiotic
therapy (including persistent bacteremia or intracardiac abscess, or involvement
of a prosthetic surface)
– (3) Evidence or high risk of recurrent embolic event because of a large
vegetation.
Prosthetic Valves
•
•
•
•
•
For patients requiring valve replacement surgery, options for the type
of prosthetic valve are biologic (xenograft or homograft) or mechanical
valves.
The major consideration regarding these types of valves is structural
valve deterioration of biologic valves versus the need for life-long
anticoagulation for mechanical valves.
Biologic valve durability is dependent on the position of implantation,
with greatest durability in right-sided valve replacements, followed by
aortic and mitral positions.
In the most common aortic location, the anticipated duration is 14 to
20 years before significant structural deterioration occurs.
Other factors in this choice include hemodynamic performance and
patient preference.
Recommendations for Prosthetic
Valves
Mechanical
Aortic
Mitral
Bioprosthetic
Mechanical valve
present in other
valve location
Age <65 years in
the absence of
contraindications to
anticoagulation
Age ≥65 years
without other risks
for
thromboembolism
Contraindication to
anticoagulation
Patient preference
Age <65 years
Age ≥65 years
Contraindication to
anticoagulation
Patient preference
Prosthetic Valves and
Antithrombotic Regimens
•
•
•
After implantation of either a biologic or mechanical prosthetic valve,
anticoagulation with warfarin is recommended for at least 3 months to
allow endothelialization of the prosthetic material (not often done). In
addition, all patients should receive aspirin (75-100 mg/d) to further
reduce the risk for thromboembolic events.
After 3 months, patients with a biologic valve replacement who are at
low risk for thromboembolic events can discontinue warfarin but must
remain on aspirin indefinitely;
Patients with a mechanical valve replacement should continue taking
low-dose aspirin and warfarin indefinitely (goal INR range 2.0-3.0 for
aortic valve replacement and 2.5-3.5 for mitral valve replacement).
Bridging Anti-Thrombotic
Therapy
•
•
Patients with mitral mechanical prosthetic valves are at higher risk for
valve thrombosis. Additional risk factors for thrombosis are AF,
previous thromboembolism, LV systolic dysfunction, hypercoagulable
conditions, non bileaflet valves, mechanical tricuspid valve, or >1
mechanical valve.
Patients with a mechanical mitral or a mechanical aortic valve with
additional risk factors undergoing an elective surgical procedure
requiring warfarin cessation should be bridged (unfractionated heparin
IV or LMW heparin before and after the procedure.
Prosthetic Valves
•
•
•
•
For patients with HIT, bivalirudin may be used for bridging of
anticoagulation.
In patients at low risk of valve thrombosis (bileaflet mechanical aortic
valve replacement with no risk factors for thrombosis), warfarin may
be stopped 48 to 72 hours before the elective procedure and restarted
within 24 hours after the procedure.
Thrombosis of a mechanical valve is an emergent situation associated
with a high risk for pulmonary edema and thromboembolism, and
therapeutic options include repeat cardiac surgery or intravenous
fibrinolytic therapy.
For baseline assessment, all patients undergoing valve replacement
surgery should have annual clinical evaluation and transthoracic
echocardiography performed 2 to 3 months after implantation.
Subsequently, however, routine annual echocardiography is not
indicated if no change in clinical status has occurred.