Valvular heart

disease

Aortic Valve Diseases

VALVULAR STENOSIS
Pressure in upstream chamber IS HIGHER
than Pressure in downstream chamber
during time of flow (when valve is normally
open).
Hemodynamic abnormality = "PRESSURE
GRADIENT"

Upstream

Down stream

High pressure

low pressure

VALVULAR
REGURGITATION
Retrograde flow of blood "upstream" during time when
valve
is normally closed.

Hemodynamic
abnormality = "VOLUME OVERLOAD"

Upstream

Volume overload

Down stream

Aortic stenosis

Anatomy of Aortic Valve

The AV is located betwn the LVOT and the ascending aorta. It forms the cente
heart and closely approximates many other important cardiac structures; sp
PV anteriorly, MV posterolaterally, and TV posteromedially. [1]
Ref:
1. Anderson RH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.

Picture : Aortic Valve.[1]

Picture ref: Anderson RH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.

Picture : Aortic Valve.[1]

Picture reference: Anderson RH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.

Pathophysiologic Variants

Bicuspid aortic valve

Bicuspid aortic valves are the most
common cardiac valvular anomaly,
occurring in 1- 2% of the general population.
It is twice as common in males as in
females.[1]

Ref:
1. Tzemos N, Therrien J, Yip J et al (September 2008)."Outcomes in adults with bicuspid aortic valves".JAMA300(1

Aortic Regurgitation:
overview
AR is a condition due to inadequate closure of
the aortic valve leaflets leading to abnormal
retrograde flow of blood through the aortic valve
during cardiac diastole.
It can be induced either by damage to and
dysfunction of the aortic valve leaflets or by
distortion or dilatation of the aortic root and
ascending aorta
In the developing world, the most common cause of
AR is rheumatic heart disease. However, in
developed countries, AR is most often due to aortic
root dilation or a congenital bicuspid aortic
valve .[1]
Ref:
1. Maurer G. Aortic regurgitation. Heart. Jul 2006;92(7):994-1000.

Causes of Aortic
Regurgitation Aortic root or ascending aorta
Leaflet abnormalities
Rheumatic fever

Systemic hypertension

Endocarditis

Aortitis (eg, syphilis)

Trauma

Reactive arthritis

Bicuspid aortic valve

Ankylosing spondylitis

Rheumatoid arthritis

Trauma/ Dissecting aneurysm

Myxomatous degeneration

Osteogenesis imperfecta

Ankylosing spondylitis

Marfan syndrome/ EDS

Acromegaly

Inflammatory bowel disease

n more commonly in men than in women. As in the Framingham study, AR wa

men versus 8.5% of women.[1]The greater prevalence of AR in men may reflect, in
e preponderance of underlying conditions such as Marfan syndrome[2]or bicusp

Ref:
1. Singh JP, Evans JC, et al. Prevalence and clinical determinants of mitral, tricuspid, and AR (the Framingham Heart Study). Am J Cardiol. M
2. Keane MG, Pyeritz RE. Medical management of Marfan syndrome. Circulation. May 27 2008;117(21):2802-13.
3. Ortiz JT, Shin DD, Rajamannan NM. Approach to the patient with bicuspid AVand ascending aorta aneurysm. Curr Treat Options Cardiova

Pathophysiology
Law of laplace
LV Volume

LV Hypertrophy

Pathophysiology : Acute AR
Sudden large regurgitant volume
imposed on LV of normal size with
normal compliance

1. Rapid LVEDP and LAP

2. LV attempts to maintain CO with HR and
Contractility
Attempts to maintain forward SV/CO may be
inadequate
Cardiogenic Shock
Forward SV/CO
Pulmonary edema
LVEDP and LAP

Angina
Coronary perfusion
demand myocardial O2

Pathophysiology: Chronic
AR
Regurgitant Volume Load

Compensatory Mechanisms:
1.LV dilatation LVED vol and chamber
compliance
2. LV hypertrophy
Decompensation
Steadily increasing regurgitant volume load
Further ventricular dilatation wall
stress
Inability to continue further hypertrophy
Contractile dysfunction EF/SV/CO
CHF symptoms
Due to both congestion and
CO

Angina
Coronary perfusion pressure &
marked LVH

Findings are a/w

hyperdynamic pulse

deMusset's
sign

A head bob occurring with each cardiac cycle

Mueller's sign Systolic pulsations of the uvula.

Becker's sign

Visible pulsations of the retinal arteries and pupils.

Quincke's
pulses

visible Capillary pulsations in the nailbeds after holding

the tip of the nail.

Duroziez's
sign

A systolic and diastolic bruit heard when the femoral

artery is partially compressed.to and fro murmur

Traube's sign

A pistol shot murmur (systolic and diastolic sounds)

heard over the femoral arteries.

Mayne's sign

More than a 15 mmHg decrease in DBP with arm

elevation from the value obtained with the arm in the
standard position.

Hill's sign

Popliteal cuff systolic pressure exceeding brachial

pressure by more than 60 mmHg.

Rosenbach's

Systolic pulsations of the liver.

 The diastolic murmur of AR begins

immediately after A2 .
It is high pitched, often blowing in
quality, and may be sustained in intensity
or decrescendo.
It may be soft and barely audible, often
appreciated only when the patient is
sitting up, leaning forward, and
holding his or her breath in
expiration.

 Patients with a longer diastolic murmur, a

displaced left ventricular impulse, a wide
pulse pressure, and the peripheral
findings of a wide pulse pressure are
considered to have severe AR.
Note: When the Diastolic murmur of AR is louder
in the 3rd /4th RICS than in the 3/4th LICS ,the AR
is likely to result from Aortic root
dilatation than deformitiy of leaflets alone.
Ref: ACC/AHA Guidelines 2006

 In a review of the literature, the presence

of an early diastolic murmur, as heard
by a cardiologist, was the most useful
finding for establishing the presence of
AR (positive likelihood ratio 8.8 [ie,
the odds of AR are increased 8.8 fold])
and its absence the most useful finding
for eliminating the presence of AR
(negative likelihood ratio 0.2 to 0.3
[ie, the odds of disease are reduced by a
factor of 0.2 to 0.3]) .[1]

Ref:
1. Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA 1

Laboratory Studies
Laboratory testing in patients with aortic
regurgitation should be guided by the
clinical scenario.
For example, in patients with AR due to
suspected
infective
endocarditis,
peripheral blood counts and cultures
may help clarify the diagnosis and
identify the causative organism.
Specific serologic tests may assist in
the diagnosis of rheumatological causes.

Imaging studies : Echo

Aortic valve structure and morphology (bileaflet versus
trileaflet, flail, thickening)
Presence of vegetations
Severity of AR
Color Doppler jet width
Vena contracta width
Regurgitant volume, fraction, and orifice area
Premature closure of the mitral valve (seen in severe AR)
Associated lesions of the aorta, including dilation, aneurysm,
dissection
LV structure and function
LV hypertrophy and dilation
EF and end-systolic dimension are key determinants of
outcome

Severity of AR: Echo

grading
MILD

MOD

SEVERE

Structural parameters
Left ventricular size

N or dilated

Dilated, except acute

AR

Aortic leaflets

N or abnormal

N or abnormal

Abnormal/flail, or wide
coaptation defect

Color Doppler jet

width

Central jet, width <25

percent of LVOT

Central jet, width 25 to

65 percent of LVOT

Central jet width >65

percent of LVOT

Doppler vena
contracta width

<3 mm

3 to 6 mm

>6 mm

Doppler parameters

Quantitative parameters
Regurgitant volume

<30 mL/beat

30 to 59 mL/beat

60 mL/beat

Regurgitant fraction

<30 percent

30 to 49 percent

50 percent

Regurgitant orifice
area

<0.10 cm2

0.10 to 0.29 cm2

0.30 cm2

Severe chronic AR is typically a/w c/f including a longer

diastolic murmur, a displaced LVI, a wide PP, and the

Echo staging of
Decompensation.[1,2,3,4,5,6,7,8]

References:
1. ACC/AHA 2006 guidelines
2. Gaasch WH, Andrias CW, Levine HJ. Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function. C
3. Schuler G, Peterson KL, Johnson AD, et al. Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of AR. Am
4. Borow KM, Green LH, Mann T, et al. End-systolic volume as a predictor of postoperative LVperformance in volume overload from valvular regurgitation.
5. Henry WL, Bonow RO, et al. Observations on the optimum time for operative intervention for AR. Evaluation of the results of AVR in symptomatic patien
6. Kumpuris AG, Quinones MA, Waggoner AD, et al. Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic
of left ventricular dilatation after valve replacement in chronic aortic insufficiency. Am J Cardiol 1982; 49:1091.
7. Gaasch WH, Carroll JD, Criscitiello MG. Chronic AR: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J
8. Stone PH, Clark RD, Goldschlager N, et al. Determinants of prognosis of patients with aortic regurgitation who undergo aortic valve replacement. J Am C
9. Bonow RO, Rosing DR, McIntosh CL, et al. The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function. Ci
10. Bonow RO, Lakatos E. Serial long-term assessment of the natural history of asymptomatic patients with chronic AR and normal left ventricular systolic
11. Siemienczuk D, Greenberg B, Morris C, et al. Chronic aortic insufficiency: factors associated with progression to aortic valve replacement. Ann Intern M

Procedures: Cardiac Cath

Class I indications for CC under current
ACC/AHA guidelines include the following:
[1]

Assessment of coronary anatomy prior

to aortic valve surgery in patients with
risk factors for coronary artery disease.

Ref:
1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update
incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease.
.

Exercise testing in AR[1]

- The weight of evidence or opinion is in favor of efficacy of the followi

patients with AR in the above settings.

Ref:
1.Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update
incorporated into the ACC/AHA 2006 guidelines for the management of patients with VHD.

Medical care
In acute severe AR, surgical intervention is
usually indicated, but the patient may be
supported medically with dobutamine to
augment cardiac output and shorten diastole
and sodium nitroprusside to reduce afterload
in hypertensive patients.
In chronic severe AR, vasodilator therapy may
be used in select conditions to reduce afterload
in patients with systolic hypertension to
minimize wall stress and optimize LV function; in
normotensive patients, vasodilator therapy is not
likely to reduce regurgitant volume (preload)
significantly and thus may not be of clinical
benefit.[1]
Ref:
1. Bekeredjian R, Grayburn PA. Valvular heart disease: aortic regurgitation. Circulation. Jul 5 2005;112(1):125-34.

Medical Care continue

The
acute
administration
of
Na
Nitoprusside , hydralazine, nifedipine or
felodipine PVR and results in an
immediate augmentation in forward
CO and a in regurgitant volume.
With nitroprusside and hydralazine ,these
acute hemodynamic changes lead to a
consistent in EDV and an in EF.
References:
1. Miller RR, Vismara LA, .Afterload reduction therapy with nitroprusside in severe AR: improved cardiac performance and reduced
regurgitant volume. AmJ Cardiol 976;38:5647
2. Greenberg BH, DeMots H. Beneficial effects of hydralazine on rest and exercise hemodynamics in patients with chronic severe
aortic insufficiency. Circulation 1980;62:4955
3. FiorettiP, BenussiB.Afterload reduction with nifedipine in aortic insufficiency. AmJ Cardiol 1982;49:172832

Medical Care Continue..

Reduced EDV and EF have also been
observed in small number of pts
receiving long term oral therapy with
hydralazine and nifedipine for a
period of 1-2 yrs. With nifedipine these
effects are A/W in LV mass.[1,2]
Reduced
BP
with
enalapril
and
quinapril has been A/W in EDV and
mass but no change in EF.[3,4]

References:
1. Scognamiglio R, Fasoli G. Long-term nifedipine unloading therapy in asymptomatic patients with chronic severe AR. J Am Coll Cardiol 19
2. Greenberg B, Massie B, et al. Long-term vasodilator therapy of chronic AI: a randomized double-blinded, placebo-controlled clinical trial
3. Lin M, Chiang HT,etal.Vasodilator therapy in chronic asymptomatic AR: enalapril versus hydralazine therapy. J Am Coll Cardiol 1994;24:1
4. Schon HR, Dorn R. Effects of 12 months quinapril therapy in asymptomatic patients with chronic AR. J Heart Valve Dis 1994;3:5009.

ACC/AHA GL on Vasodilator therapy:

Indicated for long-term therapy in patients with
chronic, severe AR and symptoms of LV
dysfunction but who are not candidates for
surgery.( CLASS I: LOE-b)
Is reasonable for short-term therapy in patients
with severe LV dysfunction and HF symptoms to
improve their hemodynamic profile before
proceeding with surgery.(CLASS IIa: LOE-c)
Is acceptable for long-term therapy in
asymptomatic patients with severe AR
and LV dilation with normal EF. (CLASS IIb: LOE-b)
Ref:

1.Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated int
guidelines for the management of patients with valvular heart disease.

Note: LOE = Level of Eviden

Prophylaxis for IE
Antibiotic prophylaxis prior to dental
procedures is no longer routinely
recommended for all patients with AR
under current ACC/AHA guidelines.[1]

Ref:
1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated in
2006 guidelines for the management of patients with valvular heart disease

Surgical care
Surgical treatment of AR usually requires
replacement of the diseased valve
with a prosthetic valve, although
valve-sparing
repair
is
increasingly
possible with advances in surgical
technique and technology.

Current ACC/AHA guideline for AV

Sx [1]
Patient is symptomatic.
Patient is asymptomatic, with a resting EF
of 55%.
Patient is asymptomatic, with LV dilation
(LV end-systolic dimension >55 mm).

Ref:
1.Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated in
2006 guidelines for the management of patients with valvular heart disease.

Mechanical Vs
bioprosthetic AV
For patients undergoing AV replacement,
careful consideration should be given to the
relative risks and benefits of mechanical
vs bioprosthetic valves.
Mechanical valves : more durable but require
long-term anticoagulation with warfarin due to
increased risk of thrombosis.
Bioprosthetic valves carry a greater risk of
long-term deterioration and risk of reoperation
but avoid the need for long-term warfarin.
[1]

Ref:
1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated in
2006 guidelines for the management of patients with valvular heart disease.
.

Further inpatient care

Inpatient care
patients with
regurgitation
symptoms
hemodynamic

is required for most

acute severe aortic
(AR), particularly with
or
evidence
of
decompensation.

Further outpatient Care

ESD

EDD

Stable Dimension

Incresing
Dimension

<45 mm

< 60 mm

Evaluate 6-12 mn
Repeat Echo in 12
mnth

3mnth
3 mnth

45-50
mm

60-70 mm

Evaluate 6 mn
Repeat Echo in 12
mnth

3 mnth
3 mnth

50-55
mm

70-75 mm

Evaluate in 6 mn
Repeat Echo 6 mnth

3 mnth
3 mnth

>55 mm

> 75 mm

Surgery

Complications
Left untreated, acute severe AR is likely
to lead to considerable morbidity and
mortality from either the underlying
cause (typically infective endocarditis or
aortic dissection) or from hemodynamic
decompensation of the LV.
Potential complications in patients with
chronic severe AR include progressive LV
dysfunction and dilation, CHF, MI,
arrhythmia, and sudden death.

Prognosis
The prognosis for patients with severe AR depends on the
presence or absence of LV dysfunction and symptoms, as
follows:[1]
In asymptomatic patients with normal EF
1.Rate of progression to symptoms &/or LVD = < 6% per
yr
2.Rate of progression to asymptomatic LVD = < 3.5% per
yr
3.Rate of sudden death = less than 0.2% per yr
In asymptomatic patients with decreased EF, rate of
progression to symptoms = >25% per year.
In symptomatic patients, mortality rate = >10% per yr.
The
strongest
predictors
of
outcome
are
echocardiographic
parameters (EF and LV end-systolic dimension).
Ref:
1.Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update
incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart
disease.

Mitral Valve
Diseases

Mitral stenosis

Uptodate 20.3

Mitral stenosis
MS is characterized by obstruction to
left ventricular inflow at the level of
MV due to structural abnormality of the
MV apparatus.1
MS
is
due
to
thickening
and
immobility of the mitral valve
leaflets.
The normal MVO has a CSA of 4-6 cm2.
Carabello, B. A. (2005). "Modern Management of Mitral Stenosis".Circulation112(3):
4327

Etiology
Rheumatic heart disease
Congenital MS
Mitral annular calcification (particularly in
patients with ESRD).
Conditions that simulate MS: IE with large
vegetation,
LA
myxoma,
ball
valve
thrombus, and cor triatriatum.
Less
common
causes:
malignant
carcinoid
disease,
SLE,
RA,
mucopolysaccharidoses,
Fabry
disease,
Whipple disease, and methysergide therapy.

Rheumatic mitral stenosis

In RMS, the MVO is slowly diminished by
progressive fibrosis, calcification of the
valve leaflets.
The flow of blood from LA to LV is restricted
and LAP rises, leading to pulmonary
venous congestion and breathlessness.
There is dilatation and hypertrophy of
the LA, and left ventricular filling becomes
more dependent on left atrial contraction.
Note: The association of atrial septal
defect with rheumatic mitral stenosis is
called Lutembacher syndrome.

Pathophysiology
LAE

Atrial Fibrillation

Thromboemboli
sm

Stroke

Ventricular filling

High pressure ruptures

Pulmonary vessels
:hemoptysis

Palpitation

LAP precipitate pul

edema Acute dyspnea

Hoarseness :due to compression of the LRLN by a dilated LA or

pulmonary artery (Ortner syndrome)

Pulmonary Hypertension
Backward transmission of the elevated left atrial pressure
Loud P2, later
becomes
palpable

JVD

Pulmonary artery pressure

Parasternal
heave

Prominent a
wave

TR

Prominent v wave

Hepatomegaly
& Pulsatile liver
Peripheral
edema

RV hypertrophy &
enlargement
Tricuspid regurgitation

RAP & development of right sided heart failure

Pathophysiology: MS
LAP

LA enlargement (compensation to attempt to

lower LAP)

LA remodelling

LAP transmitted to pulmonary venous

system

MVA

LAP, LAE

AFib

LA clot

Pul
congestion
PVR ,PHTN

Exertional
Dyspnea /Pul
edema

RV pressure overload

RVH

RV dilates & fails

Fatigue/Dyspnea/
Functional capacity

CO (first
with exercise
then at rest)

With significant obstruction

to flow from PVR & MS

History
Generally asymptomatic at rest during the early stage.
However, factors that HR such as fever, severe
anemia, thyrotoxicosis, exercise, and Afib dyspnea.
Systemic embolization may lead to stroke, renal
failure, orMI.
Hoarseness :compression of the LRLN against the
pulmonary artery by the enlarged LA. Also, compression
of bronchi by the enlarged LA can cause persistent
cough. Cough also occurs due to pul congestion
Hemoptysis may occur.
Palpitation
Chest pain (due to pul hypertension)
Oedema / Ascites (Right heart failure)
Pregnant women with mild MS may become
symptomatic during their 2nd trim (in blood vol ).

Physical examination
Presence of mitral facies (pinkish-purple
patches on the cheeks) indicate chronic
severe
MS
(reduced
CO
&
vasoconstriction).
JVD may be seen.
In
pt
with
sinus
rhythm,
a
prominentawave : RA pressure from
pul HTN & RVfailure.
A prominentvwave :is seen with TR.

Palpation
The arterial pulses are reduced in volume
due to the decreased SV.
Pulses may be irregular in Afib.
Tapping apex beat that is not displaced.
Left parasternal heave - presence of RVH
due to pulmonary HTN
A P2 may be palpable in the 2LICS.

Parasternal Heave
Grade 1 : visible but not palpable
Grade 2 : Visible & palpable and
obliterable
Grade 3: Visible & palpable but not
obliterable

Cardiac auscultation:
Heart sounds
The S1 is accentuated because of a wide
closing excursion of the mitral leaflets.
The degree of loudness of the S1 depends
on the pliability of the MV.
The intensity of the S1 as the valve
becomes more fibrotic, calcified, and
thickened.
The S2 is initially normal but, with the
development of PHTN, P2 becomes in
intensity .

Cardiac auscultation:
Opening snap
An OS of the MV is heard at the apex when
the leaflets are still mobile .
The OS is due to the abrupt halt in
leaflet motion in early diastole.
Note: The OS following S2 may be mistaken for
a split S2 (OS is best appreciated at the apex,
not the base. )

As the MS progresses and LAP is , the OS

occurs earlier after S2 or A2. Thus, the
shorter the A2-OS interval, the more
severe the MS.

Cardiac auscultation:
murmur
low-pitched diastolic rumble that is most
prominent at the apex.
Although the intensity of the diastolic murmur
does not correlate with the severity of the
stenosis, the duration of the murmur is helpful
since it reflects the transvalvular gradient and
the duration of blood flow across the valve.
The in atrial pressure after atrial contraction,
results in an increase in the loudness of the
murmur, termed "presystolic accentuation"
.

MS:
The diastolic murmur and OS are diminished with
inspiration, but augmented with expiration (in
contrast to TS). With inspiration, the A2-OS interval
widens .
Increasing venous return, eg, by lying the patient
down and lifting the legs, augments the gradient; as
a result, the diastolic murmur lengthens while
the A2-OS intervals shorten. (Similar changes
are seen in response to exercise.)
In contrast, reducing venous return with amyl
nitrate, the Valsalva maneuver, or standing after
squatting shortens the murmur and lengthens the
A2-OS interval.

MS: murmur
On auscultation of mitral area of the heart, s1 is
short ,sharp and accentuated and s2 is normal.
Opening snap is heard just after s2.
There is low pitched, mid diastolic, rumbling
murmur with presystolic accentuation of Grade
4 intensity in the mitral area without any
radiation.
The murmur is best heard at cardiac apex with
bell of steths ,in left lateral position ,at the
height of expiration and after doing mild
exercise.

MDM: D/D
It is not Carey coombs murmur (occurs in active
rheumatic vulvulitis and oedema of MV cusps gives rise to
soft MDM) because there is absence of loud s1, OS and
diastolic thrill.
It is not Austin flint murmur (which is a functional low
pitch mid diastolic murmur in pt with AI in which murmur is
produced as the regurgitant jet flow hits the anterior mitral
leaflets) because in AFM, the presystolic component is
absent, there is no thrill, and S1 is not loud. And there is no
OS. Moreover in AFM of AI ,there are features of LVH and
peripheral signs of AI which is not present in this case.
It is not MDM of TS ,because the murmur of TS would be
best heard in LSB and increases at the height of
inspiration.

CXR

CXR
Backward displacement of esophagus by
enlarged LA(in lat view)
Enlarged LA , Double shadow due to enlarged LA
Straightening of left heart border
Splaying of carina (The left main bronchus is
lifted up by the enlarged LA)
Prominent upper zone pulmonary veins (Inverted
moustache sign / Antlers horn sign /
Cephalisation pulmonary of blood flow)
Kerley B lines (indicating fluid collection in the
interlobular septa)

Management
Patients with minor symptoms should be treated
medically.
Intervention by balloon valvuloplasty, mitral
valvotomy or MVR should be considered if the
patient remains symptomatic despite medical Rx
or if PHTN develops.
Anticoagulation :to reduce the risk of systemic
embolism,
Ventricular rate control (digoxin, -blockers CCB)
in AFib
Diuretic therapy to control pulmonary congestion.
Antibiotic
prophylaxis
against
infective
endocarditis is no longer routinely recommended.

Etiology
Congenital (rare)
Acquired
1. Rheumatic (most common)
- Most common valve lesion after RF
- Stenosis occurs due to fibrosis/calcification of:
a. Commissures
b. Cusps
c. Chords
d. Combination
2. CTD (SLE, RA)
3. Obstructive masses ( Atrial Myxoma, large
vegetation)

RA

RV

Right Heart Failure:

Hepatic Congestion
JVD
Tricuspid
Regurgitation
RA Enlargement

RV Pressure
Overload
RVH
RV Failure

Pulmonary HTN
Pulmonary
Congestion
LA Enlargement
Atrial Fib
LA Thrombi
LA Pressure

LA

LV
LV Filling

Mitral Regurgitation

Overview

Mitral regurgitation (MR) is defined as an

abnormal reversal of blood flow from the left
ventricle (LV) to the left atrium (LA).
It is caused by disruption in any part of the
mitral valve (MV) apparatus.
Mitral regurgitation can be divided into 3
stages:
1.acute
2.chronic compensated
3.chronic decompensated

Pic source: www.abbottvascular.

Anatomy: Mitral valve

The mitral valve connects the
left atrium (LA) and the left
ventricle (LV).
The mitral valve opens during
diastole to allow the blood flow
from the LA to the LV.
During ventricular systole, the
mitral valve closes and prevents
backflow to the LA.
The mitral apparatus is composed of
1.the left atrial wall
2.the annulus
3.the leaflets
4.the chordae tendineae
5.the papillary muscles
6.the left ventricular wall

Pic source: www.heart-valve-surgery.com

Anatomy: MV Annulus
The mitral annulus is a fibrous ring
that connects with the leaflets.
The annulus functions as a
sphincter that contracts and
reduces the surface area of the
valve during systole to ensure
complete closure of the leaflets.
Annulus contraction during systole
promotes valve competence
Thus, annular dilatation of the
mitral valve causes poor leaflet
apposition, which results in mitral
regurgitation.
Annulus may dilate in ischemic or
dilated cardiomyopathy.
1. Figure2: http://emedicine.medscape.com

Anatomy: Mitral valve

leaflets
Harken et al have described the mitral
1

valve as a continuous veil inserted

around the circumference of the mitral
orifice.[2]
The free edges of the leaflets have
several indentations.
Two of these indentations, the
anterolateral
and
posteromedial
commissures, divide the leaflets into
anterior and posterior .
These commissures can be accurately
identified by the insertions of the
commissural chordae tendineae into
the leaflets.

Inflammatory,
degenerative,
or
infectious diseases can result in
Picture source: http://emedicine.medscape.com
perforation
poorin the
coaptation
of with
leaflets
Harken DE, Ellis LB, Dexter L, Farrand RE, Dickson JF. The
responsibility of theor
physician
selection of patients
mitral stenosis

1.
2.
Circulation. Mar 1952;5(3):349-62.

1.

Anatomy: Chordae
tendineae These are

Pic source: http://emedicine.medscape.com

small
fibrous
strings that originate either
from the apical portion of the
papillary muscles or directly
from the ventricular wall and
insert into the valve leaflets
or the muscle.
Chordal
rupture
or
foreshortening
prevents
leaflet coaptation

Anatomy: Papillary
muscles
These 2 structures
represent the
muscular components of the mitral
and left ventricular
wall
apparatus.

PM normally arise from apex and

mid third of the LV wall.
The anterolateral PM is normally
larger than the posteromedial PM &
is supplied by LAD artery or LCX
artery.
The posteromedial PM is supplied
by the RCA.
Rupture of a PM, usually the
complication of AMI, will result in
acute MR.
Infarction or LV wall motion
abnormalities may lead to valve
incompetence.
1.
http://emedicine.medscape.com
Infarction of PM itself more likely to
2.
Harken DE, Ellis LB, Dexter L, Farrand RE, Dickson JF. The responsibility of the physician in the selection of patients with mitral stenosis
Circulation. Mar 1952;5(3):349-62.
cause acute MR.

Anatomy: Mitral valve

Left atrial wall
The left atrial myocardium
extends over the proximal
portion
of the posterior
leaflet.
Thus, left atrial enlargement
can result in MR by affecting
the posterior leaflet. The
anterior
leaflet
is
not
affected, because of its
attachment to the root of the
aorta.2
1. Figure2: http://emedicine.medscape.com
2. Perloff JK, Roberts WC. The mitral apparatus. Functional anatomy of
mitral regurgitation. Circulation. Aug 1972;46(2):227-39.

Mitral regurgitation:
etiology
Acute
Chronic Primary MR
Endocarditis
Papillary muscle rupture (postMI) Trauma
Chordal rupture/leaflet flail
(MVP, IE)

Myxomatous (MVP)
Rheumatic fever
Endocarditis (healed)
Mitral annular calcification
Congenital (cleft, AV canal)
\HOCM with SAM
Radiation
Chronic secondary MR
Ischemic (LV remodeling)
Dilated cardiomyopathy

The abnormal and dilated left ventricle causes papillary muscle

displacement, which in turn results in leaflet tethering with
associated annular dilation that prevents coaptation.

Laplace Law

As stated by Laplace law: LV wall

stress is directly proportional to
the cavity pressure and inversely
proportional to wall thickness.
Due to the added regurgitant vol
there is in LV volume that leads
to an in LV cavity pressure and
it causes an in wall stress.
If
a
hypertrophic
response
occurs, thickness can return
wall stress to N.

The
hemodynamic
changes in acute MR
are more severe than
those in chronic MR due
in part to the lack of
time for the left atrium
and left ventricle to
adapt to the MR.
This is in contrast to
chronic MR where these
adaptations have time
to develop and typically
preserve hemodynamic
stability.

Chronic MR:
Pathophysiology
Vol load imposed on LA & LV (usually it gradually
over time)

LVEDP &
LAP

Compensatory dilatation of LA & LV to accommodate

vol load at lower pressure; this helps relieve pul
congestion
LV hypertrophy (eccentric) stimulated by LV
dilatation ( wall stress- Laplace Law)
Preload, LV hypertrophy, & reduced or normal
afterload (low resistance LA provides unloading of LV)
Large total SV (supra normal EF) and normal forward
SV
MR begets MR (viscious cycle in which further
LV/annular dilatation MR

Chronic MR:
Pathophysiology..

continue

MR begets MR (viscious cycle in which further

LV/annular dilatation MR

Contractile
dysfunction

EF, end-systolic
volume

Reduced forward SV/CO

LVEDP/ vol,
LAP

Pul congestion & pHTN

Basic mechanisms of acute

native valve acute MR
1. Flail leaflet due to myxomatous
disease (MVP), IE, or trauma.
2. Chordae tendineae rupture due to
trauma, IE, or acute rheumatic fever.
3. Papillary
muscle
rupture
or
displacement due to AMI or severe
ischemia or trauma.

Pathophysiology: AMR
Flail leaflet
Chordae tendineae
rupture
Papillary muscle
rupture

MR

Abnormal reversal of
blood flow from :LV
LA.

LA volume /LAP
Pulmonary congestion

Forward SV

CO

Compensatory HR

Sudden large Vol load

imposed on LA & LV of
normal size & compliance

Neurohumoral
Response :
Vascular resistance
Shock

Neurohumoral Responses
Activation
Activation
Low output
of
of
state
RAAS Contribute to maintenance of perfusion of
SNS

vital organs:
1.Maintenance of systemic pressure by
vasoconstriction, resulting in redistribution of
blood flow to vital organs
2.Restoration of CO by

myocardial
contractility and HR and by expansion of the
ECF volume
Catecholamine-stimulated contractility and HR.
Volume expansion venous return EDV SV(via FSM)

Neurohumoral Maladaptive
Responses
Activation of
RAAS

Low output state

Activation of
SNS

Catecholamine-stimulated contractility and HR.

Volume expansion venous return EDV SV(via FSM)

Maladaptive responses as below

The in diastolic pressures transmitted to the atria and

to the pulmonary circulations in capillary pressures
pulmonary congestion & peripheral edema
The in LV afterload induced by the in PVR can both
directly depress cardiac fn and enhance the rate of
deterioration of myocardial function .
Catecholamine-stimulated contractility & HR worsen
coronary ischemia (also HR EDFilling EDV SV/CO
Catecholamines and ATII promote the loss of myocytes
by apoptosis, and hypertrophy

Eccentric vs concentric
hypertrophy

EH :where the walls and

chamber of a hollow
organ undergo growth in
which the overall size
and volume are enlarged.
It is applied especially to
the LV.Sarcomeres are
added in series, as for
example in DCM (in
contrast to HOCM, a type
of CH, where sarcomeres
are added in parallel).

Pic source: www.revespcardiol.

Functional mitral
regurgitation
In patients with functional or secondary mitral regurgitation
(MR), the papillary muscles, chordae, and valve leaflets are
normal.
There are two major causes of this problem:
1.ischemia
2.any cause of dilated left ventricle.
In these settings, MR may result from one or both of the
following [1]:
Annular enlargement secondary to left ventricular dilatation
Papillary muscle displacement due to left ventricular
remodeling, which results in tethering and excess tenting of
the leaflet .2
1.Trichon BH, O'Connor CM. Secondary mitral and tricuspid regurgitation accompanying left ventricular systolic
dysfunction: is it important, and how is it treated? Am Heart J 2002; 144:373.
2.Yiu SF, Enriquez-Sarano M, Tribouilloy C, et al. Determinants of the degree of functional mitral regurgitation in
patients with systolic left ventricular dysfunction: A quantitative clinical study. Circulation 2000; 102:1400.

PREVALENCE of FMR
Some degree of functional MR is almost always
present
in
patients
with
severe
dilated
cardiomyopathy, regardless of etiology [1,2,3].
A review of 50 patients with DCM(36 idiopathic, 14
ischemic) referred for heart transplantation found that
all patients had at least moderate MR by Doppler echo
[2].
Functional MR is also a common problem in patients
with ESRD on maintenance HD. In this setting, volume
expansion rather than intrinsic cardiac disease is
primarily responsible for the cardiac enlargement.
1. Trichon BH, O'Connor CM. Secondary mitral and tricuspid regurgitation accompanying left ventricular
systolic dysfunction: is it important, and how is it treated? Am Heart J 2002; 144:373.
2. Strauss RH, Stevenson LW, Dadourian BA, Child JS. Predictability of mitral regurgitation detected by
Doppler echocardiography in patients referred for cardiac transplantation. Am J Cardiol 1987;
59:892.
3. Koelling TM, Aaronson KD, Cody RJ, et al. Prognostic significance of mitral regurgitation and tricuspid
regurgitation in patients with left ventricular systolic dysfunction. Am Heart J 2002; 144:524.

Ischemic mitral
regurgitation
Ischemic MR is a complication of coronary
heart disease.
It primarily occurs in patients with a prior
myocardial infarction (MI).
MR may also occur with acute ischemia, a
setting in which the MR typically resolves
after the ischemia resolves.
Following an MI, the MR is usually due to
infarction with permanent damage to the
papillary muscle or adjacent myocardium.

IMR:classified by the
mechanism of the valve
1.
IMR secondary to papillary muscle rupture is a
dysfunction

life-threatening complication of acute MI that

accounts for 5 % of deaths in these patients .
This complication usually occurs 2-7days after
the infarct.
2. The papillary muscle may be infarcted with
acute MI, but not ruptured.
3. The vast majority of patients have "functional"
ischemic MR. In these individuals, the papillary
muscles, chordae, and valve leaflets are normal .
However, the leaflets do not coapt and restricted
leaflet motion is frequently noted on echo.

IMR: papillary muscle

dysfunction
The term "papillary muscle dysfunction" has
been used in the literature to describe patients
with functional ischemic MR, but this is a
misnomer since papillary muscle dysfunction
does not explain the mechanism of this disorder
[1,2,3].
The mechanism for MR in this setting is better
described as "papillary muscle displacement"
due to dysfunction of underlying left ventricular
wall and associated alteration of ventricular
geometry.
1. Levine RA, Schwammenthal E. Ischemic mitral regurgitation on the threshold of a solution: from
paradoxes to unifying concepts. Circulation 2005; 112:745.
2. Kaul S, Spotnitz WD, Glasheen WP, Touchstone DA. Mechanism of ischemic mitral regurgitation. An
experimental evaluation. Circulation 1991; 84:2167.
3. Uemura T, Otsuji Y, Nakashiki K, et al. Papillary muscle dysfunction attenuates ischemic mitral
regurgitation in patients with localized basal inferior left ventricular remodeling: insights from tissue
Doppler strain imaging. J Am Coll Cardiol 2005; 46:113.

Auscultation
S1 is generally absent, soft, or buried in the
holosystolic murmur of chronic MR.
In patients with severe MR, the AV may close
prematurely, resulting in wide but physiologic
splitting of S2.
A low-pitched S3 occurring 0.120.17 s after the
AV closure sound, i.e., at the completion of the
rapid-filling phase of the LV, : DUE TO sudden
tensing of the papillary muscles, chordae
tendineae, and valve leaflets. It may be
followed by a short, rumbling, mid-diastolic
murmur, even in the absence of structural MS.
S4 is often audible in ps with acute severe MR
who are in sinus rhythm.

Auscultation
Chronic severe MR: A systolic murmur
of at least grade III/VI intensity and is
usually holosystolic.
The systolic murmur of chronic MR is
usually most prominent at the apex and
radiates to the axilla.
Acute severe MR: is decrescendo and
ceases in mid- to late systole .

Auscultation
Ruptured chordae tendineae or primary involvement
of the posterior mitral leaflet with prolapse or flail
: regurgitant jet is eccentric, directed anteriorly, and
strikes the LA wall the systolic murmur is
transmitted to the base of the heart (therefore,
may be confused with the murmur of AS).
ruptured chordae tendineae, the systolic
murmur may have a cooing or "sea gull" quality.
A flail leaflet: murmur with a musical quality.
The systolic murmur of chronic MR not due to MVP is
intensified by isometric exercise (handgrip:LVV) but
is reduced during the strain phase of the Valsalva
maneuver because of the associated decrease in
LV preload.

Mitral valve prolapse

The most important finding is the mid- or late (nonejection)
systolic click, which occurs 0.14 s or more after S 1 and is
thought to be generated by the sudden tensing of slack,
elongated chordae tendineae or by the prolapsing mitral leaflet
when it reaches its maximum excursion.
Systolic clicks may be multiple and may be followed by a highpitched, late systolic crescendo-decrescendo murmur, which
occasionally is "whooping" or "honking" and is heard best at the
apex.
The click and murmur occur earlier with standing, during the
strain phase of the Valsalva maneuver, and with any
intervention that LV volume, exaggerating the propensity of
mitral leaflet prolapse.
Conversely, squatting and isometric exercises, which LV
volume, diminish MVP; the click-murmur complex is delayed,
moves away from S1, and may even disappear.
Some patients have a mid-systolic click without a murmur;
others have a murmur without a click. Still others have both
sounds at different times.

Acute vs Chronic MR

TRICUSPID VALVE
DISEASE

Tricuspid Stenosis
Etiologi
Commonly of a multivalvular process
Rheumatic heart disease >90% cases
Carcinoid heart disease

Pathophysiology TS
TS mean diastolic pressure
gradient right atrial
pressure(RAP)systemic venous
congestion
Prominent a wave

Clinical Presentation
Fatigue
Systemic congestion signs and symptoms
Fluttering discomfort neckbecause
giant a waves

 Giant a wave
Diastolic murmur(low pitched) rivero
carvallo sign
Opening snap

Diagnostic testing
ECG: RAE, or biatrial enlargement if MS
Echo:most useful, reduction TV orifice
diameter and thickening and diastolic
doming of TV leaflets
Cath: confirmation RAP and tall a
wave

Therapy
Sodium restriction and diuretics
Ballon valvuloplasty and TV replacement

Tricuspid Regurgitation
(TR)
Primary TRanatomically abnormal valve
: congenital Ebstein anomaly, AV canal
defect and VSD
Secondary TR functional abnormality:
leaflet tethering, annular dilatation,
pulmonary hipertention etc

Clinical Presentation
Fatigue
Systemic congestion signs and symptoms
Neck pulsations because prominent cv
waves

 Pansystolic murmur (Carvallo sign)

PH: high pitched
primer: short and low pitched
Early diastolic rumble
S3 or S4

Diagnostic Testing
ECG: nonspecific,incomplete RBBB, af
Echo: right ventricular volume overload
pattern , RV enlargement, RAE
Cath: dominant v wave

Therapy
Diuretics and afterload reduction if RV
failure develops
Valve repair or replacement

TERIMAKASIH
MOHON BIMBINGAN