Transcript valvuler heart disease

VALVULER HEART
DISEASE
Yrd.Doç.Dr.Olcay ÖZVEREN
Aortic Stenosis
Pathology :
Obstruction to left ventricular (LV) outflow
Causes :
 a congenital bicuspid valve with superimposed
calcification
 calcification of a normal trileaflet valve (senile or
degenerative )
 rheumatic disease
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The risk factors of calcific AS
Similar to those for vascular atherosclerosis :
.elevated serum levels of LDL cholesterol and lipoprotein(a)
.Diabetes
.Smoking
.hypertension.
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Rheumatic Aortic Stenosis
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Rheumatic AS 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
The rheumatic valve is often regurgitant, as well as
stenotic.
Patients with rheumatic AS invariability have rheumatic
involvement of the mitral valve .
Pathophysiology
Classification of the Severity of AS
Symptoms
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exertional dyspnea (LV diastolic dysfunction, with an excessive
rise in end-diastolic pressure leading to pulmonary congestion and the limited
ability to increase cardiac output with exercise
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Angina (precipitated by exertion and relieved by rest. Angina results
from the combination of the increased oxygen needs of hypertrophied
myocardium and reduction of oxygen delivery secondary to the excessive
compression of coronary vessels
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)
Syncope (reduced cerebral perfusion that occurs during exertion when
arterial pressure declines consequent to systemic vasodilation in the presence of
a fixed cardiac output
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heart failure
)
Physical Examination
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parvus and tardus carotid impulse (slow-rising, latepeaking, low-amplitude carotid pulse . However, in patients with
associated AR or in older patients with an inelastic arterial bed,
systolic and pulse pressures may be normal or even increased. )
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The cardiac impulse is sustained and becomes
displaced inferiorly and laterally .
systolic thrill (It is palpated most readily in the second right
intercostal space or suprasternal notch and is frequently
transmitted along the carotid arteries. )
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Auscultation
The ejection systolic murmur
Typically is late peaking and heard best at the base of the heart, with radiation to the carotids .
Cessation of the murmur before A2 is helpful in differentiation from a pansystolic mitral MR murmur.
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 (Gallavardin phenomenon), in which the
murmur may be so prominent that it is mistaken for the murmur of MR.
A louder and later peaking murmur indicates more severe stenosis.
When the left ventricle fails and stroke volume falls, the systolic murmur of AS becomes
softer; rarely, it disappears altogether. The slow rise in the arterial pulse is more
difficult to recognize
The intensity of the systolic murmur varies from beat to beat when the duration
of diastolic filling varies, as in AF or following a premature contraction. This
characteristic is helpful in differentiating AS from MR, in which the murmur
is usually unaffected.
Splitting of the second heart sound
helpful in excluding the diagnosis of severe AS because normal splitting implies
the aortic valve leaflets are flexible enough to create an audible closing sound
(A2).
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Diagnostic Evaluation Modalities
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Echocardiography (definition of valve anatomy, including
the cause of AS and the severity of valve calcification, evaluation
of LV hypertrophy and systolic function, mean transaortic
pressure gradient with calculation of the ejection fraction, and
for measurement of aortic root dimensions and detection of
associated mitral valve disease.)
Cardiac Catheterization
and Angiography
 Computed Tomography
 Cardiac MR
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Clinical Outcome
Asymptomatic
Symptomatic
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2 years in patients with
heart failure
3 years in those with
syncope
5 years in those with
angina
The average rate of hemodynamic progression :
annual decrease in aortic valve area of 0.12 cm2/year
an increase in aortic jet velocity of 0.32 m/sec/year
an increase in mean gradient of 7 mm Hg/year.
Exercise test is helpful :
 Symptoms on treadmill exercise
 a decrease in blood pressure with exertion
 An elevated BNP level may be helpful when
symptoms are equivocal or when stenosis severity is
only moderate.
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Management
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Symptomatic patients with severe AS are usually
operative candidates because medical therapy
has little to offer .
Medical therapy may be necessary for patients
considered to be inoperable , HF , HT, CAD.
Diüretics ,ACE inh. ,Statins,
DC Cardiversion in AF
Surgical Treatment
Aortic Regurgitation
Causes and Pathology
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Valvular Disease
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Aortic Root Disease
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calcific AR
infective endocarditis
trauma
congenitally bicuspid valve
Rheumatic fever
SLE
rheumatoid arthritis
ankylosing spondylitis
Takayasu disease,
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Marfan syndrome;
aortic dilation related to
bicuspid valves
aortic dissection,
osteogenesis imperfecta,
syphilitic aortitis,
ankylosing spondylitis,
the Beh?et syndrome,
giant cell arteritis,
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Whipple disease,
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systemic hypertension
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Pathophysiology
Clinical Presentation
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exertional dyspnea
Angina
Syncope
heart failure
Physical Findings
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Quincke's Pulse: Capillary pulsation visible on the fingernail beds or tips
Musset's Sign: Head bobbing with each heartbeat
Müller’s Sign: Systolic pulsation of the uvula
Corrigan’s Pulse: Water-hammer pulse. Rapid distention and collapse of
arteriel pulse
Hill’s Sign: Popliteal cuff pressure more than 60 mmHg above brachial cuff
pressure
Duroziez’s Sign: To-and-fro murmur over the femoral artery with the artery
compressed
Traube’s sign: Pistol-shot sounds. Prominent systolic and diastolic sounds
over the femoral arteries
Increased pulse pressure (SBP increases and DBP decreases.)
Diastolic Murmur In AR
•In moderate AR, a relatively loud early desending diastolic murmur
is heard.
•With more severe AR, the murmur becomes longer, and will usually
decrease in intensity.
•The classic murmur caused by the regurgitant flow is best heard
along the lower left sternal border. In some cases (Marfan’s
Syndrome, VSD w/AR , aortic dissection or aneurysm) it is best
heard at the right sternal border.
• A lower-pitched mid-diastolic murmur is heard over apex this
indicates what is called an Austin Flint murmur which indicates
severe AR. (The murmur is not the regurgitant flow over the aortic
valve, but rather vibrations in a restricted Mitral Valve when the left
atrium empties and is met with the opposite flow from the aortic
valve.)
•In addition to the diastolic murmur(s), a systolic flow murmur like in
aortic stenosis may be heard. This is not necessarily indicating a
calcified valve, as the increased velocity resulting from ventricular
overload will also cause flow vibrations)
Diagnostic Evaluation Modalities
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Echocardiography (bicuspid valve, thickening of the valve
cusps, other congenital abnormalities, prolapse of the valve, a
flail leaflet, or vegetation )
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Electrocardiography (left axis deviation and a pattern of
LV diastolic volume overload, characterized by an increase in
initial forces (prominent Q waves in leads I, aVL, and V3
through V6) and a relatively small wave in lead V1 )
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Radiography
Cardiac Magnetic Resonance Imaging
Angiography
electrocardiography
Chest x ray
echocardiography
Disease Course
asymptomatic
symptomatic
Management
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Medical Treatment :There is no specific therapy to prevent
disease progression in chronic AR.
Systemic arterial hypertension, should be treated because it
increases the regurgitant flow; vasodilating agents such as ACE
inhibitors or ARB are preferred, and beta-blocking agents
should be used with great caution.
Chronic medical therapy may be necessary for some
patients who refuse surgery or are considered to be
inoperable because of comorbid conditions. These
patients should receive an aggressive heart failure
regimen with ACE inhibitors (and perhaps other
vasodilators), digoxin, diuretics, and salt restriction;
beta blockers may also be beneficial.
Surgical Treatment
Acute Aortic Regurgitation
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Causes: infective endocarditis, aortic dissection, trauma
The characteristic features of acute AR are tachycardia and an
increase in LV diastolic pressures.
The sudden increase in LV filling causes the LV diastolic pressure
to rise rapidly above left atrial pressure during early diastole .
Premature closure of the mitral valve, together with tachycardia that
also shortens diastole, reduces the time interval during which the
mitral valve is open.
The tachycardia may compensate for the reduced forward stroke
volume, and the LV and aortic systolic pressures may exhibit little
change.
Acute severe AR may cause profound hypotension and cardiogenic
shock .
Weakness, severe dyspnea, and profound hypotension secondary to
the reduced stroke volume and elevated left atrial pressure .
Physical Examination
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tachycardia, severe peripheral vasoconstriction, and
cyanosis, and sometimes pulmonary congestion and
edema.
S1 may be soft or absent because of premature closure
of the mitral valve, and the sound of mitral valve
closure in mid or late diastole is occasionally audible.
Closure of the mitral valve may be incomplete, and
diastolic MR may occur
The early diastolic murmur of acute AR is lower
pitched and shorter than that of chronic AR because as
LV diastolic pressure rises, the (reverse) pressure
gradient between the aorta and left ventricle is rapidly
reduced.
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Echocardiography:In acute AR the echocardiogram reveals a
dense, diastolic Doppler signal with an end-diastolic velocity
approaching zero and premature closure and delayed opening of
the mitral valve. LV size and ejection fraction are normal.
 Electrocardiography: In acute AR, the ECG may or may not
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show LV hypertrophy, depending on the severity and duration of
the regurgitation. However, nonspecific ST-segment and T wave
changes are common.
Radiography :In acute AR, there is often evidence of marked
pulmonary venous hypertension and pulmonary edema.
Management
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Early death caused by LV failure is frequent in patients with
acute severe AR despite intensive medical management, prompt
surgical intervention is indicated.
Even a normal ventricle cannot sustain the burden of acute,
severe volume overload.
While the patient is being prepared for surgery, treatment with
an intravenous positive inotropic agent (dopamine or
dobutamine) and/or a vasodilator (nitroprusside) is often
necessary.
In hemodynamically stable patients with acute AR secondary to
active infective endocarditis, operation may be deferred to allow
5 to 7 days of intensive antibiotic therapy . However, AVR
should be undertaken at the earliest sign of hemodynamic
instability or if echocardiographic evidence of diastolic closure of
the mitral valve develops.
MITRAL STENOSIS
MITRAL VALVE ANATOMY
Etiology
1. Rheumatic Fever
2. Congenital Mitral Stenosis
Pathophysiology
1. Increased left atrial pressure
2. Pulmonary vasoconstriction
3. Pulmonary Hypertension
4. Right Ventricular Failure
5. Decreased cardiac output
Pathophysiology
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
LV Filling
Symptoms
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Fatigue
Palpitations
Cough
Chest pain
SOB
Left sided failure
 Orthopnea
 PND
 Exercise
Palpitation
Hoarseness (Ortner’s
syndrome
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Afib
Systemic embolism
Pulmonary infection
Hemoptysis
Right sided failure
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Hepatic Congestion
Edema
Precipitating Factors
Exertion
Fever
Anemia
Pregnancy
Atrial Fibrillation
hypertiroid
Recognizing Mitral
Stenosis
Palpation:
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Small volume pulse
Tapping apex-palpable S1
+/- palpable opening snap
(OS)
RV lift
Palpable S2
ECG:
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LAE, AFIB, RVH, RAD
Auscultation:
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Loud S1- as loud as S2 in aortic
area
A2 to OS interval inversely
proportional to severity
Diastolic rumble: length
proportional to severity
In severe MS with low flow- S1,
OS & rumble may be inaudible
Mitral Stenosis: Physical Exam
S1
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S2 OS
S1
First heart sound (S1) is accentuated and snapping
Opening snap (OS) after aortic valve closure
Low pitch diastolic rumble at the apex
Pre-systolic accentuation (esp. if in sinus rhythm)
© Continuing Medical
Implementation
…...bridging the care gap
Common Murmurs and
Timing
Systolic Murmurs
 Aortic stenosis
 Mitral insufficiency
 Mitral valve prolapse
 Tricuspid insufficiency
Diastolic Murmurs
 Aortic insufficiency
 Mitral stenosis
S1
S2
os
S1
Signs: Later findings of right
ventricular failure
•Accentuated precordial thrust of right
ventricle
•Elevated neck veins
•Ascites
•Edema
Complications
Hemoptysis
Embolism
Pulmonary infection
Endocarditis
Atrial fibrillation
Radiology
Chest XRay
Double density of left atrial enlargement
Right ventricular enlargement
Posterior displacement of esophagus
Mitral valve calcification
Kerley B Lines
Echocardiogram
Mitral valve leaflet changes
Inadequate separation of valve leaflets
Valve leaflet calcification and thickening
Doppler estimates transvalvular
gradient
Mitral Stenosis - upper lobe blood
diversion
Trivial enlargement of the transverse diameter of the heart. Left atrium causes double outline (opposite
right arrow) and is somewhat dilated. Left atrial appendage is dilated, causing a prominence of the left
border (opposit left arrow). Upper lobe vessels larger than lower lobe vessels, that is, upper lobe blood
diversion. An arrow points to a dilated upper lobe vein.
Mitral Stenosis - septal line shadows.
Kerley "B"
Horizontal short line shadows, septal (Kerley "B") lines above the costo-phrenic recesses, indicating
interstitial oedema of the septa, often with haemosiderin in the adjacent alveoli.
Mitral Stenosis - hilar oedema
Hilar vessels indistinct, peri-hilar haze. Also upper lobe blood diversion and septal line shadows.
Arrow points to a Kerley "A" line, due either to septal oedema or oedema around an
intercommunicating lymphatic during its course from a perivenous to a pericardial position or vice
versa.
echocardiography
Prognosis
Slow, progressive, life-long course
Latent period of 20 to 40 years after Rheumatic
Fever
Rapid acceleration of symptoms in later life
Management
Rheumatic Fever prophylaxis until age 35 years
Benzathine Penicillin G 1.2 MU IM monthly OR
Penicillin VK 125-250 mg PO bid
Treat complications and associated conditions
Atrial Fibrillation
Congestive Heart Failure
Anticoagulation for history of emboli
Beta blocker. Digitalis.diüretics
Surgery
Open Mitral valvotomy
Percutaneous balloon valvuloplasty
Mitral Valve Replacement
MITRAL REGURGITATION
MITRAL VALVE ANATOMY
Etiology
Rheumatic Heart Disease
Mitral Valve Prolapse
Ischemic Heart Disease and papillary muscle
dysfunction
Left Ventricular dilatation
Mitral annular calcification
Hypertrophic Cardiomyopathy
Infective endocarditis
Congenital mitral regurgitation
Pathophysiology
Early or compensated mitral regurgitation
Volume overload
Left Ventricular Hypertrophy
Left atrial enlargement
Late or decompensated mitral regurgitation
Left Ventricular Failure
Decreased ejection fraction
Pulmonary congestion
Pathophysiology of mitral
regurgitation
In the normal heart, left ventricular (LV) contraction during systole forces blood exclusively through the aortic valve
into the aorta; the closed mitral valve prevents regurgitation into the left atrium (LA). In mitral regurgitation (MR), a
portion of the LV output is forced retrograde into the LA, so that forward cardiac output into the aorta is reduced. In
acute MR, the LA is of normal size and is noncompliant, such that the LA pressure rises markedly and pulmonary
edema may result. In chronic MR, the LA has enlarged and is more compliant, such that LA pressure is less
elevated and pulmonary congestive symptoms are less common if LV contractile function is intact. There is LV
enlargement and eccentric hypertrophy due to the chronic increased volume load.
Pathophysiology
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The severity of MR and the ratio of forward cardiac
flow (cardiac output) to backward flow are determined
by several, interacting factors: 1) the size of the mitral
orifice during regurgitation
2) the systemic vascular resistance opposing
forward flow from the ventricle
3) the compliance of the left atrium
4) the systolic pressure gradient between the LV
and the LA
5) the duration of regurgitation during systole (not
all regurgitation is holo-systolic)
Symptoms
Dyspnea
Fatigue
Weakness
Cough
Physical findings
Holosystolic Murmur at Apex
Harsh, medium pitched pansystolic murmur
Murmur obliterates M1
Radiation
Axilla
Upper sternal borders
Subscapular region
Soft or diminished First Heart Sound (S1)
P2 heart sound augmented
S2 Heart Sound with wide split
S3 Gallop rhythm (indicative of severe disease)
Accentuated and displaced precordial Apical Thrust
Systolic thrill
MURMUR
Laboratuary findings
Electrocardiogram
Left Ventricular Hypertrophy
Left Axis Deviation
Chest XRay
Enlarged left atrium
Dilated left ventricle
Echocardiogram
Enlarged left atrium
Hyperdynamic left ventricle
Doppler assess severity
CHEST X-RAY
echocardiography
Monitoring
Annual or semi-annual echocardiogram
Assess ejection fraction
Assess end-systolic dimension
Management
Anticoagulation in Atrial Fibrillation
Treat Congestive Heart Failure
Diuretics
Digoxin
Afterload reduction
ACE Inhibitor
Hydralazine
Nitroprusside (especially acute MR)
Surgery
Mitral Valve repair or replacement
Repair before Heart Failure develops
Keep ejection fraction >60%
Keep end-systolic dimension <45 mm
Indications
Cardiopulmonary Symptoms (NYHA Class II-IV)
Left Ventricular function impaired
Tricuspid Valve Diseases
The forgotten valve
Tricuspid Valve Anatomy
TV annuluss
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The tricuspid valve is the most apically (or caudally)
placed valve with the largest orifice among the four
valves.
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The tricuspid annulus is oval-shaped and when
dilated becomes more circular.
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20% larger than MV annulus .
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Normal TV annulus= 3.0 - 3.5 cm
Leaflets
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the tricuspid valve has three distinct leaflets
described as septal, anterior, and posterior.
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The septal and the anterior leaflets are larger.
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The posterior leaflet is smaller and appears to be
of lesser functional significance since it may be
imbricated without impairment of valve
function.
Leaflets
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The septal leaflet is in immediate proximity of
the membranous ventricular septum, and its
extension provides a basis for spontaneous
closure of the perimembranous ventricular
septal defect.
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The anterior leaflet is attached to the
anterolateral margin of the annulus and is often
voluminous and sail-like in Ebstein’s anomaly.
Papillary Muscles & Chordae
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There are three sets of small papillary muscles,
each set being composed of up to three muscles.
The chordae tendinae arising from each set are
inserted into two adjacent leaflets.
the anterior set chordae insert into half of the
septal and half of the anterior leaflets.
The medial and posterior sets are similarly
related to adjacent valve leaflets.
Etiology of Primary Tricuspid Valve
Disease
Congenital
—Cleft valve generally in association with atrioventricular canal defect
—Ebstein’s anomaly
—Congenital tricuspid stenosis
—Tricuspid atresia
• Rheumatic valve disease, generally in association with rheumatic mitral
valve disease
• Infective endocarditis
• Carcinoid heart disease
• Toxic (eg, Phen-Fen valvulopathy or methysergide valvulopathy)
• Tumors (eg, myxoma)
• Iatrogenic—pacemaker lead trauma
• Trauma—blunt or penetrating injuries
• Degenerative—tricuspid valve prolapse
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Etiology of Secondary or Functional
Tricuspid Valve Disease
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Right ventricular dilatation
Right ventricular hypertension
Global right ventricular dysfunction resulting from
cardiomyopathy, myocarditis, or longstanding right
ventricular hypertension with fibrosis
Segmental dysfunction secondary to ischemia or
infarction of the right ventricle, endomyocardial
fibrosis, arrhythmogenic right ventricular dysplasia
Clinical Presentations
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Pure or predominant tricuspid stenosis
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Pure or predominant tricuspid regurgitation
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Mixed
Tricuspid valve disease—
Symptoms
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Fatigue
Liver/gut congestion
Right upper quadrant discomfort
Dyspepsia
Indigestion
Fluid retention with leg edema
Ascites
Tricuspid valve disease ausculatory
findings
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Stenosis : Low-to medium-pitch diastolic
rumble with inspiratory accentuation
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Regurgitation : Soft, early, or holosystolic
murmur Augmented with inspiratory effort
(Caravallo’s sign)
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Prolapse : Systolic click
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Substantial tricuspid regurgitation may exist
without the classic ausculatory findings. Thus,
clinical evaluation including cardiac auscultation
cannot be used to exclude tricuspid valve disease.
Transthoracic Echo Views
Transesophageal Views
Transesophageal Views
Key Diagnostic Features
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Mild TR is seen in up to 60% and Moderate TR
in up to 15% of healthy individuals.
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Mild or worse TR in a valve with thin leaflets,
normal coaptation, and normal-appearing
supporting structures, suggests regurgitation
is physiologic or functional .
Key Diagnostic Features
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In carcinoid disease, the leaflets are thickened
and retracted with a fixed orifice usually leading
to predominant regurgitation and less severe
stenosis.
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Approximately 30% of patients with MVP have
redundancy and prolapse of the tricuspid valve,
leading to TR.
TR & TS Severity
PAP based on TR Velocity
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Mild increased PAP = 2.6 - 2.9 m/s (27-33
mmhg)
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Moderate increased PAP = 3.0 - 3.9 m/s (36-60
mmhg)
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Severe increased PAP = 4.0≤ (64 mmhg ≤ )
European Guideline for TV managment
AHA/ACC Guideline for TV managment