valvulopathies

Normal Valve Function

• Maintain forward flow

and prevent reversal of
flow.
• Valves open and close
in response to pressure
differences (gradients)
between cardiac
chambers.
 Abnormal Valve Function
• Valve Stenosis
– Obstruction to valve flow during that phase of the cardiac cycle when
the valve is normally open.
– Hemodynamic hallmark -“pressure gradient” ~ flow// VA
• Valve Regurgitation, Insufficiency, Incompetence
– Inadequate valve closure--- back leakage
• A single valve can be both stenotic and regurgitant; but both
lesions cannot be severe!!
• Combinations of valve lesions can coexist
– Single disease process
– Different disease processes
– One valve lesion may cause another
– Certain combinations are particularly burdensome (AS & MR)
1. Mitral Stenosis
 Mitral Stenosis Overview

• Definition: Obstruction of LV inflow that

prevents proper filling during diastole
• Normal MV Area: 4-6 cm2
• Transmitral gradients and symptoms begin
at areas less than 2 cm2
• Rheumatic carditis is the predominant
cause
• Prevalence and incidence: decreasing due
to a reduction of rheumatic heart disease.
Mitral Stenosis
 Mitral Stenosis:
Pathophysiology
Right Heart Failure  Pulmonary HTN
Hepatic Congestion Pulmonary Congestion
JVD Atrial Fibrillation
Tricuspid Regurgitation LA Thrombi
RA Enlargement LA Enlargement
 LA Pressure

RV Pressure Overload
RV Hypertrophy
RV Failure ↓LV Filling
↓LV Output
Mitral Stenosis
 Pathophysiology

• Limited flow into the LV has 3 major sequale:

– Elevation of Lt. Atrial pressure
– Secondary RV pressure overload, hemoptisy
– Reduced LV ejection performance
• Due to diminished preload
• Tachycardic response to compensate to
decreased SV worsens the transmitral
gradient
 Mitral Stenosis:
Pathophysiology
• Normal valve area: 4-6 cm2
• Mild mitral stenosis:
– MVA 1.5-2.5 cm2
– Minimal symptoms
• Mod mitral stenosis
– MVA 1.0-1.5 cm2 usually does not produces
symptoms at rest
• Severe mitral stenosis
– MVA < 1.0 cm2
 Etiology of Mitral Stenosis
• Rheumatic heart disease: 77-99% of all cases
• Infective endocarditis: 3.3%
• Mitral annular calcification: 2.7%
 Mitral Stenosis: Natural History
• Progressive, lifelong disease,
• Usually slow & stable in the early years.
• Progressive acceleration in the later years
• 20-40 year latency from rheumatic fever to
symptom onset.
• Additional 10 years before disabling symptoms
• Mortality: Due to progressive pulmonary
congestion, infection, and thromboembolism
2. Mitral Regurgitation
2. Mitral Regurgitation
 Pathophysiology of MR
• Pure Volume Overload
• Compensatory Mechanisms: Left atrial
enlargement, LVH and increased
contractility
– Progressive left atrial dilation and right
ventricular dysfunction due to pulmonary
hypertension.
– Progressive left ventricular volume overload
leads to dilation and progressive heart failure.
 MR Pathophysiology
• Chronic LV volume overload -» compensatory
LVE initially maintaining cardiac output
• Decompensation (increased LV wall tension) -
»CHF
• LVE – » annulus dilation – » increased MR
• Backflow – » LAE, Afib, Pulmonary HTN

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 Mitral Regurgitation:
Etiology
• Valvular-leaflets • Annulus
– Myxomatous MV – Calcification, IE (abcess)
Disease • Papillary Muscles
– Rheumatic
– CAD (Ischemia,
– Endocarditis Infarction, Rupture)
– Congenital-clefts – HCM
• Chordae – Infiltrative disorders
– Fused/inflammatory • LV dilatation &
– Torn/trauma functional regurgitation
– Degenerative
• Trauma
– IE
Chronic Mitral Regurgitation Overview

• Definition: Backflow of blood from the LV to

the LA during systole
• Mild (physiological) MR is seen in 80% of
normal individuals.
 Acute MR
• Endocarditis
• Acute MI:
• Malfunction or disruption of prosthetic valve
 Etiologies of Chronic Mitral
Regurgitation

• Myxomatous degeneration (MVP)

• Ischemic MR
• Rheumatic heart disease
• Infective Endocarditis
Pathophysiology –Acute vs Chronic Mitral
Regurgitation
• Acute MR
– Normal (noncompliant) LA
– Increase LA pressure
– large “V” waves
– Acute Pulmonary Edema
• Chronic MR
– Dilated, compliant LA
– LA pressure normal or slightly
increased
– Fatigue, low output state
– Atrial arrhythmias- a. fib.
• Most patients fall between these
two extremes!!
Pathophysiology –Acute vs Chronic
Mitral Regurgitation
 Physical Exam findings in MR
• Auscultation: soft S1 and a holosystolic
murmur at the apex radiating to the axilla
– S3 (CHF/LA overload)
– In chronic MR, the intensity of the murmur
does correlate with the severity.
• Exertion Dyspnea: ( exercise intolerance)
• Heart Failure: May coincide with increased
hemodynamic burden e.g., pregnancy,
infection or atrial fibrillation
 Imaging studies in MR

• ECG: May show, LA enlargement, atrial

fibrillation and LV hypertrophy with severe MR
• CXR: LA enlargement, central pulmonary artery
enlargement.
• ECHO: Estimation of LA, LV size and function.
Valve structure assessment
– TEE if transthoracic echo is inconclusive
 MR Symptoms
• Similar to MS
• Dyspnea, Orthopnea, PND
• Fatigue
• Pulmonary HTN, right sided failure
• Hemoptysis
• Systemic embolization in A Fib

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 The Natural History of MR
• Compensatory phase: 10-15 years
• Patients with asymptomatic severe MR have a
5%/year mortality rate
• Once the patient’s EF becomes <60% and/or
becomes symptomatic, mortality rises sharply
• Mortality: From progressive dyspnea and
heart failure
3. Aortic Stenosis
 Definition
Aortic Stenosis is the narrowing of the aortic
valve opening caused by the

failure of the valve leaflets to open normally.

Concentric LVH then develops due to an

increase in LV pressure.
 AORTIC STENOSIS
• Thickening and stiffening of the LV in the face
of increasing obstruction results in increased
LVEDP
Result = LAH and diastolic dysfunction
• Left atrium becomes critical in filling the
ventricle and Atr. Fibr. or AV dissociation are
poorly tolerated
 AORTIC STENOSIS
• In significant Ao. stenosis, the cardiac
output may be fairly well maintained at rest but
fails to augment with exercise
• Late in the course of severe AS : cardiac
output, stroke volume, and the gradient itself
all decline,……while the mean LA pressure,
capillary wedge pressure and P.A. pressure
increase
 Pathophysiology of Aortic Stenosis
• A pressure gradient develops between the left
ventricle and the aorta. (increased afterload)
• LV function initially maintained by
compensatory pressure hypertrophy
• When compensatory mechanisms are
exhausted, LV function declines.
 Aortic Stenosis Overview:

• Normal Aortic Valve Area: 3-4 cm2

• Symptoms: Occur when valve area is

1/4th of normal area.
• Types:
– Supravalvular
– Subvalvular
– Valvular
 Etiology of Aortic Stenosis
• Congenital
• Rheumatic
• Degenerative/Calcific

Patients under 70: >50% have a congenital

cause
Patients over 70: 50% due to degenerative
 Etiology
1. Tricuspid Aortic Valve Degeneration
2. Bicuspid Aortic Valve
3. Congenital Aortic Stenosis
4. Rheumatic Fever
5. Other Causes
Aortic Valve Variations

• A – Normal Valve
• B – Congenital AS
• C – Rheumatic AS
• D – Bicuspid AS
• E – Senile AS

From Brandenburg RO, et al: Valvular heart disease—When should

the patient be referred? Pract Cardiol 5:50, 1979

 Tricuspid Aortic Valve
Degeneration
• Senile Degeneration 2° to calcifications
• Most common cause of AS age > 70
• Risk factors include DM & Cholesterol
• Pathophysiology of degeneration is
unknown
 Bicuspid Aortic Valve
• Most common congenital heart anomaly
• Most common cause of AS age < 70
• 50% develop mild AS by age 50
• Increased incidence in Turners Syndrome
 Congenital AS
• Fusion of valve leaflets before birth
• More hypertrophy yet patients almost
never develop heart failure symptoms
• 15% encounter sudden death
 Rheumatic Fever

• Currently less common in the U.S.

• Still prevalent in other countries
• Almost always in combination with
mitral valve abnormality
 Other Causes
• SLE
• Severe Familial Hypercholesterolemia
• Fabry’s Disease
• Ochronosis
• Paget’s Disease of the Bone
 AORTIC STENOSIS

• In general:

• Mild Aortic Stenosis=1.5-2.0 cm2

• Moderate Stenosis=1-1.5 cm2
• Severe Aortic Stenosis=<1.0 cm2
• Critical Aortic Stenosis=<0.8 cm2
 Compensatory Mechanisms
• Adaptive and maladaptive:

- Progressive worsening of left ventricular outflow

obstruction leads to hypertrophy;
- Compensatory hypertrophy is required to maintain wall
stress (cardiac output and afterload)
- Augmented preload with increased atrial kick will
preserve LV systolic function
 Complications of the Aortic Stenosis

• Heart failure
• Angina
• Syncope
• Sudden death
 Heart Failure
• Shortness of breath (diastolic and sistolic
dysfunction)
• Changes in LV function may no longer be adequate to
overcome the outflow obstruction
– Hypertrophic remodeling leads to diastolic
dysfunction
– Afterload excess results in decreased ejection
fraction – systolic dysfunction
• 50% presentation
• 50% die in 2 years
 Angina
• = increased myocardial oxygen demand;
(demand/supply mismatch)
• Progressive LV hypertrophy from aortic
stenosis leads to increased myocardial oxygen
needs3
– Hypertrophy may compress the coronary arteries
– Reduced diastolic filling may result in classic
angina, even in the absence of coronary artery
disease4
• 35% presentation
• 50% die in 5 years
 Syncope
• exertional: cardiac output no longer increases
with exercise
• a drop in systemic vascular resistance, that
normally occurs with exertion, may lead to
hypotension and syncope
• 15% presentation
• 50% die in 3 years
 Physical Findings in Aortic Stenosis

• Slow rising carotid pulse (pulsus tardus) &

decreased pulse amplitude (pulsus parvus)

• Heart sounds- soft and split second heart

sound, S4 gallop due to LVH.

• Systolic ejection murmur- cresendo-

decrescendo character. This peaks later as
the severity of the stenosis increases.
– Loudness does NOT tell you anything about
severity
 Natural History

• Mild AS to Severe AS:

– 8% in 10 years
– 22% in 22 years
– 38% in 25 years

• The onset of symptoms is a poor prognostic

indicator.
 Evaluation of AS
• Echocardiography is the most valuable test
for diagnosis, quantification and follow-up
of patients with AS.
• Two measurements obtained are:
a) Left ventricular size and function: LVH,
Dilation, and EF
b) Doppler derived gradient and valve area
(AVA)
 Management of AS

• General- IE prophylaxis in dental procedures

with a prosthetic AV or history of endocarditis.
• Medical - limited role since AS is a mechanical
problem. Vasodilators are relatively
contraindicated in severe AS
• Aortic Balloon Valvotomy- shows little benefit.
• Surgical Replacement: Definitive treatment
 Summary

• Disease of aging
• Look for the signs on physical exam
• Echocardiogram to assess severity
• Asymptomatic: Medical management and
surveillance
• Symptomatic: AoV replacement (even in
elderly and CHF)
4. Aortic Regurgitation
 Aortic Regurgitation Overview

• Definition: Leakage of blood from aorta into

LV during diastole due to ineffective
coaptation of the aortic cusps
 Pathophysiology of AR
• Combined pressure AND volume overload

• Compensatory Mechanisms: LV dilation, LVH.

Progressive dilation leads to heart failure
Aortic Regurg – pathophysiology
Aortic Regurg – pathophysiology
 Etiology of Acute AR
• Infective endocarditis (majority of cases)
• Aortic Dissection of the root of the aorta
• Trauma

• Physical Findings:
– Wide pulse pressure
– Diastolic murmur
– Florid pulmonary edema
 Etiology of Chronic AR

• Bicuspid aortic valve

• Rheumatic
• Infective endocarditis
 Acute vs Chronic AR
Pathophysiology and Clinical Presentation

• Acute Aortic Regurgitation

– Sudden AoV incompetence
– Noncompliant LV
– Acute Pulmonary Edema
– Emergency AVR
• Chronic Aortic Regurgitation
– Long asymptomatic phase
– Progressive LV dilatation
– DOE, orthopnea, PND
– Frequent PVC’s
 Natural History of AR
• Asymptomatic until 4th or 5th decade
• Rate of Progression: 4-6% per year
• Progressive Symptoms include:
- Dyspnea: exertional, orthopnea, and
paroxsymal nocturnal dyspnea
- Nocturnal angina: due to slowing of heart rate
and reduction of diastolic blood pressure
- Palpitations: due to increased force of
contraction
 Physical Exam findings of AR
• Wide pulse pressure: most sensitive
• Hyperdynamic and displaced apical impulse
• Auscultation-
– Diastolic blowing murmur at the left sternal border
– Austin flint murmur (apex): Regurgitant jet
impinges on anterior MVL causing it to vibrate
– Systolic ejection murmur: due to increased flow
across the aortic valve
 The Evaluation of AR
• CXR: enlarged cardiac silhouette and aortic
root enlargement
• ECHO: Evaluation of the AV and aortic root
with measurements of LV dimensions and
function (cornerstone for decision making and
follow up evaluation)
• Aortography: Used to confirm the severity of
disease
 Management of AR
• General: IE prophylaxis in dental procedures
with a prosthetic AV or history of
endocarditis.
• Medical: Vasodilators (ACEI’s), Nifedipine
improve stroke volume and reduce
regurgitation only if pt symptomatic or HTN.
• Serial Echocardiograms: to monitor
progression.
• Surgical Treatment: Definitive Tx
Acute valvulpopathies
 Introduction
• There may be abnormalities of cusps, chordae,
or papillary muscles causing valvular
dysfunction.
• Significant valvular abnormality increases
stroke rate 3.2 times and death rate 2.5 times
 Diagnosing a New Murmur
• A diastolic murmur or new murmur warrants
cardiology referral for evaluation/echo.
• Urgency for accurate diagnosis and referral or
admission depends on severity of symptoms not
presence of murmur unless aortic stenosis and
syncope is suspected. Patient may be at risk for
recurrent cardiovascular event.
 Innocent or Physiologic Murmur
• No abnormal symptoms or signs
• Soft, systolic ejection murmur begins after S1
and ends before S2, and heart sounds are
normal
• Review of symptoms reveals no symptoms
compatible with cardiovascular disease, and
complete physical exam is normal.
 Acute Valve Disease
• Acute valve disease can result in dramatic
symptoms.
• Consider murmur in context of patient’s
medical condition
• Patient may have normal cardiac anatomy, but
murmurs can be associated with other disease
states.
• Examples include anemia, thyrotoxicosis,
sepsis, fever, renal failure, and pregnancy
 Chronic Valve Disease
• There may be decades between onset of
dysfunction and symptoms
• Dilation or hypertrophy may preserve cardiac
function
• Account for around ninety percent of valvular
disease