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Disorders of the heart valves
Disorders of the heart valves
Damage and dysfunction of the heart valves most commonly occurs as a result of :
Infective endocarditis or
Congenital defects or abnormalities of the heart valves
Two major types of changes are seen in heart valves:
Stenosis and Regurgitation (also called insufficiency or incompetence)
• Acute and Chronic
• Acute and Chronic
The valve opening narrows
The valve leaflets may become fused or thickened that the valve cannot open freely
obstructs the normal flow of blood
EFFECTS: the chamber behind the stenotic valve is subject to
o greater stress must generate more pressure or work
o hard to force blood through the narrowed opening
initially, the heart compensates for the additional workload by gradual
hypertrophy and dilation of the myocardium heart failure
Valvular Insufficiency or Regurgitation
Scarring and retraction of valve leaflets or weakening of supporting structures
incomplete closure of the valve result to leakage or backflow of blood from the previous
o causes the Heart to pump the same blood twice (as the blood comes back into the
o the Heart dilates to accommodate more blood (the usual blood it needs to pump
+ regurgitated blood)
o ventricular dilation and hypertrophy eventually leads to heart failure
Heart Murmur: is an extra or unusual sound heard during a heartbeat.
Mnemonic: Systolic Murmurs ( ASaMR) Diastolic Murmurs (ARMS)
Aortic Stenosis Overview:
Normal Aortic Valve Area: 3-4 cm2
Symptoms: Occur when valve area is 1/4th
of normal area.
The normal aortic valve consists of three thin and pliable valve leaflets
Bicuspid aortic valve (BAV) is a congenital condition of the aortic valve where two of
the aortic valvular leaflets fuse during development resulting in a valve that is bicuspid (2
leaflets) instead of the normal tricuspid configuration. Persons born with an abnormal
bicuspid valve are particularly susceptible to calcification later in life.
Normally the only cardiac valve that is bicuspid is the mitral valve (bicuspid valve).
Aortic Stenosis causes & Consequences
may be due to rheumatic heart disease, atherosclerosis, congenital valvular disease or
narrowing of the aortic valve flow of blood from the left ventricle to the aorta
blood volume and pressure in the left ventricle
Left ventricle hypertrophy develops as a compensatory mechanism to continue pumping
blood through the narrowed opening
Patients under 70: >50% have a congenital cause
Patients over 70: 50% due to degenerative
Pathophysiology of Aortic Stenosis
fatigue & exertional dyspnea – 1st
symptoms – due to CO and pulmonary congestion
chest pain (angina) – most common symptom
o occurs during exercise – due to inability of the heart to increase coronary blood
flow to cardiac muscle
exertional syncope, vertigo, periods of confusion -- CO
weakness, orthopnea, PND, pulmonary edema (severe cases)
signs of right-sided heart failure –- end-stage symptoms
- if untreated, survival rate: 1.5-3 years
Auscultation: harsh, rough, mid-systolic ejection murmur
Management of AS
General- IE prophylaxis in dental procedures with a prosthetic AV or history of
o limited role since AS is a mechanical problem.
o restrict activity
o Na+ restriction, diuretics
o Nitroglycerin – for chest pain
o Aortic Balloon Valvotomy- shows little benefit.
o Surgical Replacement: Definitive treatment (even in elderly and CHF)
Mitral stenosis Definition
Mitral stenosis is characterized by thickening, fibrosis and hardening of the mitral
annulus, such as mitral orifice narrows and blood cannot pass by to the left ventricle.
obstruct blood flow from left atrium to the left ventricle that prevents LV proper filling
The consequence of this is the accumulation of blood in the left atrium and then to the
lungs (heart failure and pulmonary edema).
Normal MV Area: 4-6 cm2
, symptoms begin at areas less than 2 cm2
Mitral Stenosis Overview
Most common valvular disorder in Rheumatic Heart Disease (RHD)
Considered late complications of rheumatic fever.
Rheumatic fever is a late sequela to Group A β-hemolytic streptococcal infection of the
However, most often strep infection is asymptomatic and thereby properly left untreated
(treatment consist in eradication of infection with penicillin).
14 days after the onset of infection a series of immune complexes are formed with high
affinity for connective tissue (like heart valves – M protein).
Mitral stenosis occurs after a free interval of 10-20 years from initial rheumatic attack,
but is often asymptomatic in the early stages.
The incidence of rheumatic mitral stenosis decreased in recent years due to the
identification and proper treatment of beta-hemolytic streptococci infection. However,
the condition is quite common in cold and wet climates.
Mitral Stenosis Pathophysiology
MS Symptoms & Signs
Progressive Dyspnea (70%): LA dilation pulmonary congestion (reduced emptying) :
worse with exercise, fever, tachycardia, and pregnancy
Increased Transmitral Pressures: Leads to left atrial enlargement Arrhythmia (irregular
heart beats) called atrial fibrillation.
Atrial fibrillation is the most common arrhythmia in mitral stenosis and can cause serious
complications such as systemic embolisms.
Anticoagulant medication (Warfarin “Coumadin” : is still used prophylactically, it helps
to prevent thrombus formation at the level of the dilated left atrium.
Right heart failure symptoms: due to Pulmonary venous HTN
Hemoptysis (Coughing Blood): due to rupture of bronchial vessels due to elevated
Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism
Physical Exam Findings of MS
Presence of bilateral peripheral edema, especially in the ankle, with warm skin, slightly
The present of hepatojugular reflux ( blood outpouring in the veins of the neck,
secondary to liver stasis); prominent "a" wave in jugular venous pulsations (JVP): Due to
pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure: in advanced disease
Lung auscultation may reveal the present of hyperemia rales, at the level of lung bases
Mitral facies:(Malar flush) When MS is severe and the cardiac output is diminished, there
is vasoconstriction, resulting in pinkish-purple patches on the cheeks
exertional dyspnea and fatigue (most common)
orthopnea, paroxysmal nocturnal dyspnea, cough, hemoptysis
Right-sided heart failure – distended neck veins, peripheral edema, hepatomegaly,
o Mid diastolic murmur (apex)
Evaluation of MS
ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and
mitral valve area
Management of MS
MS like AS is a mechanical problem and medical therapy does not prevent progression
Medical Therapy is aimed at preventing the complications of systemic embolization and
bacterial endocarditis as well as atrial fibrillation.
Patients who have asymptomatic mitral stenosis require only antibiotic prophylaxis.
IE prophylaxis: also with Patients with prosthetic valves or a Hx of IE for dental
Patients with mild pulmonary congestion can be managed with diuretics alone. β -
Blockers can be used to reduce heart rate and improve diastolic filling time.
When patients have atrial fibrillation, digoxin, β-blockers, or calcium channel blockers
can be used for ventricular response rate control.
Patients with atrial fibrillation require anticoagulation to prevent thrombus formation in
Once the patient has symptoms despite adequate medical management, mechanical
correction of mitral stenosis by:
Balloon valvuloplasty :. It is minimally invasive procedure; done by cardiac
Surgery: by Commissurotomy which is an open-heart surgery that repairs a mitral
valve that is narrowed from mitral valve stenosis.
Mitral valve replacement – when stenosis is severe
MS Surgical Treatment
o is the leaking of the aortic valve that causes blood to flow in the reverse direction
during ventricular diastole, from the aorta into the left ventricle.
o LV dilation, LVH. Progressive dilation leads to heart failure
o Rheumatic Fever – most common cause
o Bicuspid aortic valve disease
o Severe hypertension
o Congenital anomaly
Symptoms & Signs of AR
Asymptomatic until 4th
Rate of Progression: 4-6% per year
Progressive Symptoms include:
o Dyspnea: Shortness of breath
o Orthopnea : is shortness of breath which occurs when lying flat, causing the
person to have to sleep propped up in bed or sitting in a chair
o Paroxsymal Nocturnal Dyspnea (PND): refers to attacks of severe shortness of
breath and coughing that generally occur at night.
o Nocturnal angina: due to slowing of heart rate and reduction of diastolic blood
o Palpitations: due to increased force of contraction
Physical Findings of AR
Wide pulse pressure : most sensitive
Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex) -mid-diastolic or presystolic murmur:
Due to diastolic displacement of the anterior leaflet of the mitral valve by the
aortic regurgitation stream causing it to vibrate.
Systolic ejection murmur: due to increased flow across the aortic valve
Florid pulmonary edema
Pulmonary edema is accumulation of fluid in the interstitial spaces of the lungs
(Interstitial Edema) due to an imbalance in the oncotic and hydrostatic pressure in
Florid pulmonary edema: the excess fluid is filled in the space between the
capillary and lung interstitial spaces.
Pathophysiology of AR
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
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
Simplified Indications for Surgical Treatment of AR
o ANY Symptoms at rest or exercise
o Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated
Definition: Backflow of blood from the LV to the LA during systole
Mild (physiological) MR is seen in 80% of normal individuals.
Acute MI: papillary muscle rupture or rupture of a chorda tendinea secondary to MI
Malfunction or disruption of prosthetic valve
Acute rheumatic fever with carditis is the predominant cause.
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
Mortality: From progressive dyspnea and heart failure
Clinical Manifestations of MR
Fatigue & weakness – due to CO – predominant complaint
exertional dyspnea & cough – pulmonary congestion
palpitations – due to atrial fibrillation (occur in 75% of pts.)
Right-sided heart failure – distended neck veins, edema, ascites, hepatomegaly
Auscultation: holosystolic murmur at the apex radiating to the axilla
Pathophysiology of MR
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 (TransEsophageal Echocardiogram) if transthoracic echo is inconclusive.
Management of MR
The treatment of acute aortic regurgitation is surgery to repair or replace the valve.
Medical therapy may be used to stabilize the patient en route to surgery; however,
surgery should not be delayed in favor of efforts at medical management.
Do not attempt to alleviate tachycardia with beta-blockers. Mild-to-moderate tachycardia
is beneficial in these patients because it allows less time for the heart to have backfill,
which lowers regurgitant volume.
o Vasodilator such as hydralazine
o Rate control for atrial fibrillation with β-blockers, CCB, digoxin
o Anticoagulation in atrial fibrillation and flutter
o Diuretics for fluid overload
o Mild: 2-3 years, Moderate: 1-2 years, Severe: 6-12 months
IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.
MV Replacement in Severe MR
Mitral Valve Prolapse
When 1 or both of the valve leaflets bulge into the left atrium during ventricular
more common in women
Cause: due to an inherited connective tissue disorder enlargement of one or both
Elongates/stretches the chordae tendinae & papillary muscles regurgitation may occur
Extra heart sound (Mitral click) – an early sign that a valve leaflet is ballooning into the
fatigue, shortness of breath
arrhythmias may develop – dizziness, chest pain, dyspnea, palpitations, syncope
high-pitched late systolic murmur
Mitral Valve Prolapse
antibiotic prophylaxis to prevent endocarditis
If w/ dysrhythmia – avoid caffeine, alcohol, stop smoking
for chest pain – nitrates, calcium channel blockers, beta blockers
surgery not indicated
usually occurs together w/ aortic or mitral stenosis
may be due to rheumatic heart disease
blood flow from right atrium to right ventricle
right ventricular output
left ventricular filling CO
blood accumulates in systemic circulation
S/Sx: symptoms of right-sided heart failure
o peripheral edema
o neck vein engorgement
o CO – fatigue, hypotension
TR is most commonly secondary, caused by dilation of the right ventricle (RV) with
malfunction of a normal valve, RV dysfunction–induced heart failure (HF), and
pulmonary outflow tract obstruction.
TR is less commonly primary, due to valvular abnormalities caused by infective
endocarditis in users of illicit IV drugs, blunt chest trauma, rheumatic fever, congenital
An insufficient tricuspid valve allows blood to flow back into the right atrium venous
congestion & right ventricular output blood flow towards the lungs
Clinical Manifestations of TR
Symptoms of TR are often nonspecific, and severe TR may be well tolerated, producing
few overt symptoms for a prolonged period.
With isolated severe TR, Patients may complain of :
o fatigue and decreased exercise tolerance as a result of low cardiac output. Elevated
right atrial (RA) pressure also leads to peripheral edema and hepatic congestion with
decreased appetite and abdominal fullness.
o Long-standing severe TR results in right-heart failure:
o Ascites (accumulation of fluid in the peritoneal cavity, causing abdominal swelling)
o Anasarca (severe generalized, massive edema)
o Decreased urine output
o Active pulsing in the neck veins (Jugular venous distention)
o The murmur of TR is frequently not heard. When evident, it is a holosystolic murmur
rare, usually congenital in origin
flow of blood to the pulmonary artery due to narrowing
blood flows back to right ventricle and right atrium
right ventricle hypertrophy to compensate for
blood volume and force blood to the pulmonary artery
Symptoms & Signs
harsh systolic murmur
fatigue, dyspnea on exertion, cyanosis
poor weight gain or failure to thrive in infants
hepatomegaly, ascites, edema
a rare condition caused by infective endocarditis, tumors or RF
blood flows back into Right ventricle Right ventricle and atrium hypertrphy
symptoms of Right-sided heart failure
Is repair of cardiac valve
patient does not require continuous anti-coagulant medication
usually require cardiopulmonary bypass machine
1. Commissurotomy – to separate the fused leaflets
performed in the cardiac cath. lab.
balloon inflated for 10-30 secs., w/ multiple inflations
common used for mitral and aortic stenosis
Closed surgical valvuloplasty
done in the OR under GA
Midsternal incision, a small hole is cut into the heart, the surgeon’s finger or a
dilator is used to open the commissure
done w/ direct visualization of the valve, thrombus and calcifications may be
identified and removed
Is repair of valve annulus (junction of the valve leaflets and the muscular heart
narrows the diameter of the valve’s orifice, useful for valvular regurgitation
Is repair of chordae tendineae , done for mitral valve regurgitation
caused by stretched, torn or shortened chordae tendineae
Example: Caged ball valve, Tilting-disk valve
more durable, used for younger pts.
risk of thromboembolism – long-term use of anti-coagulants
Tissue or biological valves:
xenografts – porcine or bovine heterografts (7-10 yrs viability)
homografts – from cadaver tissue donations (10-15 yrs)
autografts – excising the pts.’s own pulmonic valve and portion of pulmonary artery
for use as the aortic valve
Long-term anticoagulant therapy