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Aortic stenosis

Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta. It is most commonly caused by calcification and fibrosis of the aortic valve. Symptoms include dyspnea, exertional dizziness, and exertional angina as the left ventricle has to work harder to maintain adequate cardiac output against the increased resistance. On examination, the carotid pulse is weak and delayed while auscultation reveals a crescendo-decrescendo systolic murmur best heard at the right upper sternal border that radiates to the carotid arteries. Management involves prompt aortic valve replacement for symptomatic severe aortic stenosis.

Health & Medicine◦

Aortic Valve: Aortic Stenosis
en.wikipedia.org

Aortic stenosis
• Aortic stenosis (AS) is narrowing of the aortic
valve resulting in obstruction of blood flow
from the left ventricle to the ascending aorta
during systole.

Etiology
Infants, children, adolescents
Congenital aortic stenosis
Congenital subvalvular aortic stenosis
Congenital supravalvular aortic stenosis
Young adults to middle-aged
Calcification and fibrosis of congenitally bicuspid AV
Rheumatic aortic stenosis
Middle-aged to elderly
Senile degenerative aortic stenosis
Calcification of bicuspid valve
Rheumatic aortic stenosis

William Syndrome
boyerpd1bio.wikispaces.com

↑ intraventricular pressure to maintain CO
Pathophysiology: AS
Angina , Syncope,
Dyspnea
Valve
obstruction
Impaired passive fillingLVH ↓ Compliance
↑preload dependance on
atrial contraction
↑LVEDP Subendocardial ischemia (↓ myocardial perfusion pressure)
Progressive valvular obstruction & increrasing wall stress
↑ Filling pressure , ventricular dilatation, contractile
dysfunction, ischemia, arrythmia
Ventricular wall hypertrophy (to reduce wall stress)

Symptoms
• The classic symptoms due to AS are heart failure
(HF), syncope, and angina. However, these
“classic” symptoms reflect end-stage disease.
• Now, with earlier diagnosis by echocardiography
and prospective followup of patients, the most
common presenting symptoms are:
1. Dyspnea on exertion or decreased exercise
tolerance
2. Exertional dizziness
3. Exertional angina

Dyspnea and decreased exercise
tolerance
• The MC symptom of AS is dyspnea, usually with exertion.
• 2 factors can contribute: diastolic dysfunction, with an ↑ in
LV filling pressures with exercise, and an inability of LV to ↑
the CO during exercise because the stiff AV obstructs flow.
• Systolic LVdysfunction is rare and overt HF is a late, end-
stage finding, usually in who havent received regular
medical care. Once overt HF occurs, the patient may
complain of SOB, easy fatigability, debilitation, and other
S/S of a low CO state.
• AF, which is uncommon in isolated AS, often accompanies
HF.

Inspection: Carotid pulse
• The quality of the arterial pulse reflects the obstruction
to blood flow into the peripheral arterial circulation.
• The arterial pulse :as "parvus and tardus", ie, it is small
or weak and rises slowly.
• Best appreciated in the carotid artery where the pulse
is reduced in amplitude and delayed in occurrence.
• The delay can be appreciated by simultaneous
palpation of the apex (PMI) and the carotid artery.
• There may be :an associated carotid artery thrill or
coarse vibration ("shuddering") due to the marked
turbulence of blood flow across the stenotic valve.

Palpation of Precordium
• The cardiac impulse at the apex is sustained
and is initially normal in location. (However, it
becomes displaced late in the course of AS
when left ventricular failure occurs. )
• A systolic thrill :at the base of the heart (2nd
ICS ), especially during full expiration with the
patient leaning forward.

Cardiac auscultation :Heart Sounds
• S2 :soft and single since A2(due to Avclosure), is delayed and tends
to occur simultaneously with P2(due to PV closure).
• S2 may become paradoxically split when the stenosis is severe and
associated with LV dysfunction .
• With increasingly severe, fixed AS, the A2 closing sound may
disappear.
• The presence of a normal split S2 is the most reliable finding to
exclude severe AS in adults.
• The S1 is usually N. However, an aortic ejection click, which is more
commonly heard with a congenital bicuspid valve, may be heard
after S1 (when the leaflets are stiff, but still somewhat compliant
and mobile) .
• Vigorous LA contraction can lead to a S4.

AS: MURMUR
• The hallmark finding is a crescendo-decrescendo
ejection murmur, heard best with the diaphragm of
the stethoscope at the right upper sternal border when
a patient is sitting upright leaning forward.
• The murmur typically radiates to one or both carotid
arteries and has a harsh or grating quality.
• The intensity of the systolic murmur does not
correspond to the severity of AS; rather, the timing of
the peak and the duration of the murmur corresponds
to the severity of AS. The more severe the stenosis, the
longer the duration of the murmur and the more likely
it peaks at late systole.

• In elderly persons with calcific AS, however, the murmur
may be more prominent at the apex, because of radiation
of its high-frequency components (Gallavardin
phenomenon). This may lead to its misinterpretation as a
murmur of MR.
• The murmur is soft when stenosis is less severe, grows
louder as stenosis progresses, and becomes longer and
peaks in volume later in systole (ie, crescendo phase
becomes longer and decrescendo phase becomes shorter)
as stenosis becomes more severe.
• As LV contractility decreases in critical AS, the murmur
becomes softer and shorter. The intensity of the murmur
may therefore be misleading in these circumstances.

• The murmur of AS typically increases with maneuvers
that increase LV volume and contractility (eg, leg-
raising, squatting, Valsalva release,) and decreases with
maneuvers that decrease LV volume (Valsalva
maneuver) or increase afterload (isometric handgrip).
• These dynamic maneuvers have the opposite effect on
the murmur of hypertrophic cardiomyopathy, which
can otherwise resemble that of AS.
• The murmur of MR due to prolapse of the posterior
leaflet may also mimic AS.

other
• A high-pitched, diastolic blowing murmur may be
present if the patient has associated aortic
regurgitation.
• Rarely, right ventricular failure with systemic venous
congestion, hepatomegaly, and edema precede LV
failure. This is probably due to the bulging of the
interventricular septum into the right ventricle, with
impedance in filling, elevated jugular venous pressure,
and a prominent a wave (Bernheim effect).
•

Management
• Patients with symptomatic severe AS should have
prompt AV replacement.
• Old age is not a contraindication to valve
replacement .
• Aortic balloon valvuloplasty is useful in
congenital aortic stenosis but is of no value in
older patients with calcific aortic stenosis.
• Anticoagulants are only required in patients who
have Afib or those who have had a valve
replacement with a mechanical prosthesis.

End of slides
References:
• Medscape
• Uptodate 20.3
• Harrison’s Internal medicine
• Davidson’s
• Merck’s mannual

Aortic stenosis

1.
Aortic Stenosis Pratap SagarTiwari
2.
Aortic Valve: AorticStenosis en.wikipedia.org
3.
Aortic stenosis • Aorticstenosis (AS) is narrowing of the aortic valve resulting in obstruction of blood flow from the left ventricle to the ascending aorta during systole.
4.
Etiology Infants, children, adolescents Congenitalaortic stenosis Congenital subvalvular aortic stenosis Congenital supravalvular aortic stenosis Young adults to middle-aged Calcification and fibrosis of congenitally bicuspid AV Rheumatic aortic stenosis Middle-aged to elderly Senile degenerative aortic stenosis Calcification of bicuspid valve Rheumatic aortic stenosis
5.
William Syndrome boyerpd1bio.wikispaces.com
6.
↑ intraventricular pressureto maintain CO Pathophysiology: AS Angina , Syncope, Dyspnea Valve obstruction Impaired passive fillingLVH ↓ Compliance ↑preload dependance on atrial contraction ↑LVEDP Subendocardial ischemia (↓ myocardial perfusion pressure) Progressive valvular obstruction & increrasing wall stress ↑ Filling pressure , ventricular dilatation, contractile dysfunction, ischemia, arrythmia Ventricular wall hypertrophy (to reduce wall stress)
7.
Symptoms • The classicsymptoms due to AS are heart failure (HF), syncope, and angina. However, these “classic” symptoms reflect end-stage disease. • Now, with earlier diagnosis by echocardiography and prospective followup of patients, the most common presenting symptoms are: 1. Dyspnea on exertion or decreased exercise tolerance 2. Exertional dizziness 3. Exertional angina
8.
Dyspnea and decreasedexercise tolerance • The MC symptom of AS is dyspnea, usually with exertion. • 2 factors can contribute: diastolic dysfunction, with an ↑ in LV filling pressures with exercise, and an inability of LV to ↑ the CO during exercise because the stiff AV obstructs flow. • Systolic LVdysfunction is rare and overt HF is a late, end- stage finding, usually in who havent received regular medical care. Once overt HF occurs, the patient may complain of SOB, easy fatigability, debilitation, and other S/S of a low CO state. • AF, which is uncommon in isolated AS, often accompanies HF.
9.
Inspection: Carotid pulse •The quality of the arterial pulse reflects the obstruction to blood flow into the peripheral arterial circulation. • The arterial pulse :as "parvus and tardus", ie, it is small or weak and rises slowly. • Best appreciated in the carotid artery where the pulse is reduced in amplitude and delayed in occurrence. • The delay can be appreciated by simultaneous palpation of the apex (PMI) and the carotid artery. • There may be :an associated carotid artery thrill or coarse vibration ("shuddering") due to the marked turbulence of blood flow across the stenotic valve.
10.
Palpation of Precordium •The cardiac impulse at the apex is sustained and is initially normal in location. (However, it becomes displaced late in the course of AS when left ventricular failure occurs. ) • A systolic thrill :at the base of the heart (2nd ICS ), especially during full expiration with the patient leaning forward.
11.
Cardiac auscultation :HeartSounds • S2 :soft and single since A2(due to Avclosure), is delayed and tends to occur simultaneously with P2(due to PV closure). • S2 may become paradoxically split when the stenosis is severe and associated with LV dysfunction . • With increasingly severe, fixed AS, the A2 closing sound may disappear. • The presence of a normal split S2 is the most reliable finding to exclude severe AS in adults. • The S1 is usually N. However, an aortic ejection click, which is more commonly heard with a congenital bicuspid valve, may be heard after S1 (when the leaflets are stiff, but still somewhat compliant and mobile) . • Vigorous LA contraction can lead to a S4.
12.
AS: MURMUR • Thehallmark finding is a crescendo-decrescendo ejection murmur, heard best with the diaphragm of the stethoscope at the right upper sternal border when a patient is sitting upright leaning forward. • The murmur typically radiates to one or both carotid arteries and has a harsh or grating quality. • The intensity of the systolic murmur does not correspond to the severity of AS; rather, the timing of the peak and the duration of the murmur corresponds to the severity of AS. The more severe the stenosis, the longer the duration of the murmur and the more likely it peaks at late systole.
13.
• In elderlypersons with calcific AS, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardin phenomenon). This may lead to its misinterpretation as a murmur of MR. • The murmur is soft when stenosis is less severe, grows louder as stenosis progresses, and becomes longer and peaks in volume later in systole (ie, crescendo phase becomes longer and decrescendo phase becomes shorter) as stenosis becomes more severe. • As LV contractility decreases in critical AS, the murmur becomes softer and shorter. The intensity of the murmur may therefore be misleading in these circumstances.
14.
• The murmurof AS typically increases with maneuvers that increase LV volume and contractility (eg, leg- raising, squatting, Valsalva release,) and decreases with maneuvers that decrease LV volume (Valsalva maneuver) or increase afterload (isometric handgrip). • These dynamic maneuvers have the opposite effect on the murmur of hypertrophic cardiomyopathy, which can otherwise resemble that of AS. • The murmur of MR due to prolapse of the posterior leaflet may also mimic AS.
15.
other • A high-pitched,diastolic blowing murmur may be present if the patient has associated aortic regurgitation. • Rarely, right ventricular failure with systemic venous congestion, hepatomegaly, and edema precede LV failure. This is probably due to the bulging of the interventricular septum into the right ventricle, with impedance in filling, elevated jugular venous pressure, and a prominent a wave (Bernheim effect). •
16.
Management • Patients withsymptomatic severe AS should have prompt AV replacement. • Old age is not a contraindication to valve replacement . • Aortic balloon valvuloplasty is useful in congenital aortic stenosis but is of no value in older patients with calcific aortic stenosis. • Anticoagulants are only required in patients who have Afib or those who have had a valve replacement with a mechanical prosthesis.
17.
End of slides References: •Medscape • Uptodate 20.3 • Harrison’s Internal medicine • Davidson’s • Merck’s mannual

Editor's Notes

#4 In individuals with normal aortic valves, the effective area of valve opening equals the cross-sectional area of the left ventricular outflow tract, which is about 3.0 to 4.0 cm 2 in adults. As AS develops, the antegrade velocity remains normal and there is a minimal valve gradient until the orifice area reaches less than half of normal. Calcific aortic valve disease without a significant gradient (defined as an aortic jet velocity ≤2.5 m/sec) is called aortic valve sclerosis. Aortic stenosis is present when the antegrade velocity across an abnormal valve is at least 2.6 m/sec. In general, symptoms in patients with aortic stenosis and normal left ventricular systolic function rarely occur until the valve area is <1.0 cm 2 , the jet velocity is over 4.0 m/sec, and/or the mean transvalvular gradient exceeds 40 mm Hg
#5 Extra notes : infant- 0-3months baby- 3months- 12months toddler-12months- 4 years child-5 years- 9 years adolescent-10 years - 12 years teen- 13 years- 17 years adult- 18 years + Middle age:40-60 Elderly:above 60 The aortic valve is the second most frequently affected by rheumatic fever, and commonly both the aortic and mitral valves are involved. Rheumatic valve disease is characterized by fusion of the commissures between the leaflets. Calcific aortic valve disease is characterized by aortic valve leaflet thickening and calcification in patients with a congenital bicuspid valve or an anatomically normal trileaflet valve In elderly patients, the most common precursor is aortic sclerosis, a degenerative aortic valve disease with thickening of aortic valve structures by fibrosis and calcification initially without causing significant obstruction. Over years, aortic sclerosis progresses to stenosis in as many as 15% of patients. Aortic sclerosis resembles atherosclerosis, with deposition of lipoproteins and inflammation and calcification of the valves; risk factors are similar. Degenerative calcific aortic stenosis is now the leading indication for aortic valve replacement. Calcific aortic valve disease may progress to obstruction to blood flow because the thickened, stiff leaflets do not open fully with ventricular ejection. Unlike atherosclerosis, where clinical events are due to plaque rupture and thrombosis, obstruction in calcific AS is due to the bulk of the lesion, with no evidence for plaque instability. In patients < 70 yr, the most common cause is a congenital bicuspid aortic valve. Congenital AS occurs in 3 to 5/1000 live births and affects more males; it is associated with coarctation and progressive dilatation of the ascending aorta causing dissection. In developing countries, rheumatic fever is the most common cause in all age groups.
#8 Congenital AS is usually asymptomatic until age 10 or 20 yr, when symptoms develop insidiously. In all forms, progressive untreated AS ultimately results in exertional syncope, angina, and dyspnea (SAD triad). Other symptoms and signs may include those of heart failure and arrhythmias, including ventricular fibrillation leading to sudden death. The classic symptoms due to AS are heart failure (HF), syncope, and angina. However, these “classic” symptoms reflect end-stage disease. Now, with earlier diagnosis by echocardiography and prospective followup of patients, the most common presenting symptoms are: Dyspnea on exertion or decreased exercise tolerance Exertional dizziness Exertional angina Heyde's syndrome is a syndrome of aortic valve stenosis associated with gastrointestinal bleeding from colonic angiodysplasia. It is named after Dr. Edward C. Heyde, who first described the association in 1958. It is due to the induction of von Willebrand disease type IIA by the valvular stenosis.
#9 Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years. Exertional dyspnea or fatigue is the most common initial complaint. Ultimately, most patients experience the classic triad of chest pain, heart failure, and syncope Angina pectoris — Angina with effort occurs in about two-thirds of patients with severe AS. Approximately one-half of these patients have underlying coronary artery disease. Angina in the remaining patients has been attributed to left ventricular hypertrophy, which can cause coronary ischemia by other mechanisms: Increased left ventricular oxygen demand as a result of increased left ventricular mass; the myocardial oxygen uptake per gram is normal Compression of intramyocardial coronary arteries from prolonged contraction and impaired myocardial relaxation Reduced diastolic coronary perfusion time during tachycardia Reduced coronary flow reserve Dizziness and syncope — There are several proposed explanations for exertional dizziness or syncope, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension A transient bradyarrhythmia that can occur during or immediately after exertion Abnormalities in the baroreceptor response with an ensuing failure to appropriately increase the blood pressure An arrhythmia, such as atrial fibrillation; ventricular arrhythmias are uncommon.
#10 There are no visible signs of AS. In severe aortic stenosis, the carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus). However, in elderly individuals with rigid carotid vessels, this sign may not be present. A lag time may be present between the apical impulse and the carotid impulse. Systolic hypertension can coexist with aortic stenosis. However, a systolic blood pressure higher than 200 mm Hg is rare in patients with critical aortic stenosis. Pulsus alternans can occur in the presence of LV systolic dysfunction. The jugular venous pulse may show prominent a waves reflecting reduced right ventricular compliance consequent to hypertrophy of the interventricular septum.
#11 A hyperdynamic LV is unusual and suggests concomitant aortic regurgitation or mitral regurgitation. An apical impulse that is sustained (thrusts with the 1st heart sound [S1] and relaxes with the 2nd heart sound [S2]) because of LV hypertrophy. The LV impulse may become displaced when systolic dysfunction develops.
#12 Cardiac auscultation — Stenosis of the aortic leaflets is associated with reduced mobility and delayed closure. This leads to the following changes in the heart sounds. An ejection click is common in children and young adults with congenital aortic stenosis, but it is rare in elderly individuals with acquired calcific aortic stenosis, in whom the cusps become immobile and severely calcified. This sound occurs approximately 40-60 milliseconds after the onset of S1 and is frequently heard best along the mid to lower left sternal border; it is often well transmitted to the apex and may be confused with a split S1. An ejection click may also be audible early after S1 in patients with congenital bicuspid AS when valve leaflets are stiff but not completely immobile. The click does not change with dynamic maneuvers. A prominent S4 can be present and is due to forceful atrial contraction into a hypertrophied left ventricle. The presence of an S4 in a young patient with aortic stenosis indicates significant aortic stenosis, but with aortic stenosis in an elderly person, this is not necessarily true.
#13 The classic crescendo-decrescendo systolic murmur of aortic stenosis begins shortly after the first heart sound. The intensity increases toward midsystole, then decreases, and the murmur ends just before the second heart sound. It is generally a rough, low-pitched sound that is best heard at the second intercostal space in the right upper sternal border. It is harsh at the base and radiates to 1 or both carotid arteries. In elderly persons with calcific aortic stenosis, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardin phenomenon). This may lead to its misinterpretation as a murmur of mitral regurgitation. Accentuation of the aortic stenosis murmur following a long R-R interval (as in atrial fibrillation or following a premature beat) distinguishes it from the mitral regurgitation murmur, which usually does not change. The murmur of valvular aortic stenosis is augmented upon squatting or following a premature beat; the murmur intensity is reduced during Valsalva strain. This is contrary to what occurs with hypertrophic obstructive cardiomyopathy, in which a Valsalva maneuver increases the intensity of the murmur. When the left ventricle fails and cardiac output falls, the aortic stenosis murmur becomes softer and may be barely audible. Atrial fibrillation with short R-R intervals can also decrease the murmur intensity or make it inaudible.
#16 The murmur generally begins after S1 and ends before S2. The intensity of the murmur reflects the amount and velocity of blood flow across the valve and the turbulence produced by the stenosis. A loud murmur (grade 4 or greater) has a high specificity for severe aortic stenosis. However, most patients with severe stenosis have a grade 3 murmur and many have only a grade 1 or 2 murmur. The timing of the murmur also correlates with the severity of the stenosis, similar to the timing of the carotid pulse. An early peaking murmur is typical for mild to moderate AS, while a late peaking murmur is consistent with severe AS. However, evaluation of the timing of the murmur is not reproducible among examiners and is therefore of limited clinical utility. In almost all patients, AS is associated with a small degree of aortic regurgitation since the stiff, calcified, and rigid aortic valve leaflets may not coapt normally. In this setting, a soft diastolic murmur of aortic regurgitation may be heard.
#17 The only definitive treatment for aortic stenosis is aortic valve replacement. The development of symptoms due to aortic stenosis provides a clear indication for replacement. For patients who are not candidates for aortic replacement, percutaneous aortic balloon valvuloplasty may provide some symptom relief.[ Medical treatment (such as diuretic therapy) in aortic stenosis may provide temporary symptom relief but is generally not effective long term. In truly asymptomatic patients with severe aortic stenosis, the issue of valve replacement is less clear.

Aortic stenosis

1.
Aortic Stenosis Pratap SagarTiwari
2.
Aortic Valve: AorticStenosis en.wikipedia.org
3.
Aortic stenosis • Aorticstenosis (AS) is narrowing of the aortic valve resulting in obstruction of blood flow from the left ventricle to the ascending aorta during systole.
4.
Etiology Infants, children, adolescents Congenitalaortic stenosis Congenital subvalvular aortic stenosis Congenital supravalvular aortic stenosis Young adults to middle-aged Calcification and fibrosis of congenitally bicuspid AV Rheumatic aortic stenosis Middle-aged to elderly Senile degenerative aortic stenosis Calcification of bicuspid valve Rheumatic aortic stenosis
5.
William Syndrome boyerpd1bio.wikispaces.com
6.
↑ intraventricular pressureto maintain CO Pathophysiology: AS Angina , Syncope, Dyspnea Valve obstruction Impaired passive fillingLVH ↓ Compliance ↑preload dependance on atrial contraction ↑LVEDP Subendocardial ischemia (↓ myocardial perfusion pressure) Progressive valvular obstruction & increrasing wall stress ↑ Filling pressure , ventricular dilatation, contractile dysfunction, ischemia, arrythmia Ventricular wall hypertrophy (to reduce wall stress)
7.
Symptoms • The classicsymptoms due to AS are heart failure (HF), syncope, and angina. However, these “classic” symptoms reflect end-stage disease. • Now, with earlier diagnosis by echocardiography and prospective followup of patients, the most common presenting symptoms are: 1. Dyspnea on exertion or decreased exercise tolerance 2. Exertional dizziness 3. Exertional angina
8.
Dyspnea and decreasedexercise tolerance • The MC symptom of AS is dyspnea, usually with exertion. • 2 factors can contribute: diastolic dysfunction, with an ↑ in LV filling pressures with exercise, and an inability of LV to ↑ the CO during exercise because the stiff AV obstructs flow. • Systolic LVdysfunction is rare and overt HF is a late, end- stage finding, usually in who havent received regular medical care. Once overt HF occurs, the patient may complain of SOB, easy fatigability, debilitation, and other S/S of a low CO state. • AF, which is uncommon in isolated AS, often accompanies HF.
9.
Inspection: Carotid pulse •The quality of the arterial pulse reflects the obstruction to blood flow into the peripheral arterial circulation. • The arterial pulse :as "parvus and tardus", ie, it is small or weak and rises slowly. • Best appreciated in the carotid artery where the pulse is reduced in amplitude and delayed in occurrence. • The delay can be appreciated by simultaneous palpation of the apex (PMI) and the carotid artery. • There may be :an associated carotid artery thrill or coarse vibration ("shuddering") due to the marked turbulence of blood flow across the stenotic valve.
10.
Palpation of Precordium •The cardiac impulse at the apex is sustained and is initially normal in location. (However, it becomes displaced late in the course of AS when left ventricular failure occurs. ) • A systolic thrill :at the base of the heart (2nd ICS ), especially during full expiration with the patient leaning forward.
11.
Cardiac auscultation :HeartSounds • S2 :soft and single since A2(due to Avclosure), is delayed and tends to occur simultaneously with P2(due to PV closure). • S2 may become paradoxically split when the stenosis is severe and associated with LV dysfunction . • With increasingly severe, fixed AS, the A2 closing sound may disappear. • The presence of a normal split S2 is the most reliable finding to exclude severe AS in adults. • The S1 is usually N. However, an aortic ejection click, which is more commonly heard with a congenital bicuspid valve, may be heard after S1 (when the leaflets are stiff, but still somewhat compliant and mobile) . • Vigorous LA contraction can lead to a S4.
12.
AS: MURMUR • Thehallmark finding is a crescendo-decrescendo ejection murmur, heard best with the diaphragm of the stethoscope at the right upper sternal border when a patient is sitting upright leaning forward. • The murmur typically radiates to one or both carotid arteries and has a harsh or grating quality. • The intensity of the systolic murmur does not correspond to the severity of AS; rather, the timing of the peak and the duration of the murmur corresponds to the severity of AS. The more severe the stenosis, the longer the duration of the murmur and the more likely it peaks at late systole.
13.
• In elderlypersons with calcific AS, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardin phenomenon). This may lead to its misinterpretation as a murmur of MR. • The murmur is soft when stenosis is less severe, grows louder as stenosis progresses, and becomes longer and peaks in volume later in systole (ie, crescendo phase becomes longer and decrescendo phase becomes shorter) as stenosis becomes more severe. • As LV contractility decreases in critical AS, the murmur becomes softer and shorter. The intensity of the murmur may therefore be misleading in these circumstances.
14.
• The murmurof AS typically increases with maneuvers that increase LV volume and contractility (eg, leg- raising, squatting, Valsalva release,) and decreases with maneuvers that decrease LV volume (Valsalva maneuver) or increase afterload (isometric handgrip). • These dynamic maneuvers have the opposite effect on the murmur of hypertrophic cardiomyopathy, which can otherwise resemble that of AS. • The murmur of MR due to prolapse of the posterior leaflet may also mimic AS.
15.
other • A high-pitched,diastolic blowing murmur may be present if the patient has associated aortic regurgitation. • Rarely, right ventricular failure with systemic venous congestion, hepatomegaly, and edema precede LV failure. This is probably due to the bulging of the interventricular septum into the right ventricle, with impedance in filling, elevated jugular venous pressure, and a prominent a wave (Bernheim effect). •
16.
Management • Patients withsymptomatic severe AS should have prompt AV replacement. • Old age is not a contraindication to valve replacement . • Aortic balloon valvuloplasty is useful in congenital aortic stenosis but is of no value in older patients with calcific aortic stenosis. • Anticoagulants are only required in patients who have Afib or those who have had a valve replacement with a mechanical prosthesis.
17.
End of slides References: •Medscape • Uptodate 20.3 • Harrison’s Internal medicine • Davidson’s • Merck’s mannual

Editor's Notes

#4 In individuals with normal aortic valves, the effective area of valve opening equals the cross-sectional area of the left ventricular outflow tract, which is about 3.0 to 4.0 cm 2 in adults. As AS develops, the antegrade velocity remains normal and there is a minimal valve gradient until the orifice area reaches less than half of normal. Calcific aortic valve disease without a significant gradient (defined as an aortic jet velocity ≤2.5 m/sec) is called aortic valve sclerosis. Aortic stenosis is present when the antegrade velocity across an abnormal valve is at least 2.6 m/sec. In general, symptoms in patients with aortic stenosis and normal left ventricular systolic function rarely occur until the valve area is <1.0 cm 2 , the jet velocity is over 4.0 m/sec, and/or the mean transvalvular gradient exceeds 40 mm Hg
#5 Extra notes : infant- 0-3months baby- 3months- 12months toddler-12months- 4 years child-5 years- 9 years adolescent-10 years - 12 years teen- 13 years- 17 years adult- 18 years + Middle age:40-60 Elderly:above 60 The aortic valve is the second most frequently affected by rheumatic fever, and commonly both the aortic and mitral valves are involved. Rheumatic valve disease is characterized by fusion of the commissures between the leaflets. Calcific aortic valve disease is characterized by aortic valve leaflet thickening and calcification in patients with a congenital bicuspid valve or an anatomically normal trileaflet valve In elderly patients, the most common precursor is aortic sclerosis, a degenerative aortic valve disease with thickening of aortic valve structures by fibrosis and calcification initially without causing significant obstruction. Over years, aortic sclerosis progresses to stenosis in as many as 15% of patients. Aortic sclerosis resembles atherosclerosis, with deposition of lipoproteins and inflammation and calcification of the valves; risk factors are similar. Degenerative calcific aortic stenosis is now the leading indication for aortic valve replacement. Calcific aortic valve disease may progress to obstruction to blood flow because the thickened, stiff leaflets do not open fully with ventricular ejection. Unlike atherosclerosis, where clinical events are due to plaque rupture and thrombosis, obstruction in calcific AS is due to the bulk of the lesion, with no evidence for plaque instability. In patients < 70 yr, the most common cause is a congenital bicuspid aortic valve. Congenital AS occurs in 3 to 5/1000 live births and affects more males; it is associated with coarctation and progressive dilatation of the ascending aorta causing dissection. In developing countries, rheumatic fever is the most common cause in all age groups.
#8 Congenital AS is usually asymptomatic until age 10 or 20 yr, when symptoms develop insidiously. In all forms, progressive untreated AS ultimately results in exertional syncope, angina, and dyspnea (SAD triad). Other symptoms and signs may include those of heart failure and arrhythmias, including ventricular fibrillation leading to sudden death. The classic symptoms due to AS are heart failure (HF), syncope, and angina. However, these “classic” symptoms reflect end-stage disease. Now, with earlier diagnosis by echocardiography and prospective followup of patients, the most common presenting symptoms are: Dyspnea on exertion or decreased exercise tolerance Exertional dizziness Exertional angina Heyde's syndrome is a syndrome of aortic valve stenosis associated with gastrointestinal bleeding from colonic angiodysplasia. It is named after Dr. Edward C. Heyde, who first described the association in 1958. It is due to the induction of von Willebrand disease type IIA by the valvular stenosis.
#9 Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years. Exertional dyspnea or fatigue is the most common initial complaint. Ultimately, most patients experience the classic triad of chest pain, heart failure, and syncope Angina pectoris — Angina with effort occurs in about two-thirds of patients with severe AS. Approximately one-half of these patients have underlying coronary artery disease. Angina in the remaining patients has been attributed to left ventricular hypertrophy, which can cause coronary ischemia by other mechanisms: Increased left ventricular oxygen demand as a result of increased left ventricular mass; the myocardial oxygen uptake per gram is normal Compression of intramyocardial coronary arteries from prolonged contraction and impaired myocardial relaxation Reduced diastolic coronary perfusion time during tachycardia Reduced coronary flow reserve Dizziness and syncope — There are several proposed explanations for exertional dizziness or syncope, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension A transient bradyarrhythmia that can occur during or immediately after exertion Abnormalities in the baroreceptor response with an ensuing failure to appropriately increase the blood pressure An arrhythmia, such as atrial fibrillation; ventricular arrhythmias are uncommon.
#10 There are no visible signs of AS. In severe aortic stenosis, the carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus). However, in elderly individuals with rigid carotid vessels, this sign may not be present. A lag time may be present between the apical impulse and the carotid impulse. Systolic hypertension can coexist with aortic stenosis. However, a systolic blood pressure higher than 200 mm Hg is rare in patients with critical aortic stenosis. Pulsus alternans can occur in the presence of LV systolic dysfunction. The jugular venous pulse may show prominent a waves reflecting reduced right ventricular compliance consequent to hypertrophy of the interventricular septum.
#11 A hyperdynamic LV is unusual and suggests concomitant aortic regurgitation or mitral regurgitation. An apical impulse that is sustained (thrusts with the 1st heart sound [S1] and relaxes with the 2nd heart sound [S2]) because of LV hypertrophy. The LV impulse may become displaced when systolic dysfunction develops.
#12 Cardiac auscultation — Stenosis of the aortic leaflets is associated with reduced mobility and delayed closure. This leads to the following changes in the heart sounds. An ejection click is common in children and young adults with congenital aortic stenosis, but it is rare in elderly individuals with acquired calcific aortic stenosis, in whom the cusps become immobile and severely calcified. This sound occurs approximately 40-60 milliseconds after the onset of S1 and is frequently heard best along the mid to lower left sternal border; it is often well transmitted to the apex and may be confused with a split S1. An ejection click may also be audible early after S1 in patients with congenital bicuspid AS when valve leaflets are stiff but not completely immobile. The click does not change with dynamic maneuvers. A prominent S4 can be present and is due to forceful atrial contraction into a hypertrophied left ventricle. The presence of an S4 in a young patient with aortic stenosis indicates significant aortic stenosis, but with aortic stenosis in an elderly person, this is not necessarily true.
#13 The classic crescendo-decrescendo systolic murmur of aortic stenosis begins shortly after the first heart sound. The intensity increases toward midsystole, then decreases, and the murmur ends just before the second heart sound. It is generally a rough, low-pitched sound that is best heard at the second intercostal space in the right upper sternal border. It is harsh at the base and radiates to 1 or both carotid arteries. In elderly persons with calcific aortic stenosis, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardin phenomenon). This may lead to its misinterpretation as a murmur of mitral regurgitation. Accentuation of the aortic stenosis murmur following a long R-R interval (as in atrial fibrillation or following a premature beat) distinguishes it from the mitral regurgitation murmur, which usually does not change. The murmur of valvular aortic stenosis is augmented upon squatting or following a premature beat; the murmur intensity is reduced during Valsalva strain. This is contrary to what occurs with hypertrophic obstructive cardiomyopathy, in which a Valsalva maneuver increases the intensity of the murmur. When the left ventricle fails and cardiac output falls, the aortic stenosis murmur becomes softer and may be barely audible. Atrial fibrillation with short R-R intervals can also decrease the murmur intensity or make it inaudible.
#16 The murmur generally begins after S1 and ends before S2. The intensity of the murmur reflects the amount and velocity of blood flow across the valve and the turbulence produced by the stenosis. A loud murmur (grade 4 or greater) has a high specificity for severe aortic stenosis. However, most patients with severe stenosis have a grade 3 murmur and many have only a grade 1 or 2 murmur. The timing of the murmur also correlates with the severity of the stenosis, similar to the timing of the carotid pulse. An early peaking murmur is typical for mild to moderate AS, while a late peaking murmur is consistent with severe AS. However, evaluation of the timing of the murmur is not reproducible among examiners and is therefore of limited clinical utility. In almost all patients, AS is associated with a small degree of aortic regurgitation since the stiff, calcified, and rigid aortic valve leaflets may not coapt normally. In this setting, a soft diastolic murmur of aortic regurgitation may be heard.
#17 The only definitive treatment for aortic stenosis is aortic valve replacement. The development of symptoms due to aortic stenosis provides a clear indication for replacement. For patients who are not candidates for aortic replacement, percutaneous aortic balloon valvuloplasty may provide some symptom relief.[ Medical treatment (such as diuretic therapy) in aortic stenosis may provide temporary symptom relief but is generally not effective long term. In truly asymptomatic patients with severe aortic stenosis, the issue of valve replacement is less clear.

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