Professional Documents
Culture Documents
• The aortic valve is the last of four cardiac valves through which the blood is pumped before it goes to the
rest of the body.
• It separates the left ventricular outflow tract from the aorta.
• Its main function is to prevent backward blood flow from the aorta to the left ventricle, while allowing the
blood to flow forward during systole with minimal resistance.
AORTIC ROOT
• The aortic sinuses facilitate closure of the aortic valve by creating eddies and currents between the cusps
and arterial wall .
• They also prevent the cusps from occluding the coronary artery orifices during systole, thus guaranteeing
myocardial perfusion during the entire cardiac cycle.
• entire right coronary sinus lies adjacent to
the RVOT.
RIGHT CORONARY SINUS
• central part lies adjacent to the crista
supraventricularis,
• left part is adjacent to the area of the
RVOT in the angle between the crista
supraventricularis and the pulmonary
valve.
• posterior (noncoronary) part of the right
coronary sinus is related to the area of the
right ventricle posteroinferior to the crista
supraventricularis.
• Inferiorly, the entire right coronary sinus
is related to the interventricular septum;
the muscular septum lies under the
central and left parts, while either
membranous or muscular septum may lie
under the posterior part of the right
coronary sinus.
NONCORONARY SINUS
• The atrialchambers with the intervening
atrial septum lie adjacent to the
noncoronary sinus.
• right and central parts of the
noncoronary sinus are related to the
right atrium and the interatrial septum,
• left part is related to the left atrium.
• Inferiorly, the right part, like the
posterior part of the right coronary
sinus, may be related either to the
membranous or the muscular septum
depending on the size of the
membranous septum. However,
beneath the central part of the
noncoronary sinus, the membranous
septum is a constant structure. The left
part of the noncoronary sinus inserts
into the anterior mitral leaflet
LEFT CORONARY SINUS
• Isolated aortic stenosis (AS) is more common in men than in women and is found in 2% of people 65 years of
age and older.
• The most common causes of AS include age related calcific degeneration, bicuspid aortic valve, and
rheumatic aortic valve.
• The distribution of these causes varies across age groups and geographic regions.
• Age related degeneration is the most common cause of AS in patients older than 70 years.
• In contrast, bicuspid aortic valve calcification accounts for most surgical cases in patients younger than 70
years.
• Valvular AS has three principle causes
1. Congenital bicuspid valve with superimposed calcification
2. Calcification of normal trileaflet valve
3. Rhumatic disease.
• Fixed obstruction to LVOT may occur above the valve(supravalvular stenosis)
• Below the valve (subvalvular stenosis)
CONGENITAL BICUSPID VALVE WITH SUPERIMPOSED
CALCIFICATION
• Calcific aortic valve disease affecting a congenital bicuspid or normal trileaflet valve is the most commone
cause of AS in adults
RHEUMATIC AORTIC STENOSIS
• It Results from adhesions and fusion of the comissures and cusps and vascularazation of the leaflets of the
valve ring
• Leading to retraction and stiffening of the free borders of the cusps
• Calcific nodules deveope on bothe surface and orifice is reduced to small round or triangular opening.
• It can be regurgitant as well as stenotic.
PATHOPHYSIOLOGY
• No appreciable gradient exists across the normal aortic valve during systole.
• In AS, gradual obstruction of the left ventricular outflow leads to an increased left ventricular afterload
and left ventricular wall stress, elevated left ventricular systolic and diastolic pressures, decreased
aortic pressure, and prolonged left ventricular ejection time.
• Over time, this results in compensatory concentric left ventricular hypertrophy (LVH) to maintain
ejection fraction.
• In patients with chronic severe AS, this compensatory mechanism may become insufficient, leading to
gradual dilation and thinning of the left ventricle, and result in a decrease in ejection fraction and in
congestive heart failure.
PATHOPHYSIOLOGY
• The classic symptoms of AS are angina, exertional syncope, and symptoms of congestive heart failure such as
shortness of breath.
• Two-dimensional transthoracic echocardiography is the most common modality for the diagnosis and
grading of AS
• X ray chest
• EKG
• CARDIAC CT
• CARDIAC CATHETERIZATION
• TMT
NATURAL HISTORY
• Without intervention,
• Multiple studies consistently reported survivals of 3 years for angina and syncope
• 1.5 to 2 years for dyspnea and heart failure.
• These findings have driven recommendations for early surgical intervention in patients with symptomatic AS.
• One third of asymptomatic patients with severe AS will become symptomatic in 2 years with an estimated
cardiac death of less than 1% each year to 5% each year.
• Patients with higher grades of AS severity seem to progress at a faster rate than lower grades of AS.
• After AS becomes moderate, aortic valve area decreases on average by 0.1 cm2 per year, the pressure
gradient across the valve rises on average by 7 mm Hg per year, and the jet velocity increases by 0.3 m/sec
per year.
AORTIC REGURGITATION
• disturbance in any of the components of the functional unit of the aortic valve (e.g., cusps, sinuses of
Valsalva, sinotubular junction, ventriculoaortic junction).
• In general, the causes can be divided into
• affect the valve cusps (e.g., calcific degeneration, congenitally bicuspid valve, infective endocarditis,
rheumatic disease, myxomatous degeneration)
• affect the aortic root (e.g., aortic dissection, aortitis of various etiologies such as syphilis, connective tissue
disorders such as Marfan syndrome)
Leaflet perforation
Vegetation
Commissure detachment
Type IlIa: Restricted leaflet closure and opening Leaflet thickening Commissure fusion Calcification
• ACUTE AR :usually exhibit sudden or rapidly progressive cardiovascular collapse, which can be life threatening if
not addressed promptly.
• They often exhibit ischemic symptoms because of the decrease in coronary blood flow and increased myocardial
oxygen demand.
• CHRONIC AR : asymptomatic for a long period of time because of the compensatory LV changes.
• Once the compensatory response is exhausted, the patients start having heart failure symptoms
• Aortic root disorders murmur is best heard along right sternal border musical murmur Longer the duration
of murmur severer the aortic regurgitation
• Becomes short - cardiac failure
• Austin flint murmur
• Soft, low pitched rumbling mid diastolic murmur.
• Diastolic displacement of the anterior leaflet of the mitral valve by the aortic regurgitation stream.
• Classic signs of widened pulse pressure may also be found, including
1. Corrigan or water-hammer pulse,
2. De Musset sign (bobbing of the head with heart beats),
3. Quincke pulse (pulsations of the lip and fingers),
4. Traube sign (pistol shot sounds over the femoral artery),
5. Müller sign (pulsations of the uvula).
6. Becker sign - Visible systolic pulsations of the retinal arterioles
7. Light-house sign – Alternate flushing & blanching of forehead
8. Landolfi’s sign - Change in pupil size with each systole
9. Gerhardt’s sign - Visible systolic pulsations of spleen
10. Rosenbach’s sign - Visible systolic pulsations of liver
11. Corrigan’s sign – Dancing carotid in neck
12. Hill sign: Popliteal cuff systolic pressure exceeding brachial cuff systolic pressure by more than 20 mmHg.
DIAGNOSTIC CRITERIA
• Transthoracic echocardiography with Doppler colorflow is the most useful tool for the diagnosis of AR.
• The jet width and vena contracta width on Doppler color-flow are used to qualitatively assess the severity of
AR, whereas the regurgitant volume, regurgitant fraction, and regurgitant orifice area are used for the
quantitative assessment.
CHEST X RAY
• acute AR, there may be minimal cardiac enlargement, but marked enlargement is a common finding in chronic AR.
ECG
•LV hypertrophy
•Left axis deviation
•Left atrial enlargement
•LV volume overload pattern - Prominent Q waves in leads I, aVL, and V3 to V6 and relatively small R waves in
V1
• AORTIC ANGIOGRAPHY
1. Mild (1+) - A small amount of contrast enters the LV during diastole and clears with each systole
2. Moderate AR (2+) - Contrast enters the LV with each diastole, but the LV chamber is less dense than the
aorta
3. Moderately severe AR (3+) - The LV chamber is equal in density to the ascending aorta.
4. Severe AR (4+) - Complete, dense opacification of the LV chamber occurs on the first beat, and the LV is
more densely opacified than the ascending aorta
• CARDIAC MRI :CMR provides accurate measurements of regurgitant volumes and the regurgitant orifice in
AR. It is the most accurate noninvasive technique for assessing LV end systolic volume, diastolic volume, and
mass
CARDIAC CATHETERIZATION