Aortic valve stenosisAortic valve regurge
Aortic valve disease
By Prof. Hatem Abdel Rahman
MD cardiology Dr. Mohamd Ashraf Ahmad
MD cardiology
Aortic Stenosis
Definition Aortic stenosis
refers to obstruction of flow from the LV to aorta.
Anatomically, It may be:1-Valvular:2- Subvalvular:3-Supravalvular :
Aortic valve Stenosis
Etiologies
Congenital 0-30 yrsBicuspid 30-50 yrsRheumatic 30-60 yrsDegenerative >60 yrs
Aortic valve Stenosis
Pathophysiology
Valvular aortic stenosis results in chronic left ventricular pressure overloading.
Compensatory concentric LVH allows the ventricle to maintain stroke volume with increases in diastolic pressure, and patients remain asymptomatic for many years.
Later on, LVH causes either Diastolic dysfunction with the onset of
congestive symptomsMyocardial oxygen needs in excess of
supply with the onset of angina. Some patients might also experience
exertional syncope, probably reflecting the inability to increase cardiac output and maintain blood pressure in response to vasodilation.
Clinical presentation- Asymptomatic - The classic symptoms of severe AS:
1- Angina. 2- Syncope. 3- Congestive heart failure. 4-Sudden cardiac death.
Aortic Stenosis
Natural history of aortic stenosis. At the onset of symptoms (arrow), there is a rapid progression and survival is severely limited
On examination:
Delayed slow-rising carotid upstroke (pulsus parvus et tardus).
Sustained left ventricular apical impulse. Fourth heart sound. Harsh systolic murmur of aortic stenosis,
loudest at the base of the heart and radiating to the carotids, is often but not always prominent. Low output states, obesity, or chronic lung disease may mask the findings.
Other hallmarks of significant aortic valve stenosis include a single (pulmonic) component of the second heart sound.
InvestigationsECG often shows changes of left ventricular
hypertrophy. The chest X ray occasionally shows heavy
calcification of the valve or ascending aortic dilation.
Echocardiography: Test of choice in the evaluation of patients with suspected valvular disease. It allows assessment of the valve anatomy as well as of chamber size and ventricular function. Doppler studies permit estimation of pressure gradients and estimations of aortic valve area .
Stress ECG:Cardiac catheterization: It is generally performed as preoperative
coronary angiography in men older than 35 years, women older than 45 years to exclude coronary artery disease.
TreatmentMedical:
To date, no medical therapy exists for the treatment of calcific aortic stenosis.
Prophylaxis against recurrent rheumatic fever in rheumatic patients.
Antibiotic prophylaxis against infective endocarditis in conditions associated with bacteraemia.
Surgical:Aortic valve replacementPercutaneous:
TAVR
Indications for surgery 1- Symptomatic patients (i.e., those
with angina, syncope, or dyspnea) with severe aortic stenosis should undergo valve replacement.
2- Patients with severe AS undergoing coronary artery bypass grafting
3- Patients with severe AS undergoing
surgery on the aorta or other heart valves .
3- Asymptomatic Patients with severe AS and left ventricular ejection fractions less than 0.50.
4- Patients with moderate aortic stenosis undergoing coronary artery bypass grafting or surgery on the aorta or other heart valves (Class IIa indication).
5- Aymptomatic patients with severe AS who exhibit an abnormal response to exercise (hypotension).
Questions???
Aortic Regurgitation
Aortic RegurgitationEtiologyPhysical ExaminationAssessing SeverityNatural History PrognosisTiming of Surgery
Etiology of AR
CongenitalBicuspid valve
AcquiredRheumatic heart
diseaseDilated aorta (e.g.
hypertension..)DegenerativeConnective tissue
disorders E.g. ankylosing
spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis )
AortopathyCystic medial
necrosisCollagen disorders
(e.g. Marfan’s)Ehler-DanlosOsteogenesis
imperfecta.
Acute AI: aortic dissection, infective endocarditis, trauma
:Pathophysiology of ARAcute or subacute significant AR
causes the abrupt introduction of a large volume of blood into a noncompliant LV, thus increasing LV end-diastolic and pulmonary venous pressures and leading to acute dyspnea or pulmonary edema.
In chronic AR, compensatory LV changes occur over time. The excess volume load causes stretching and elongation of myocardial fibers, which in turn increase wall stress.
When the ventricle can not dilate further, diastolic pressure increases and results in dyspnea, another sign of decompensation.
Symptoms of ARDyspnea, orthopnea, PNDPalpitations.Chest pain.
Nocturnal angina >> exertional angina ( diastolic aortic pressure and increased
LVEDP thus coronary artery diastolic flow).
With extreme reductions in diastolic pressures (e.g. < 40 mmHg) may see angina
Peripheral Signs of Severe ARQuincke’s sign:
capillary pulsationCorrigan’s sign:
water hammer pulse
De Musset’s sign: systolic head bobbing
Mueller’s sign: systolic pulsation of uvula
Durosier’s sign: femoral retrograde bruits
Traube’s sign: pistol shot femorals
Hill’s sign: BP Lower extremity >BP Upper extremity by > 20 mm Hg - mild AR> 40 mm Hg – mod AR> 60 mm Hg – severe
AR
Cardiac Signs of Severe AR
Apex:DisplacedHyper-dynamicPalpable S3 Austin-Flint
murmur
Murmur of aortic regurge:High pitched,
blowing, decrescendo diastolic murmur at LSB best heard at end-expiration & leaning forward
length correlates with severity (chronic AR)
in acute AR murmur shortens as Aortic DP=LVEDP
Assessing Severity of AR Assess severity by impact on peripheral
signs and LV peripheral signs = severityDilated LV = severityS3Austin –FlintRadiological cardiomegaly
Investigations ECGChest X rayEchocardiographyStress ECGCoronary angiography (preop.)
Echo Indications for Valve Replacement in Asymptomatic AR & MR
Type of Regurgitatio
n
LVESD mm
EF %
FS
Aortic >55 < 55 < 0.27
Mitral >45 < 60 <0.32
Indication for Valve Replacement in severe AR :
ACC/AHA Class ISymptomatic patients with preserved LVF
(LVEF >50%)Asymptomatic
Patients with mild to moderate LV dysfunction (EF 25-49%)
Patients undergoing CABG, aortic or other valvular surgery
ACC/AHA Class II aAsymptomatic patients with preserved
LVEF but severe LV dilatation (EDD>75 mm or ESD > 55mm)
Questions????
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