Aortic Stenosis PHYSICAL FINDINGS Aortic Stenosis SYMPTOMS, PATHOPHYSIOLOGY  with Aortic Stenosis TREATMENT

 

Aortic Stenosis Definition —

Aortic stenosis is the narrowing of the left venticular outlet usually at the valve. Aortic stenosis is the commonest valvular heart dis­ease in adults and elderly persons. It is more com­mon in males. Aortic Stenosis An impairment of blood flow from the left ventricle to the aorta, as a result of aortic valve disease or obstructions just above or below the valve Aortic Stenosis causes Left ventricular outflow obstruction in adults is most often due to aortic valve stenosis; less common causes are subvalvular or supravalvular disease

Aortic Stenosis ETIOLOGY

   

• This may result from inflammatory disorders, or excessive development, embryonic maldevelopment, hypertrophy and thickening of a sphincter muscle, of fibrous tissue.
• Rheumatic valve disease
• Aortic sclerosis
• Degenerative / calcific / senile
• Rheumatic heart disease
• Calcific disease of a trileaflet valve
• Congenital AS
• – Bicuspid aortic valve
• – Subaortic stenosis-Discrete
• – Supra valvular AS
• Hypertrophic cardiomyopathy (also called IHSS­Idiopathic hypertrophic subaortic stenosis).

 

Aortic Stenosis PATHOPHYSIOLOGY

   

• There is obstruction at the outlet of the left ventricle. his leads to increased pressure in the left ventricle and decreased pressure in the aorta.
• Rheumatic valve disease is characterized by fusion of the commissures between the leaflets, with a small central orifice.
• The LV hypertrophies and maintains the cardiac out­ Jut. As the disease becomes chronic, the LV dilates a d the cardiac output falls.
• hen there is severe obstruction to LV outflow, the Peak systolic pressure gradient (difference of pres­: e between LV and aorta) is more than 50 mmHg : d area of aortic orifice is less than 1 cm²•
• Many of the risk factors for atherosclerosis are also associated with aortic valve sclerosis,
• adually LVEDP (left ventricular end diastolic pressure) rises and there is left ventricular failure. The  , LA, PA and RV pres;iures increase.

 

Aortic Stenosis SYMPTOMS OF AORTIC STENOSIS

   

• Patient may be asymptomatic for many years.
• Patient has exortional dysnoea is due to increased LV diastolic pressure creased pulmonary capillary pressures.
• Angina pectoris is due to LV hypertrophy (increased  ement of oxygen), decreased supply due to outflow obstruction and sometimes coincidental coro­nary artery disease.
• Many patients with mild or moderate aortic stenosis (e.g., with a valve area that is more than 1 cm² or a valve gradient that is less than 50 mm Hg)
• Syncope is due to vasodilatation of exercising muscles resulting in decreased cardiac output.
• Syncope usually occurs only during exertion.
• Later there is weakness, fatigue, peripheral cyanosis and other features of low cardiac output.
• There is orthopnea, paroxysmal nocturnal dyspnoea, and other symptoms of pulmonary edema and LV fail­ure.
• However, in patients with known AS who are followed prospectively, the most common symptoms are decreased exercise tolerance and dyspnea on exertion.
• Very late findings are pulmonary hypertension with right ventricular failure, systemic venous congestion, hepatomegaly, atrial fibrillation, tricuspid regurgita­tion.
• When aortic stenosis occurs along with mitral steno­sis, there is severe reduction in cardiac output and severe symptoms early in the course of the disease.
• When aortic stenosis occurs along with aortic regur­gitation, there is early left ventricular failure and pul­monary edema.

 

Aortic Stenosis PHYSICAL FINDINGS

   

• Rhythm is regular. If there is coexistent MS or MR there is atrial fibrillation.
• Blood pressure is usually normal. Later there is fall in systolic pressure and narrow pulse pressure.
• The presence of hypertension rules out severe aortic stenosis.
• A slow rate of rise in the carotid pulse Mid to late peak intensity of the murmur Reduced intensity of the second heart sound
• The murmur of aortic stenosis is best heard by placing the stethoscope over the base of the heart.
• Peripheral arterial pulse is slow and delayed called pulsus parvus et tardus.
• A bisferiens pulseis found in AS with AR or severe AR but never in pure AS.
• Palpation of the arteries in severe aortic stenosis may reveal a delayed and weakened pulse (e.g., at the carotids).
• The sound is typically described as being “diamond-shaped”;i.e., it starts softly, increases in intensity, and then diminishes to a whisper
• In the late stages of AS the pulse is very low volume and so the delay in upstroke is difficult to feel.
• JVP is normal but in greatly hypertrophied interven­tricular septum the RV cavity is reduced and there may be a prominent ‘a’ wave in the JVP.
• The left ventricular impulse is displaced laterally and downwards due to left ventricular hypertrophy.
• In pure AS, the left ventricular hypertrophy is a con­centric hypertrophy and therefore apex may not be shifted grossly.
• In the left lateral position a double apical impulse may be felt as in IHSS.
• A systolic thrill is present at the base of the heart (right second intercostal space and left third intercostal space), in the jugular notch and along the ca­rotid arteries.
• Systolic thrill is always present in AS except in very mild AS.

Aortic Stenosis Auscultation

   

• There is an early systolic ejection sound (an opening snap of the aortic valve) heard in noncalcific valvular AS as in congenital AS in children.
• Ejection sound is absent in calcified and rigid valves. The A₂ is delayed, (normally A₂ or aortic closure sound comes before P₂ or pulmonary closure sound) and may overlap the P₂. If it is further delayed as in severe AS then it may come after P₂. This is called paradoxic or reversed split of S2′
• A₂ is heard only if aortic valve is noncalcified and mobile.
• S4 is audible at the apex when there is LV hypertro­phy and increased LV end diastolic pressure.
• S3 is heard when the LV dilates and there is frank or incipient heart failure.
• The characteristic murmur of AS is ejection systolic or mid-systolic murmur beginning just after S1′
• This increases in intensity and reaches a peak around the middle of ejection. The murmur then diminishes in intensity gradually and ends just before aortic valve closure (AJ.
• It is low pitched, rough and rasping in character, best heard at the base of the heart i.e. right second inter­costal space and the left third intercostal space.
• It radiates along the carotid arteries upwards in the neck.
• It increases in expiration.
• In IHSS the murmur increases on standing but in val­vular aortic stenosis the murmur decreases on stand­ing.
• The systolic murmur may also be heard at the apex. The murmur is intense and usually loud i.e. grade III and above.
• In severe AS with heart failure, the apex is feeble and the murmur is soft.

 

INVESTIGATIONS in Aortic Stenosis

Aortic Stenosis ECG :

 

• ECG shows LVH, ST de ression, T inversion in Ll’ AVL, and left precordial leads.

Aortic Stenosis Echocardiography :

 

• · There is LV hypertrophy
• · Calcification of aortic valves may be seen
• · Congenital bicuspid aortic valve may be diag­nosed by eccentric aortic valve cusps.
• · There may be thickened aortic cusps and root
• · TEE shows the obstruction clearly
• · Doppler echocardiography measures LV function and associated AR
• · Other valvular diseases can be seen
• · Supravalvular, valvular and subvalvular AS and IHSS (Idiopathic Hypertrophy Subaortic Steno­sis) can be distinguished.

Aortic Stenosis X–ray:

   

• · LVH
• · Post-stenotic dilatation of ascending aorta in
• severe AS.
• · Aortic calcification in fluoroscopy.
• · Pulmonary congestion
• ·LAE

 

Aortic Stenosis Catheterization:

   

• Before operative treatment catheterization of left side of heart and coronary arteriography should be done to :
• · Rule out coronary artery disease
• · Multivalvular disease
• · Feasibility of balloon valvotomy of aortic valve
• · Level of obstruction of the LV outflow

 

Aortic Stenosis PROGNOSIS

   

• The average time a patient of AS lives after develop­ment of angina pectoris is 3 years, after syncope is 3 years, after dyspnoea is 2 years and after CHF is 2 years.

 

Aortic Stenosis TREATMENT

• A congenitally bicuspid valve is a common cause of aortic stenosis requiring surgery in all age groups.
• The only definitive therapy for aortic stenosis is aortic valve replacement.
• In severe AS i.e. valve area less than 1 sq cm patient should avoid any physical strain even if asymptom­atic.
• Salt restriction, and diuretics for heart failure Digitalis glycosides for heart failure Nitroglycerin for angina pectoris
• Among the 7 percent of patients who underwent surgery at ≤ 50 years of age, approximately two-thirds had a bicuspid valve and one-third had a unicuspid valve.
• Among the remaining patients over age 70, approximately 60 percent had a tricuspid valve and 40 percent had a bicuspid valve.
• Among the 40 percent of patients who underwent surgery between the ages of 50 and 70, approximately two-thirds had a bicuspid valve and one-third a tricuspid valve; a unicuspid valve was rare.
• Statins for prevention of calcification and aortic valve shrinkage in degenerative AS.
• Surgical treatment is AVR (aortic valve replacement). AVR is indicated in severe AS (valve area <1 sqcm), symptomatic patients, patients with LV dysfunction.
• In asymptomatic AS, if ejection fraction is more than 50%, AVR is not done especially in calcific AS, even if severe.
• Surgery should be done before LV failure occurs and ejection fraction falls.
• Operative risk is 4% in most cases but 20% in pa­tients of LVF.
• Aortic valvuloplasty: Percutaneous balloon aortic valvuloplasty can be done in children and young adults with non-calcific AS, and in patients where risk of surgery is high.

 

PHYSICAL ACTIVITY AND EXERCISE —

• the presence of severity of aortic regurgitation, and the presence of aortic root dilatation.
• Recommendations for physical activity and exercise in patients with bicuspid aortic valves needs to take into account three issues: the presence and severity of aortic stenosis.