Management of Aortic Stenosis
Four categories of severity:
1) Valve area > 1.2 cm2 – mild
2) Valve area 1.0-1.2 cm2 - moderate
3) Valve area 0.8-1.0 cm2 - severe
4) alve area < o.8 cm2 - critical

Surgical treatment,
For symptomatic ptnts- w/out valve replacement:
- 50% presenting with angina will die within five years,
- 50% presenting with syncope will die within three years
- 50% presenting with dyspnoea will be dead within two years

- Aortic valve replacement (AVR)- for most adult with calcific AS and severe obstruction
- Indicated in patients with severe AS who are symptomatic and those who exhibit LV dysfunction
- Surgery on patients with severe AS who are asymptomatic with normal LV function should be postponed since they may continue to do well for many years – risk of surgical mortality exceeds that of sudden death in asymptomatic patients

Aortic Valve replacement
- Mechanical vs bioprosthetic valve
1) Bioprosthetic valve- doesn’t require long-term oral anticoagulation but has relatively limited durability
2) Mechanical valve- offers long- term durability but requires lifelong warfarin therapy- can develop significant hemorrhagic complications

- Palliative, not curative
- Commits a patient to continued IE prophylaxis, regular cardiac follow-up and continued med therapy (inc anticoagulation with warfarin-those with mechanical valves)
- Re-operation- malfunction of the prosthetic valve.
- some patients may require implantation of a permanent pacemaker after valve surgery.

Percutaneous balloon aortic valvuloplasty
- preferable in children and young adults with congenital, noncalcific AS
- not commonly used in adult with severe calcific AS – because of ↑ restenosis rate


Asymptomatic patients with mild to moderate AS
- Should be on under regular review for assessment of symptoms eg changes in exercise tolerance and echocardiography
- Should avoid strenuous act, and post-prandial exertion
- a/biotic prophylaxis against IE is important
- HPT occurs in about 20%-30% of patients
1) Managed with ACE inhibitors or ARB titrated slowly
2) Beta-blockers are also used in selected ptnts


Management of HPT

Lifestyle
- Stop smoking
- Weight ↓ if necessary- maintain ideal BMI of 18-23
- ↓salt intake, total fat, saturated fat and cholesterol intake
- ↑ polyunsaturated, monosaturated fats
- ↑ fruit, vege, whole grains, fish
- Cut alcohol intake
- Regular exercise
- Relaxation therapy can help

Antihypertensive drugs

Main agents used:
1)Thiazide diuretics
- Actions:
i.↑ salt and H2O excretion-->↓ ECF vol
ii.↓ cardiac output through ↓ plasma vol

2)Beta-blockers
-Actions:
i.↓ CO
ii.↓sympathetic act-->↓vasoconstriction-->↓peripheral resistance
iii.↓renin release-->↓ATI and II-->↓vasoconstriction

3)Calcium channel blockers
-Action:
i.Block Ca entry through Ca channels-->vasodilation-->↓arterial p

4)ACE inhibitors
-Actions:
i.Inhibit ACE-->ATI not converted to AT II-->↓vasoconstriction

The electrocardiogram (ECG)
Although aortic stenosis does not lead to any specific findings on the ECG, it still often leads to a number of electrocardiographic abnormalities. ECG manifestations of left ventricular hypertrophy (LVH) are common in aortic stenosis and arise as a result of the stenosis having placed a chronically high pressure load on the left ventricle (with LVH being the expected response to chronic pressure loads on the left ventricle no matter how caused).
As noted below, the calcification process which occurs in aortic stenosis can progress to extend beyond the aortic valve and into the electrical conduction system of the heart. Evidence of this phenomenon may include heart block that is apparent on the ECG but otherwise undetectable.

the pathophysiology of aortic stenosis can be explained from the following equation;

wall stress = (Pressure)x(heart radius)/muscle mass

since the aorta is narrowed, the pressure required for the Left Ventricle, LV to maintain a constant cardiac output is increased. this is turn will also increase the stress (pressure) that is absorb by the walls of the blood vessels (the body does not want this to happen as increase wall stress will damage the vessels). therefore as a compensation mechanism,the muscle mass of the LV will increase over a period of time (LV hypertrophy). increase muscle mass (LV hypertrophy) will reduce the compliance of the LV (LV is thick, so it is harder to expand). as compliance is reduced the end diastolic pressure will rise. the pressure required for the left atrium, LA to pump blood into the LV will also increase. as time goes, the LA will also become hypertrophied leading to an increase pressure in the pulmonary arteries. increase pressure of the pulmonary arteries will then causes pulmonary edema (fluid leakage - increase filtration). patient will show symptoms of breathlessness. as this condition progress, the heart is unable to increase the muscle mass of the LV anymore. from here, the LV will start to dilate and the patient will have cardiomegaly. ultimately, this will progress into left heart failure. the patient's condition may also lead to ride heart failure (if left untreated).

the concept is the same for hypertension.

some other stuff:
* LA hypertrophy may also lead to atrial fibrillation

Rheumatic Fever and Valvular Heart Disease
Aortic Stenosis
Causesà congenitalà valvularà bicuspid aortic valves (1 -2% of population, undergo accelerated degenerative changes)
à non-valvularà discrete subaortic membrane (formation of fibrous ridge or diaphragm below aortic valve) and supravalvular aortic stenosis (congenital fibrous diaphragm above the aortic valve often associated with mental retardation and hypercalcaemia; William’s Syndrome)

àRheumatic Feverà results in progressive fusion, thickening and calcification of the valve. Second most common valve involved after mitral valve

àCalcific Valvular diseaseà common cause of stenosis in the elderly. Usually due calcification of lipoprotein in the subendotheluim matrix in atherosclerosis. Thus increasing leaflet stiffness and reducing systolic opening.

Pathophysiology--> AS causes fixed outflow obstruction and left ventricular pressure overload. Compensatory left ventricular hypertrophy increases myocardial demand and ischemia can develop even in the absence of CAD. Hypertrophy causes decreased chamber compliance and diastolic left ventricular dysfunction LVF.

Clinical Presentation--> Midsystolic murmur heard loudest in the second right intercostals space and transmitted to the neck. Also when patient is sitting up and in full expirationSmall and slow-rising arterial pulse, systolic thrill in the second right intercostals space or suprasternal notch and sustained apical impulse.Aortic ejection sound is present and second heart sound is normal but sometimes reversed split can occur in severe obstruction.Symptoms= angina pectoris, exertional syncope and LVF. Atrial fibrillation can occur as well.

Aortic Regurgitation
Causesà acuteà Valvular-Infective EndocarditisAortic root- Marfan’s syndrome, dissecting aneurysm of the aortic root
à chronicà Valvular- Rheumatic (infective endocarditis)Congenital- bicuspid valve, ventricular septal defectAortic root dilatation- Marfan’s syndrome, aortitis (seronegative arthropathies, rheumatoid arthritis, tertiary syphilis) and dissecting aneurysm.

Pathophysiologyà Regurgitation causes reflux of blood from aorta through the aortic valve into the left ventricle during diastole. Thus reduces CO. To compensate LV has to pump harder to maintain COLeft ventricular volume overloadà left ventricular dilatation enhances chamber compliance and end-diastolic volumes can be accommodated without a rise in filling pressure.In long termà progressive ventricular dilatation eventually leads to congestive heart failure.In large regurgitant volumes, it can result in rapid increasing diastolic filling pressure, pulmonary oedema and shock.

Clinical Presentationà Patient present with complaint of heart pounding and vigorous pulsation, shortness of breath and angina pectoris.Pulse- characterized as collapsing (a water hammer pulse) and BP with wide pulse pressure.Diastolic thrill can be felt at the left sternal edge when patient sits up and expire.A decrescendo high-pitched mid-diastolic murmur beginning immediately after the 2nd heart sound at left sternal edge.An Austin murmur (mid-systolic) at mitral area, mimicking mitral stenosis.

Mitral Stenosis
Causesà Most common valve to be affected in rheumatic heart disease following an acute rheumatic fever.Congenital parachute valve- all chordae insert into one papillary muscle. (rare)

Pathophysiologyà Commissural fusion and degeneration change in the mitral apparatus obstruct left ventricular inflow. This causes an increase in left atrial pressure to maintain left ventricular filling àleft atrial chamber dilation, pulmonary venous congestion and secondary pulmonary arterial hypertension à right heart failure.

Clinical Presentationà symptoms- dypsnoea, ortopneoa, paroxysmal norturnal dyspnoea, haemoptysis; ascites, oedema.à Atrial fibrillation can occur due to atrial dilation.àPalpable S1- tapping quality of the apex beat, and right ventricular heave.à On auscultation- Loud S1(valve cusps widely apart at the onset of systole. Low pitched mid-diastolic murmur at mitral area (best heard with a bell with patient in the left lateral position)

Mitral Regurgitation
Causesà Rheumatic heart disease (infective endocarditis, myocarditis)Papillary muscle dysfunction secondary to IHDDilated Cardiomyopahy (IHDConnective tissue disease (SLE)Collagen abnormalities (Marfan’s syndrome and Ehlers-danlos syndromeDegeneration of the valve cusps or mitral annular calcification.Drugs- fenfluramine

Pathophysiologyà In acute mitral regurgitation, the normal compliance of the left atrium does not allow much dilation but atrial pressure rises. In chronic regurgitation, atrial and ventrical dilation can occur since a proportion of the stroke volume is regurgitatedà the stroke volume increases to maintain the forward cardiac outputà left ventricular failure.Pulmonary venous hypertension is common either due to increase pressure in atrial chamber or left ventricular failure.

Clinical presentationàSymptoms are related to left heart failure and atrial or ventricular arrhythmiaà Dyspnoea and ortopnoeaà laterally displaced (forceful) diffuse apex beat and systolic thrill at apex areaà Parasternal heave due to left atrium enlargementà Pansystolic murmur maximal in the apex and radiating towards the axilla. Soft or absent S1(atrial and ventricular pressures have equalized and the valve cusps have drifted back together) and left ventricular S3 which is due to rapid left ventricular filling in the early diastole.

Task for PBL paper 1

1. Rheumatic fever (sareeta)
   
• what is it?
• epidemiology
  
• cause
• clinical presentation
• complication
2. Valvular heart disease
   
1. aortic + mitral (alvin)
   
2. pulmonary + tricuspid (christine)
   
• for stenosis and regurgitation
• clinical presentation
• causes
3. pathophysiology of aortic stenosis (yazid)
   
• how does it cause SOB
• alcohol and smoking on the heart
• effect of BP and AS on heart
4. Investigation (chris)
   
• for aortic stenosis
• narrowing of pulse pressure
5. Management of AS and high BP (maze)
   
• non pharm/pharm
• surgical
• other