IOD Valvular heart disease

Question 1

stenosis?

Answer 1

• failure of a valve to open completely → impede forward flow. [there is also usually failure of full valve closure]
• stenosis is virtually always caused by a chronic process.
The gradual development of stenosis allows time for compensatory changes
in heart, blood vessels and other organs.

Question 2

regurgitation?

Answer 2

• failure of a valve to close completely → reverse flow occurs.
• regurgitation may be caused by an acute or chronic process.

Question 3

aortic stenosis?

Answer 3

Aortic stenosis is the most common valve disease in developed countries. The prevalence of clinically significant aortic stenosis in patients over 70yo in Europe is about 1-3%.

Question 4

causes?

Answer 4

• age-related calcification of a normal valve.
• the normal aortic valve has three leaflets.
• cumulative ‘wear and tear’ due to valve movement over many years leads to endothelial and fibrous damage, causing gradual calcification and stenosis of an otherwise normal valve.
• cusp calcification of a bicuspid valve.
• bicuspid valve is a congenital abnormality in which the valve is made up of two leaflets. It occurs in about 1-2% of the population and has a strong association with aortic coarctation.
• it is thought that years of turbulent flow across the abnormal valve disrupt the endothelium and collagen matrix of the leaflets, resulting in gradual calcium deposition. The calcification develops by approximately 30yrs, with progressive stenosis
post rheumatic fever valve disease-fish-mouth short thick fused cusps

Question 5

Pathophysiology of aortic stenosis?

Answer 5

As stenosis progresses, blood flow through the aortic valve becomes more and more impeded during systole. ie. there is development of leN ventricle (LV) outflow obstruction. In order to maintain cardiac output, the LV must produce more force to drive blood through the aortic valve and into the aorta.
Since aortic stenosis develops over a chronic course, the LV is able to do this by undergoing compensatory hypertrophy.
ie. gradual development of LV ouBlow obstruction causes gradual pressure overload of LV and results in compensatory LV hypertrophy.
However, the hypertrophy reduces the compliance of the ventricle. The resulting elevation of diastolic LV pressure also causes LA hypertrophy in order to fill the ‘stiff’ LV.

As a consequence of the compensatory changes, there is a long asymptomatic period.

Question 6

decompensation in aortic stenosis?

Answer 6

Eventually the heart decompensates and there is deterioration in cardiac function, leading to the the development of symptoms.
The classic clinical presentation of aortic stenosis is the triad of:
• angina.
• syncope on exertion.
• development of congestive cardiac failure.
[AS is also an important cause of unexpected sudden death (due to arrhythmias).]
Once symptoms develop, there is marked reduction in survival. There is no effective medical treatment. The two options for valve intervention are conventional aortic valve replacement and transcatheter aortic valve implantation.

AS is associated with an ejection systolic murmur.

Question 7

aortic sclerosis?

Answer 7

thickening and calcification of aortic valve leaflets without motion restriction ie. the valve still opens and closes normally

Question 8

mitral regurgitation?

Answer 8

second most common valve lesion

Question 9

causes of MR?

Answer 9

• LV dilatation (eg. due to any cause of leN ventricular failure) causes secondary stretching of the valve ring so that the valve cannot close properly
• mitral valve prolapse
• infective endocarditis
• post-rheumatic fever (scarring and fusion of cusps) [rare in the UK]
• Rupture post MI
• Ischaemia due to coronary artery atheroma (impaired contraction of the papillary muscle causes failure of complete valve closure)

Question 10

Acute MR?

Answer 10

Due to infective endocarditis or rupture of papillary muscles after MI
sudden onset means not enough time for heart to undergo compensation so blood flows back into the LA
increased pressure in the LA so increased pressure in the pulmonary veins so acute pulmonary oedema and LHF

Question 11

chronic MR?

Answer 11

dilatation of mitral valve ring and prolapse, post-rheumatic fever, or papillary ischaemia
gradual onset means enough time to compensate
LA dilates to accommodate backflow so no increase in LA or pulmonary pressure
LVH to maintain CO
Asymptomatic until decompensation and progression to LV failure

Question 12

mitral valve prolapse?

Answer 12

commonest cause of MR
incidence of 5%
complication of CT disorders

Question 13

mitral valve prolapse cause?

Answer 13

In MVP the normal dense collagen and elastin matrix of the valve is replaced with loose myxomatous connective tissue containing abundant glycosaminoglycans (so-called ‘myxomatous degeneration’). The leaflets become enlarged and one of the leaflets ‘prolapses’ back into the LA during systole.

MVP may or may not be associated with regurgitation:
• MVP without MR is generally considered by cardiologists to be asymptomatic (majority of cases).
• MVP with MR: symptomatic. Only a minority of patients have severe enough MR to warrant surgery