Valvular Heart Disease

Question 1

General anatomy of heart valves

Answer 1

Aortic- tricuspid/3 commissures/semilunar valves CUSPS
Pulmonary- tricuspid semilunar valves CUSPS
Tricuspid- tricuspid flaps supported by chordae tendinae
Mitral - bicuspid flaps supported by chordae tendinae—pap Mm
(Latter 2 atrioventricular valves and have leaflets)

Question 2

Function of heart valves

Answer 2

Maintain unidirectional blood flow

Function dependant on mobility/pliability/structural integrity of leaflets and cusps

Question 3

Heart valve morphology

Answer 3

Lined by endo
Dense collagenous core at outflow surface
Loose CT rich central core
Elastin rich layer at inflow surface

Question 4

HV response to injury

Answer 4

Mechanical- fibrotic thickening over preserved architecture
Inflammation- vascularisation and fibrosis (reduced size and surface area)
Degeneration- distortion and increase in size due to chol/calcium deposits
Consequences- stenosis (reduced blood flow) incompetence (back flow of blood)

Question 5

Common causes of VHD

Answer 5

Calcific aortic stenosis- wear and tear/calcific deposits heaped up (affects 70-80years w/ normal Aortic valve and 50-60years w/ bicuspid aortic valve)
Mitral annular calcification
Myxomatous degeneration of mitral valve
ARF and RHS

Question 6

Aortic valve stenosis location

Answer 6

Supra valvular 
Sub valvular 
Valvular 
NV- 3-4 CM2 
Symptomatic when area reduced to 1 CM2

Question 7

AVS Etiology

Answer 7

Congenital- bicuspid aortic valve/unicuspid aortic valve
Early onset 30-50 years and ass. To aneurysm, dissection and coarctation
Acquired- RHD/degeneration/calcification
Late onset 70-80 years and ass. To adhesions and fusions of commissures and cusps/SLE/RA/post radiation/infectious vegetations

Question 8

AVS pathophysiology

Answer 8

P gradient develops between LV and aorta increasing after load
LV function is maintained by compensatory hypertrophy
LV function declines when compensatory mechanisms exhausted

Question 9

AVS natural history

Answer 9

Mild to severe in 25years

Onset of symptoms is a poor prognostic indicator

Question 10

Mitral valve stenosis

Answer 10

Obstruction of LV inflow which prevents proper filling during diastole
NV- 5-6 CM2 symptomatic at <2 CM2
Primary causes- ARF/RHD/IE/mitral annular calcification

Question 11

MVS M&M

Answer 11

Infection
Pulmonary congestion
Thromboembolism

Question 12

MVS pathophysiology

Answer 12

Progressive dyspnea (70%) > LA dilation/pulm congestion/reduced emptying (worsened by PA/fever/pregnancy)
Increased transmitral P> LA dilation and atrial fibrillation
RHS HF as a result of p-HTN
Hemoptysis as a result of bronchial BV rupture under high P

Question 13

MVS natural history

Answer 13

Mild to severe in 30 years

Question 14

Mitral annular calcification

Answer 14

Increased in F >60 years
Degenerative calicific deposits in MV ring (no alteration of MV function)
May lead to mitral regurgitation
Source of thromboembolism and increases risk of IE

Question 15

Aortic regurgitation

Answer 15

Leakage of blood into LV during diastole due to ineffective joining of aortic cusps
Acute- IE/dissection
Chronic- bicuspid aortic valve/RHD/IE
Symptoms- diastolic murmur/wide pulse P/pulm edema

Question 16

Aortic regurgitation pathophysiology

Answer 16

Combined P/V overload
Compensatory mechanisms
LV dilation and hypertrophy leads to HF

Question 17

Mitral regurgitation

Answer 17

Back flow of blood from LV to LA during systole
Acute- IE/ malfunction of prosthetic valve
Chronic - RHD/IE/ischemia/myxomatous degeneration
Mild chronic form In 80% of normal people

Question 18

Mitral regurgitation pathophysiology

Answer 18

Pure V overload
Compensatory mechanisms
LA enlargement/hypertrophy/increased contractility
> progressive LV dilation and volume overload/RV dysfunction/p-HTN/HF

Question 19

Mitral valve prolapse

Answer 19

Tenting of valve leaflets
Cause of myxomatous degeneration of valves and leaflets
Valvular cusps balloon/leaflets become thick and rubbery
Could be due to CT disorder Marfans syndrome (alteration in gene encoding fibrillin)