Valvular heart disease Flashcards
Causes of valvular heart disease
Degenerative
- aortic > mitral
Infective
- any valve
- right atypical organism
Rheumatic
Congenital
Degenerative valve disease epidemiology
Reflects ageing population
Infective valve disease epidemiology
Most common on abnormal valves
Virulent organisms
Immunocompromised
Rheumatic valve disease epidemiology
Post streptococcal rheumatic fever
Children and young adults
Disease of poverty and overcrowding
Congenital heart disease epidemiology
Low static incidence in all populations
Pathology of valvular heart disease
Stenosis
- fibrosis: fusion of leaflets
- calcification: immobility of leaflets
Regurgitation
- supporting structures: papillary muscles
- dilatation of valve ring
Aortic stenosis aetiology
Congenital syndromes <60
Bicuspid valves 40-60
Degenerative >60
Post rheumatic fever
What is aortic stenosis?
Obstruction to blood flow- pressure overload in ventricle
Similar signs in other causes of obstruction
- HOCM, subvalvular/ supravalvular stenosis
Generation of high LV systolic pressure to force blood through the obstruction
Left ventricular hypertrophy
Eventually LV decompensation/ dilation
Aortic stenosis physiology
As ventricle contracts, pressure goes up forcing leaflets open
If stenosed it can’t open properly, producing turbulent flow- murmur
At beginning of systole pressure gradually rises so crescendo decrescendo sound, ejection systolic murmur
As the valve gets even thicker, doesn’t open properly or close properly so no second heart sound
Aortic stenosis symptoms
Chest pain
- normal coronary arteries- supply/ demand
- coronary artery disease
Breathlessness
Dizziness/ syncope
- bradyarrhythmias
- insufficient cardiac output
Sudden death
Aortic regurgitation aetiology
Aortic dilatation - loss of support
- connective tissue disease, hypertension, aortic dissection, degenerative, cystic medial necrosis, syphilis
Valvular
- bicuspid valve, infective endocarditis
Aortic regurgitation
At the end of systole the pressure in the ventricle falls and the valve leaflet closes
If it can’t close blood falls back into the ventricle
Early diastolic murmur
Normally abnormal valve so turbulence as blood comes out, commonly also systolic murmur
What is aortic regurgitation?
Blood falls back into LV during diastole
Resultant volume overload
LV dilatation to accommodate volume
Late decompensation of LV function
High volume circulation (as in pregnancy, anaemia, thyrotoxicosis)
Symptoms
Often asymptomatic
Chest pain
- normal coronary arteries - supply demand
- coronary artery disease
Breathlessness
Syncope- uncommon
Catastrophic decompensation if acute
Mitral regurgitation aetiology
Valvular
- prolapse
- infective
- degenerative
Chordal/ papillary muscle failure
- acute/ chronic
Annular dilatation- secondary to left ventricular dilatation
Mitral regurgitation
As pressure in systole increases with ventricular contraction, the mitral valve is forced shut
If leaflets fail to coapt, blood squirts back into left atrium
Left atrium is low pressure and during systole the elft ventricle is high pressure, blood regurgitates back almost immediaitely and for the whole of systole
Mitral regurgitation classically produces pan-systolic murmur
What is mitral regurgitation?
Blood ejected backwards during systole into the left atrium
Leads to transient elevation of left atrial pressure
Chronically affects the right heart raised PAP
Results in volume overload in subsequent cardiac cycles of left ventricle
As a result left ventricular dilatation and decompensation develops
Symptoms of mitral regurgitation
Breathlessness- mitral valve next in line to lungs
Lethargy
Palpitations- atrial fibrillation
Peripheral oedema, hepatomegaly, JVP- decompensation (RHF consequence)
Chest pain- concomitant CAD
Mitral prolapse
Initially valve shuts during early part of systole but then either because leaflet is too baggy or abnormal sub-valvular apparatus, the leaflets prolapse back into left atrium
Potentially allows through jet of regurgitation
As it prolapses back into LA mid-systolic click
If blood then flow into the atrium there’s a late systolic murmur
Mitral stenosis aetiology
Almost always due to rheumatic fever
Congenital
Storage diseases
Malignancy
Mitral stenosis
Problem with leaflets as well as the sub-valvular apparatus
Restricts blood flowing across the mitral valve from the left atrium into the left ventricle during diastole
Mid diastolic rumbling murmur
Opening snap as the restricted leaflets snap open
May have loud first heart sound if the leaflets are stiff but still relatively mobile
What is mitral stenosis?
Failure of ejection of left atrial volume
Dominates by lung. right heart consequences
Left ventricle preserved
Exacerbated when atrial contraction lost or when high circulating volume
Symptoms of mitral stenosis
Breathlessness
- pulmonary oedema
- pulmonary hypertension
Palpitations
- AF
Systemic emboli
Peripheral oedema
Fatigue
Haemoptysis
Compressive symptoms- stridor, dysphagia
Prosthetic heart sounds
Position
First heart sound metallic- mitral/ tricuspid
Second heart sound metallic- aortic
Systolic murmurs common and not necessary pathological
Diastolic murmurs usually pathological
Valvular heart disease treatments
Medical
- HF
- arrhythmias
Surgical
- valve repair
- valve replacement
Percutaneous intervention
- BAVI
- TAVI
- mitraclip
- paravalvular leak closure
Tricuspid regurgitation
Organic tricuspid valve disease is rare
- infective endocarditis
- carcinoid
Infective endocarditis
Microbial infectrion endothelial surface heart
Wide range bacteria and fungi but typically
- streptococci
- staphylococci
- enterococci
Characteristic lesion is a vegetation
Heart valve typically affected
May present acutely with or sub acutely with a several week history
Mimics
Infective/ sepsis
Embolic
Immunological
Symptoms and signs of infective endocarditis
Constitutional symptoms
Emboli
Arthralgia
Splinter haemorrhages
Osteomyelitis/ discitis
Osler’s nodes
Glomerulonephritis
Vasculitic rash
Peripheral manifestations of IE
Mycotic aneurysms
Septic emboli
Risk embolisation greatest 2 weeks anti-microbial therapy and for vegetations >1cm
20-40% patients clinical evidence emboli
Diagnosis and management of IE
Duke criteria help
Blood cultures before antibiotics
Echocardiography to detect vegetations/ abscess formation
Antimicrobial therapy 2-6 weeks duration
Surgery
- ongoing sepsis
- worsening valve regurgitation
- recurrent emboli
- vegetations >1.5cm
- removal intra-cardiac device
IVDU associated with IE
Typically right heart valves but not exclusive
40-6-% pulmonary septic emboli
60% cases staphylococcus
Increased risk of death if left sided valves involved
Patients may have co-existent HIV infection
Congenital heart disease
Failure of normal development of cardiac structures in utero
Severe
- stillbirth
- neo-natal heart failure
Mild
- presents in childhood or early adult life
Left to right shunts
Atrial
Patent ductus arteriosus
Ventricular
