Valvular Heart Disease
·
= Stenosis,
insufficiency/regurgitation or mixed
·
Insufficiency may be due to
diseased cusp or supporting structures (valve ring, chordae tendinae, papillary
muscles, ventricular wall). Can be acute or chronic
·
Stenosis: disease of valve cusps,
usually always chronic
· See Heart Murmurs(Topic), for clinical descriptions
·
Compared with
regurgitation/incompetence:
o Have different effects on the LV (can‟t have severe stenosis and severe
regurgitation together):
o Stenosis: pressure but no in volume. LV tolerates pressure loads less well than volume loads ® stenosis
is the worse of the two
o Regurgitation: volume but no in pressure. However, some in afterload due to stroke
volume
·
Causes or aortic stenosis:
o Post inflammatory scarring (eg rheumatic fever): 10%
o Senile (degenerative) aortic stenosis: commonest, in 8th – 9th decade
o Calcification of deformed valve in 6th – 7th decade (associated with coarctation Þ check for radio-femoral delay)
o Congenital stenosis
o Infective
·
Symptoms: Occur late
o Dyspnoea and chest tightness related to exertion
o Exertional syncope: due to inability to increase CO and transient
ventricular arrhythmias
o Angina pectoris/MI, fibrosis, ventricular arrhythmia and sudden death
due to impact on myocardial
o O2 supply and demand:
o · O2
demand due to pressure and LV mass (LV workload ® concentric hypertrophy) · ¯¯coronary blood flow due to ¯diastolic
aortic pressure coronary vascular resistance and
§ systole
compared with diastole ® ¯time for perfusion · ® ischaemia
o No pulmonary oedema unless eg mitral problems secondary to LV
hypertrophy, etc
·
Signs:
o Sounds:
·
Harsh systolic ejection murmur
(unless in severe LV failure) +/- systolic ejection click and a short aortic
diastolic murmur. Heard in base, apex and carotids
·
May have paradoxic (reversed)
splitting of S2 if severe stenosis or LBBB. 3rd and 4th sounds common
o ¯Pulse
pressure and low blood pressure
o Slowing and shuddering of the carotid upstroke
o LV hypertrophy on ECG or x-ray and heave on examination. Palpable LV
hypertrophy with a dynamic quality is more related to incompetence – the
ventricular impulse reflects stroke volume more than pressure
o LV failure: progression from LV hypertrophy to LV dilation in late
stages
o AF in 10%
·
Diagnosis:
o Often a discrepancy between symptoms and severity. Pre-symptomatic
progression is highly variable
o Usually at least some regurgitation as well
o ECG: LV hypertrophy, occasionally left or right BBB
o Pressure differential with Doppler ® estimate valve area
·
Gross:
o Look for commissural fusion (rheumatic)
o Heaped up calcified masses in leaflets. Beginning at the base Þ senile,
beginning at the edge Þ abnormal valve
·
Management:
o If mild/moderate (ie < 50 mmHg pressure gradient across the valve)
then monitor
o Fix/replace valve before LV
failure
·
Complications:
o Sudden death
o LVF
o Conduction defects
o Infective endocarditis
o Embolisation
·
Differential:
o Can rarely be due to supraventricular or subvalvular lesions, with no
problem with the valve
o Left ventricular failure
o Hypertrophic obstructive cardiomyopathy: pulse is jerky and upstroke
rapid. Longer, harsher murmur best heard at the left sternal edge
o Hard to confuse with mitral regurgitation (!!): Pansystolic murmur and
rapid upstroke
o Coarctation
·
Causes:
o Intrinsic valvular disease:
§ Acute lesions: Rheumatic fever, infective
endocarditis (have high index of suspicion), traumatic rupture, aortic
dissection (may also have dissected coronary arteries ® MI)
§ Chronic lesions: Congenital lesions, rheumatic heart disease, arteritis,
aortic aneurysm, collagen diseases, ankylosing spondylitis and Reiter‟s
Syndrome (may be secondary to aortitis)
o Aortic disease: degenerative aortic dilatation, syphilitic aortitis,
Ankylosing Spondylitis, rheumatoid arthritis, Marfan‟s syndrome
·
Key features:
o LV hypertrophy
o Large aorta
o Stroke
volume
o Wide pulse pressure eg 140/50 (systolic due to extra work of the
heart, ¯diastolic due to back flow)
·
Symptoms:
o Acute: dyspnoea – often paroxysmal, orthopnea, pink frothy sputum. Chest
pain, sudden death, etc. If sub-acute, possibly embolisation
o Chronic: Symptoms unrelated to severity. Either awareness of force of
contraction (palpitations) or LV disease/failure
·
Signs:
o Pulses: prominent pulsations in the neck (Corrigan‟s Sign), throbbing
peripheral pulses, prominent apex beat over a wide area
o Auscultation: high-pitched, blowing diastolic murmur beginning
immediately after S2. The more severe the longer it lasts. Systolic flow murmur
·
Pathogenesis:
o Acute: LV blood volume ® left atrial and pulmonary pressure ® oedema. Pressure
inside a non-compliant pericardium ® RH pressures. ¯Myocardial
flow due to ¯aortic diastolic pressure and constricted pericardium ®
ischaemia, further dysfunction, etc
o Chronic/Gradual: ® eccentric hypertrophy with low filling pressure. Stroke
volume ® systolic pressure ® baroreceptor reflex ® peripheral vasodilation ® further widening of the pulse
pressure. Copes with tachycardia better than stenosis: ¯proportion
of cycle in diastole ® ¯proportion of blood flowing back into the ventricle. However, peripheral
resistance (eg cold, iso-tonic exercise, sympathetic nervous stimulation) ® pressure
load on the heart
·
Complications:
o LV failure + myocardial fibrosis (secondary to hypertrophy, ischaemia,
etc) late in the progression
o Infective endocarditis
o Conduction defects less common
o No pulmonary oedema unless LV hypertrophy
·
Differential diagnosis:
o Pulmonary regurgitation + pulmonary hypertension
o Other causes of rapid run-off: patent ductus, arterio-venous fistula
·
Causes: rheumatic heart disease,
infection (less common than aortic) ® fusion of the leaflets
·
Symptoms: dyspnoea, PND,
haemoptysis, arrhythmia (® palpitations), RH signs if pulmonary hypertension
·
Signs:
o Loud S1, opening snap after S2 (loudest at apex)
o Long, loud diastolic murmur accentuated just before S1 (atrial systole –
not if AF). Loudest with bell at apex and left lateral side
o Pulmonary oedema is worse than in other causes (eg mitral regurgitation)
o If pulmonary hypertension then low cardiac output failure® thin
patient, peripheral cyanosis, cool extremities, small pulse volume. Dilated
veins and cyanosis of cheeks = mitral facies
·
Leads to:
o LA enlargement:
§ ®
pulmonary hypertension (> 7.5 mmHg/L/min) and pulmonary oedema
§ ® AF
o Bronchitis
·
Investigations:
o ECG: broad P wave, RV hypertrophy (NB – LV enlargement is not typical –
key differential with mitral regurgitation)
o X-ray: LA enlargement, RH enlargement
o Echo: good at imaging the mitral valve
·
Differential: Left atrial myxoma
(much less common)
·
Treatment:
o Prophylaxis for RF (till 20) and infective endocarditis (eg dental work)
o Surgery: valvotomy, balloon valvuloplasty, replacement
·
Causes:
o Abnormalities of leaflets:
§ Rheumatic heart disease ® post inflammatory scarring
§ Infective endocarditis
§ Degenerative change
§ Floppy valve syndrome = mitral valve prolapse. Immaterial haemodynamic
changes (Þ normal heart size, etc). Common - ?5-10% of young women. Mid/late
systolic murmur +/-mid/late systolic click. Complications (3% of affected) are
infective endocarditis, mitral regurgitation, and embolism of leaflet thrombi
§ Congenital
§ SLE can cause Libman-Sacks endocarditis: sterile immune mediated
endocarditis mainly affecting underside of mitral valve (cf other vegetative
endocarditis on top)
o Abnormalities of tensor apparatus: Previous MI: e.g. fibrosis or rupture
of papillary muscle
o Abnormalities of LV cavity or valve ring:
§ Calcification of mitral ring (especially elderly women)
§ LV enlargement (whole ventricle expands). Dilatation of the mitral
annulus and lateral displacement of the papillary muscles
§ Hypertrophic cardiomyopathy (thickening in parts of wall – e.g. enlarged
septum disrupts flow to aortic valve). Anterior displacement of the anterior
leaflet
o Existing MR – begets MR.
Enlargement of LV pulls posterior leaflet away from the mitral orifice
·
Signs:
o Pan-systolic murmur: regurgitation throughout the whole of systole.
Loudest at apex. Radiates over precordium and into axilla. No S1. No opening snap
unless concurrent stenosis. Early diastolic flow murmur
o In severe MR, Aortic valve closes prematurely ® split S2
o S3 caused by sudden tensing of papillary muscles, chordae tendinae and
valve leaflets
o Small volume pulse
·
Significant difference between
acute and chronic presentations:
o Pulmonary oedema and RV overload much more significant if acute. In
chronic, enlargement of the LA reduces pulmonary „back flow‟
o AF better tolerated than in mitral stenosis
o RHF rare unless acute presentation or LVF
·
Leads to:
o Eventually leads to LV and LA hypertrophy (may take decades)
o AF common – mostly correlated with age
o Infective endocarditis (in 20%)
o Systemic embolisation
o Pulmonary hypertension (but much later compared with mitral stenosis)
·
Differential:
o Hypertrophic cardiomyopathy: both long systolic murmurs, but MR radiates
to the axilla, hypertrophic cardiomyopathy radiates centrally
o VSD
·
Commonest cause is right heart
failure/enlargement secondary to left ventricular failure. Left atrium is also
likely to be enlarged ® AF common too
·
= Infection of mural endothelium
or heart valves. May also include the
proximal aorta
· See also Rheumatic Fever(Topic)
·
Now all called infective
endocarditis
·
Acute bacterial endocarditis
(ABE):
o < 6 weeks duration
o Virulent organisms
o Normal valves (eg IVDU)
o Bulky friable vegetations: may extend to adjoining endocardium and
chordae tendinae. Destructive (directly proportional to virulence of organism).
Much more destructive than Rheumatic Fever. Microscopically vegetations show a
suppurative exudate, fibrinous thrombi, and large bacterial colonies destroying
valve substance
·
Sub-acute bacterial endocarditis
(SBE)
o > 6 weeks duration
o Avirulent organisms: normal flora
o Abnormal valves
o Evolution slower, gradual valvular dysfunction, flatter vegetations with
deeper chronic inflammatory component including a vascular fibrous tissue
healing response
·
1950s: rheumatic heart disease
(most cases) – affect 15 – 35 year olds
·
1990s: degenerative, rheumatic,
congenital (low pressure side of a septal defect gets infected), prosthetic
valves – affects 50 year olds
·
Circulatory factors:
o Regurgitant blood stream (incompetent valve)
o Large pressure gradient across valve (i.e. rarely right heart except
IVDU)
·
Nearly always where there‟s a
pre-existing abnormality
·
Usually on the top of the valve
·
Incompetent mitral and aortic
valves: 40% mitral, 40% mitral and aortic valve
·
Calcific aortic stenosis
·
Prosthetic heart valves
·
Congenital septal or valve
defects
·
Also in Intra-venous drug users
(IVDU) with normal hearts (Right side commonly affected).
·
In theory: any organism
(including fungi and chlamydiae)
·
In practice:
o Native valves:
§ Streptococci: 70%
§ Staph: 20 – 25%
§ Miscellaneous (including enteroccoci) 5%
§ Culture negative 5%
o Prosthetic valves:
§ < 3 months (early PVE): staphylococci > streptococci
§ > 3 months: staph = streptococci
·
Streptococcal causes of
endocarditis:
o Oral Commensals: Viridians Streps – more in younger people, good at
sticking, don‟t cause much
o infection elsewhere: S. sanguis, s. salivarius, s. mitis, s. milleri, s.
mutans
o Faecal: called enterococcal
·
Staphylococcal causes:
o S. aureus: coag +ive – 60% mortality (common in intravenous drug user)
o S. epidermidis + 20 others: coag –ive – 40% mortality
·
Miscellaneous causes:
Haemophilus, Actinobacillus, Cadriobacterium/Candida Albicans (in
prosthetic valves, mortality 100%), Eikenella, Kingella
·
Abnormal valve ®
o NBTE (non-bacterial thrombotic endocarditis) – little blood clots – we
all have them but risk on a deformed valve ®
§ Transient bacteraemia from possibly trivial infection ®
adherence of bacteria ® Acute inflammatory reaction – WBCs, fibrin & platelets laid down ®
o Mature vegetation – sheds bacteria
·
Always a differential in pyrexia
of unknown origin. Malaise, weakness
·
Existing immunosuppression,
neutropenia, diabetes, and alcohol increases risk
·
Heart murmur, isolated petechiae
(eg nail beds, retinal) and splenomegaly significant
· Blood culture: 3 times – organism load in blood may be low
·
Echocardiogram (although may miss
flat vegetations)
·
Valvular insufficiency or
stenosis (aortic stenosis ® LV hypertrophy ® coronary artery insufficiency)
·
Local extension: down septum,
into wall of aorta, perforated valve, suppurative pericarditis, ring abscesses
· Embolism: small infarcts (e.g. in kidney cortex) or abscess (each emboli has bacteria in it) eg in lungs
·
Mycotic aneurysms, focal and
diffuse glomerulonephritis
·
Septicaemia
·
Antigenaemia: antigen/antibody
complexes ® skin lesions, clogged up kidneys
·
Identify causal organism with
antibody sensitive tests (MIC & MBC)
·
Empiric antibiotic therapy -
regimes:
o Staphylococcal: Flucloxacillin (or vancomycin) 2g iv 4 hourly for 2
weeks, then 1 g orally 6 hourly for 4 weeks
o Streptococcal: penicillin + gentamycin or amoxycillin + gentamycin iv
for 2 weeks, then 4 weeks oral
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