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Chapter: Medicine Study Notes : Cardiovascular

Valvular Heart Disease

Insufficiency may be due to diseased cusp or supporting structures (valve ring, chordae tendinae, papillary muscles, ventricular wall). Can be acute or chronic

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


Aortic Stenosis


·        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


Aortic Regurgitation


·        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


Mitral Stenosis


·        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


Mitral Regurgitation (MR)


·        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


Tricuspid Regurgitation


·        Commonest cause is right heart failure/enlargement secondary to left ventricular failure. Left atrium is also likely to be enlarged ® AF common too


Infective Endocarditis


·        = 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


Predisposing Factors


·        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)


Anatomic sites of infection


·        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).


Causal organisms


·        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


Pathogenesis of infection


·        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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