JC05 - Valvular heart disease Flashcards
Pathophysiology of acute and chronic rheumatic fever
Acute: molecular mimicry
- Delayed immune response to infection with certain strains of Group A Strep
- Cross-reactiveness targeting cardiac proteins (anti-M)
- Result: inflammation in ALL layers: endocardium, myocardium and pericardium
Chronic:
- Repeated ARF attacks over decades → progressive fibrosis and fusion of heart valves
S/S of acute rheumatic fever
- Preceded by Strep throat 2-3m weeks before
- Fever, anorexia, lethargy
- Pancarditis: SOB, Palpitation, Angina, Murmurs
- Associated: Arthritis, Skin (subcutaneous nodules), Sydenham’s chorea
- Valvular involvement: Commonly Mitral (MS > MS+MR > MR) and Aortic
Type of murmur associated with acute rheumatic fever
Transient MR/AR murmur, MDM at apex (Carey-Coombs murmur)
Name of diagnostic criteria for rheumatic fever
Jone’s criteria
2 major manifestation or 1 major + 2 minor + evidence of preceding streptococcus infection
Investigation and treatment of acute rheumatic fever
Ix:
□ Throat swab (rarely positive) and serology for ↑ASO titres
□ ESR/CRP
□ Echocardiogram: MR ± AR, MVP, pericardial effusion
Tx:
Acute: single dose IM benzylpenicillin
Heart valves affected by rheumatic fever
Site: MV alone (most common)
AV+MV, AV alone
TV (rare)
Pathophysiology of IE
Endothelial damage → attract platelet/fibrin deposits → protects vs host defense
→ favours colonization by blood-borne organisms
Fibrin/platelet accumulation → growth of vegetation → obstruction/embolism
Infection destroy adjacent tissues → abscess formation
Risk factors of IE
Prior rheumatic HD (30%) Normal valves (40%) IVDU (10%) Congenital defects (10%) Prosthetic heart valve (10%)
Complications of IE
□ Systemic infection due to continuous bacteraemia
□ Valvular heart disease due to vegetation formation
□ Septic embolization due to dislodging of vegetation materials
□ Immune complex deposition due to systemic inflammatory response
Groups of pathogens that cause IE
S. aureus: most common
Viridans strep: 2nd most common cause (eg. S. sanguis, S. mutans)
Group A/B streptococci, i.e. S. pyogenes and agalactiae
Group D streptococci, i.e. Enterococcus, S. bovis
HACEK: group of slow-growing fastidious G- bacilli
Others:
- Animal contact: Coxiella burnetti (Q fever), Brucella
- Fungal (IV line, immunocompromised)
- Coagulase -ve staphylococcus (prosthetic valve)
Primary sources of bacteria that cause IE
S. aureus - skin/ skin infection/ IVDU
Viridans strep. - Oropharyngeal commensal, dental procedure, brushing
Group D strep. - GI/ GU tract diseases [classically a/w colonic ulcerative lesions, eg. CA colon, ulcerative colitis]
HACEK - oropharynx
Antibiotics sensitivity of causative bacteria of IE
S. aureus: variable, often penicillin-resistant
Viridans strep, Group A/B strep - Penicillin
Group D strep:
- S. bovis: penicillin
- Enterococcus: penicillin-resistant, need aminoglycoside
Staphylococcus/ HACEK: variable, often penicillin-resistant
Causes of negative blood culture for IE
Culture-negative endocarditis:
- Inadequate technique
- Prior antibiotics
- Fastidious organisms (require prolonged culture) e.g. Mycoplasma, HACEK
- Fungal (mainlining addicts, immunocompromised)
May take additional 3 cultures in these cases
Causes of Non-bacterial thrombotic endocarditis
Deposition of sterile thrombus on valve leaflets
Causes: metastatic malignancy (marantic, esp mucin-producing adenocarcinoma), thrombophilia, SLE Libman-Sacks endocarditis
S/S of systemic infection complication in IE
S/S:
- Persistent fever
- Chills and rigors
- General malaise
- weight loss
- Pallor
S/S of Cardiac involvement in IE
S/S
- Chest pain
- S/S of heart failure
- Changing murmurs (esp regurgitation murmurs)
S/S, associated conditions for Septic embolism due to IE
Conditions:
- Stroke
- Brain abscess
- Cold limbs
- Splenic/renal/visceral infarcts/abscesses
S/S:
- Skin petechiae
- Roth spots
- Janeway lesions
- Splinter haemorrhage
- Splenomegaly
S/S, associated conditions for systemic immune deposition due to IE
associated conditions:
- Arthralgia/myalgia
- Tenosynovitis
- Glomerulonephritis
P/E:
- Arthritis
- Uraemia
- Vascular phenomena
- Osler’s nodes
- Finger clubbing
Sample collection method for microbiological workup of IE
3 venous cultures taken at different sites, separated by ≥0.5h + 3 cultures if initially negative (esp if prior Abx)
Microbiological diagnosis:
>2 of 3 venous blood cultures(taken at different sites and separated by at least 0.5h) showingpersistent bacteraemia of typical organisms:
Imaging modalities for IE
Indications for each approach
Trans-thoracic echo - first line for screening
Trans-esophageal echo - see vegetation, cardiac complications, first line for prosthetic valve
- Indications:
(1) Prosthetic valve/ intracardiac device (difficult to visualize)
(2) TTE non-diagnostic or –ve but high clinical suspicion
(3) TTE +ve but high risk for complications
First-line investigations for IE
Blood culture
Echocardiogram
Blood: leukocytosis, ESR, CRP
Urine: proteinuria, haematuria, pyuria, RBC casts
ECG: AV block or conduction delays
CXR: HF, cardiomegaly, septic pulmonary emboli
Clinical diagnostic criteria for IE
Duke’s criteria: Pathologic + Clinical criteria:
Diagnosis made when one of following is met
□ Pathologic criteria:
→ Micro-organisms demonstrated in a vegetation
→ IE confirmed by histology
□ Clinical criteria:
→ Definite IE = 2 major OR 1 major + 3 minor OR 5 minor
→ Possible IE = 1 major + 1 minor OR 3 minor
List all major criteria in Duke’s criteria for IE
1) Positive blood culture: demonstrate persistent bacteria
→ Typical organisms grown in 2 separate blood C/ST or >12h apart
→ Skin contaminants grown in 3 or majority of ≥4 separate C/ST (with 1st and last drawn ≥1h apart)
→ Coxiella burnetii: single +ve C/ST or phase I IgG titre >1:800
2) Evidence of endocardial involvement:
→ Echo: vegetation, abscesses or prosthetic valve dehiscence
→ New valvular regurgitation
List all minor criteria in Duke’s criteria for IE
□ Predisposition: VHD/cardiac conditions or IVDU
□ Fever ≥38.0oC
□ Vascular phenomena, eg. embolism, septic PE, mycotic aneurysm, Janeway lesion, conjunctival haemorrhage
□ Immunological phenomena, eg. GN, Osler’s nodes, Roth spots, ↑RF
□ Suggestive blood cultures: organism grown but does not meet major criterion or serologic evidence
of active infection with organism consistent with IE
Main mechanisms of heart valve defect and effect on heart chambers
Valvular stenosis (cannot open properly):
Hypertrophy of the proximal chamber (e.g. aortic stenosis - left ventricular hypertrophy)
Dilatation occurs as the chamber fails (e.g. mitral stenosis - left atrial enlargement)
Valvular regurgitation (cannot close properly): Dilatation of the chambers on either side of the valve (e.g. mitral regurgitation - left atrium and left ventricle enlarged)
S/S of valvular heart disease
- Left heart failure - progressive exertional dyspnea (SOB)
- Right heart failure (progressive to involve right heart) - ankle oedema, hepatic pain (hepatic congestion)
- Myocardial ischaemia - chest pain
- Atrial fibrillation etc. - palpitations
- Low output - easy fatigability
- Complications:
a) Thromboembolism (esp atrial fibrillation)
b) Infective endocarditis
c) Problems during pregnancy (higher demand of cardiac output)
First-line investigations for valvular heart diseases
- ECG: chamber enlargement, atrial fibrillation
- CXR
- Echocardiogram*
- Exercise testing: objective assessment of functional capacity
- Cardiac catheterization (to assess status before valvular surgery):
a) Associated coronary artery disease
b) Pressure gradient
c) Inject contrast to assess regurgitant lesions
Outline tests done on Echocardiogram in assessment of valvular heart diseases
Echocardiogram* (accurate, noninvasive):
Valvular architecture
Chamber size
Chamber function
Doppler: assess valvular gradient/regurgitation
Low dose dobutamine (β-adrenergic receptor stimulant) to assess ischaemia and contractile reserve
Symptoms of IE
Systemic:
Fever (FUO), chills, rigor
Septic emboli: Stroke, Cold limb (PAD), Renal symptoms
Cardiac:
Heart failure: Chest pain, dyspnea, palpitations
Immunological reaction: Arthralgia Myalgia Tenosynovitis Glomerulonephritis
Signs of IE
Systemic: Fever, secondary sinus tachycardia (increase 10bpm/oC) Pallor Weight loss Splenomegaly
Intravascular lesions: Changing murmurs Splinter haemorrhages Osler’s nodes Janeway lesions (unpainful) Signs of heart failure (bilateral basal crackles) Petechiae Roth spots
Immunological reaction: Arthritis Uraemia Vascular phenomena Finger clubbing
First- line investigations for IE
Systemic:
- CBC: Anaemia, Leucocytosis (PMN)
- Inflammatory: Raised ESR
- Microbiology: Blood culture with C/ST, Sepsis workup (swab oral cavity, nasopharynx, vagina etc.)
Intravascular lesions:
- RBC in urine, albumin negative (acute nephritic syndrome)
- CXR
- Echocardiogram
- Arteriography
- Liver-spleen scans
- Fundoscopy
Immunological reactions: Proteinuria, casts Polyclonal Ig High rheumatoid factor Low complements, immune complexes
First-line management options for IE
- Eradicate source of infection
- Bactericidal agents:
- Streptococcus: penicillin + gentamicin
- Penicillin-resistant or allergic: vancomycin
- Methicillin-resistant Staphylococcus: vancomycin - IV high dose antibiotics (4-6 weeks)
- Surgery and complications management:
i) Large emboli/ hemodynamically unstable
ii) Prosthetic valve endocarditis
iii) Fungal endocarditis
Methods to monitor treatment for IE
- Physical signs; body weight
- Urine testing
- Renal function and blood counts (ESR may take weeks to decrease, drug level)
- Echocardiogram
- Fever may take 1-2 week to decrease
Antibiotics prophylaxis for IE
- type of antibiotics
- typical indications for prophylaxis
- Reasons for revision of IE prophylaxis guidelines
2g amoxicillin
Procedures:
All dental procedures that involve manipulation of gingival tissues or periapical region of teeth or perforation of oral mucosa only
Procedures on respiratory tract or infected skin, skin structures, or musculoskeletal tissue
Not recommended for GU or GI tract procedures (e.g. no need for OGD, colonoscopy)
Reasons for revision of guidelines:
- IE is much more likely to result from frequent exposure to random bacteremias associated with daily activities
- Prophylaxis may prevent an exceedingly small number of cases of IE
- The risk of antibiotic-associated adverse events exceeds the benefit
- Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia
Cardiac conditions associated with poor prognosis in IE
- Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
- Previous IE
- Congenital heart diseases:
- Unrepaired cyanotic CHD
- Acute infection within 6 months of complete prosthetic repair
- Prosthetic defect in repaired CHD - Cardiac transplantation recipients who develop cardiac valvulopathy
Mitral stenosis
Etiologies
95% chronic rheumatic heart disease
5% congenital malformation of mitral valve
Rare: Mitral annular calcification Anorectic drugs Carcinoid syndrome SLE Infective endocarditis
Mitral stenosis
Hemodynamic changes
Obstruction to LV inflow
Increase LA pressure (blood accumulates in left atrium)
Increase pulmonary venous pressure and thickness of pulmonary vascular beds
pulmonary arterial hypertension (second stenosis)
right heart failure
Mitral stenosis
Symptoms
- Respiratory symptoms: SOB on exertion, paroxysmal nocturnal dyspnea
- Chronic RV failure: congestive cardiac failure
- Atrial fibrillation
- Systemic embolization caused by blood stasis in LA
Mitral stenosis
Signs
Malar flush (LA pressure increased + pulmonary hypertension) Pulse volume: small, irregular if in AF Venous: Loss of a wave in AF Increase JVP if RHF
Precordium: Parasternal heave / tapping apex Loud S1 Opening snap Mid-diastolic rumble May be enhanced with exercise, lying on the left side
Signs of complications:
Pulmonary oedema (basal crepitation in lungs)
Embolisation – peripheral vessels (reduced pulses), stroke
Mitral stenosis
Causes of acute decompensation
First-line investigations
Acute decompensation:
- Atrial fibrillation
- Chest infection
- Pregnancy (high intravascular volume)
Investigations:
CXR: Left atrial enlargement, Pulmonary edema, Kerley’s A and B lines
ECG: bifid P wave, AF, RVH
Echo: thickened and dome-like LA
Cardiac catheterization (for associated CAD)
Mitral stenosis
Medical and surgical treatment options
Medical:
- Diuretics for congestion symptoms
- Digoxin, beta-blocker, CCB if Atrial fibrillation
- Anticoagulation if high risk of stroke
- Antibiotic prophylaxis against infective endocarditis
Surgical:
- Valvuloplasty (balloon) if no calcification or MR
- Mitral valvotomy (closed or open)
- MVR (mitral valve replacement) if calcified or destroyed: Mechanical with lifelong warfarin or Bioprosthetics
Mitral stenosis
Prognosis
Major causes of mortality
Time lapse from rheumatic fever to symptoms = 16 years
Untreated, symptomatic MS: 10 years survival at 50%
Concurrent pulmonary hypertension: median survival < 3 years
Major causes of mortality: Progressive heart failure (60-70%) Systemic embolism (20-30%) Pulmonary embolism (10%) Infection (1-5%)
Mitral regurgitation
Etiologies
- Rheumatic
- Mitral valvular prolapse: a/w secundum ASD, Turner’s syndrome, PDA, Wolff- Parkinson-White syndrome
- Ruptured chordae tendinae:
Degenerative or collagen disease e.g. Marfan syndrome
Infective e.g. IE
Active rheumatic heart disease - Ischaemia/ myocardial infarction- papillary muscle dysfunction
- Left ventricular dilatation - enlarged MV ring
Mitral regurgitation
Haemodynamic changes
High LA pressure only during systole
Volume overload of LV can lead to LV enlargement and failure
- asymptomatic if cardiac hypertrophy with reduced LV function
- Functional MR with poor LV function and refractory HF
Mitral regurgitation
Symptoms and signs
Complications
Symptoms: can be asymptomatic
- Exercise limitation
- Heart failure/ acute LV failure
- Atypical chest pain and palpitations
Signs:
LV dilatation
S1 not increased, S2 obscured by murmur, S3 usual
Pansystolic murmur best heard at apex radiating to axilla
For mitral valvular prolapse: Mid systolic click(s), Late systolic murmur (accentuated by standing)
Complications:
- Progressive severe MR
- Emboli
- Atrial fibrillation
Mitral regurgitation
First line investigations
CXR:
left atrial and ventricular enlargement
Pulmonary oedema
Kerley’s A and B lines
Echocardiogram:
MVP, LV dilatation
Cardiac catheterization for asso. CAD
Mitral regurgitation
Medical and surgical management options
Medical: Anticoagulants for symptomatic heart failure, treat underlying cause
Surgical: Mitral valve replacement or mitral valve repair
Aortic stenosis
Etiologies
Etiologies by age:
Commonest = Degeneration and calcification (>75 years old)
60-75: Calcified bicuspid valve
<60: Rheumatic heart disease, Congenital valvular defect (unicuspidal/ bicuspid valve)
Aortic stenosis
Hemodynamic changes
AV cannot open properly in systole
blood accumulates in LV
compensatory LVH
Progressive LV dysfunction, reduced ejection fraction and eventual LV dilatation, HF
Aortic stenosis
S/S
Tx
Symptoms:
- Exertional dyspnoea
- Angina pectoris (e.g. during exercise)
- Congestive cardiac failure
- Syncope or sudden death
Signs:
Slow rising pulse
LVH (heaving apex)
Weak A2 (if calcified & severely stenotic)
Thrill + murmur at aortic area (ejection systolic murmur), radiating to neck
Tx:
Aortic valvular replacement
Define severe Aortic stenosis
AV area <1cm2 and/or mean pressure gradient > 50mmHg
Aortic regurgitation
Etiologies
- Degeneration
- Rheumatic heart disease
- Seronegative rheumatoid syndrome – ankylosing spondylitis, Reiter’s syndrome, psoriatic arthropathy
- Infective endocarditis
- Syphilis (syphilitic heart disease): Dilatation of aortic valvular ring and aortitis, calcification of aorta
- Congenital – Marfan syndrome, congenital bicuspid valve
- Traumatic – aortic dissection, rupture sinus of Valsalva, external trauma
Aortic regurgitation
Haemodynamics changes
Increase End-diastolic volume in LV
LV dilatation (not hypertrophy) to increase stroke volume Early mitral valve closure and heart failure if LV function worsens
More blood goes to LV instead of coronary arteries during diastolic phase
Aortic regurgitation
S/S
More blood goes to LV instead of coronary arteries during diastolic phase
Symptoms
- Exertional dyspnoea
- Angina pectoris (e.g. during exercise)
- Congestive cardiac failure
- Syncope or sudden death
Signs:
- Collapsing pulse (if pulse pressure >50mmHg)
- LV dilatation (displaced apex)
- Early blowing diastolic murmur following S2 (lower sternal border, exaggerated when lean forward in full expiration)
Eponyms/ special signs of aortic regurgitation
- Corrigan’s pulse (rapid upstroke and collapse of the carotid artery)
- De Musset’s head bobbing sign
- Austin-Flint murmur – diastolic murmur across MV
- Duroziez sign – to and fro murmur over femoral arteries
- Quincke’s pulse – capillary pulsation in finger tips or mucous membranes
- Tranle’s sign – pistol shot murmur
Tricuspid regurgitation
Etiologies
Etiologies: Right heart failure/ functional TR (90%): due to left-sided heart disease Infective endocarditis Rheumatic Infiltrative
Tricuspid regurgitation
Symptoms and signs
Tx
S/S: Right heart failure, cardiac cirrhosis Systolic S wave (giant v wave in JVP RV heave Pansystolic murmur over lower sternal border (increase with inspiration) Pulsatile liver
Tx:
Bed rest
Diuretics + spironolactone
Valvuloplasty
Tricuspid regurgitation
Symptoms and signs
Tx
S/S: Right heart failure, cardiac cirrhosis Systolic S wave (giant v wave in JVP RV heave Pansystolic murmur over lower sternal border (increase with inspiration) Pulsatile liver
Tx:
Bed rest
Diuretics + spironolactone
Valvuloplasty
