The cardiovascular system - Coronary artery disease 2 Flashcards
What is infective endocarditis (IE)?
Refers to any infection of the endocardial surface of the heart
Describe the epidemiology of infective endocarditis
- Men are predominately affected
- In the developed world, IE is mostly a disease seen in elderly patients and commonly occurred in patients with pre-existing valvular disease from rheumatic heart disease
Causes of endocarditis can be divided into 5. Give the 5 causes
- Native valve endocarditis
- Prosthetic valve endocarditis (PVE)
- IV drug users (IVDU)
- Culture-negative IE
- Non-infective endocarditis
a) What is native valve endocarditis (NVE) commonly due to?
b) What is the most common organisms causing NVE?
a) Rheumatic heart disease, congenital heart disease or structural disease
b) Usually due to streptococcal species and presents with a subacute course
- Streptococcal species (alpha-haemolytic, S.bovis) and enterococci: implicated in around 70% of cases
- Staphylococcal species: implicated in around 25% of cases. More aggressive disease
a) What does the prosthetic valve endocarditis (PVE) depend on?
b) What is the most common organisms causing early and late PVE?
a) Aetiology of PVE depends on it occurs early (<1 year) or late (>1 year)
b) Coagulase-negative staphylococcus (CoNS) account for 30% of PVE
- Early PVE: occurring shortly after surgery. Staphylococcal species commonly implicates. Acute course (that can cause local abscess, fistula formation, and valvular dehiscence)
- Late PVE: occurring a medium-to-long period after surgery. Streptococcal species commonly implicates. Has a more subacute course
a) What organism is most commonly implicated in IV drugs users (IVDU) associated IE?
b) Explain which valve is most commonly affected?
a) Staphylococcus aureus
b) The tricuspid valve (together with the mitral valve) is commonly affected in IVDU.
Blood from the venous circulation encounters the tricuspid valve first, so bacterial load from repeated injections with contaminated drug paraphernalia is more likely to result in right-sided endocarditis
a) What is culture-negative infective endocarditis defined as?
b) What are 4 possible causes of culture negative IE may be due to?
a) Defined as endocarditis with no definite microbiological aetiology despite adequate sampling
b)
- Typical pathogens
- Pathogens with complex growth
- Intracellular bacteria
- Non-bacterial pathogens (e.g., fungi)
What are 4 possible causes of non-infective endocardiitis
- Physical trauma caused by IV catheters or placing wires
- Systemic lupus erythematosus (SLE)
- Metastatic lung, GI, and pancreatic cancers
- Chronic infections e.g., tuberculosis, osteomyelitis
What are the 3 most common organism species causing IE?
Staphylococcal, streptococcal and enterococcal
Staphylococcal species is one of the most common cause of IE
a) What specific staphylococcal species is most common?
b) What is another common species and what is it commonly associated with?
a) Staphylococcus aureus
b) Coagulase negative staphylococcus (CoNS) and commonly associated with prosthetic devices
Streptococcal species is one of the most common cause of IE.
Give the two most common streptococcal species
Alpha-haemolytic streptococci e.g., Strep Viridans
Beta-haemolytic streptococci e.g., Strep. Bovis
Strep.bovis is a beta-haemolytic streptococci that can cause IE
a) What type of people is this organism commonly seen in?
b) What conditions is the organism associated with and what investigation is required?
a) Elderly
b) Adenomas/adenocarcinomas of the colon and IBD. Colonoscopy is indicated
Enterococcal species is one of the most common cause of IE.
a) What is the most common organism of enterococcus species causing IE?
b) What % of all enterococcus species is caused by this organism?
a) Enteroccous facecialis
b) 90%
S.epidermis is a common organism that causes IE. What type of IE does it cause?
Causes early prosthetic valve IE
Aside from staphylococcus, streptococcal and enterococcus species. What other organisms can cause IE?
- Q fever - Coxiella burnetii
- Brucella
- Pseudomonas aerugionsa
- Fungal - Candida e.g., C.albicans, C.stellatoidea
- HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella –> fastidious (hard to culture) group of gram-negative staining bacteria
When should you suspect Q fever (Coxiella burnetii) causing IE?
Suspect if contact with farm animals and cats/dogs
When should you suspect Brucella causing IE?
Suspect if recent travel or at risk occupation e.g., farmers
75% of fungal infections are caused by the Candida (e.g., C.albicans, C. stellatoidea) . These can cause IE.
What type of people are particularly affected?
IVDU and immunocompromised
Name the two main disease processes underpinning infective endocarditis
- Endocardial injury
- Baceraemia
a) Describe patient-associated risk factors of IE
b) Describe cardiac risk factors of IE
c) Aside from patient-associated and cardiac risk factors of IE. What are other risk factors of IE?
a)
- Age - occurs in patients aged > 60 years
- Male predominance - sex dominance varies from 3:2 to 9:21
- IVDU
- Dentition - poor dental hygiene, dental infections and certain procedures increase risk
b)
- Structural heart disease (75% of IE patients have underlying structural heart disease)
- Valvular heart disease
- Congenital heart disease (e.g., bicuspid aortic valve, ventricular septal defect and cyanotic heart disease)
- Prosthetic heart valves
- Previous IE
- Intravascular devices
b)
- Immunosuppression (e.g., HIV)
- Haemodialysis
a) Describe the symptoms of IE
b) Describe the signs of IE
a)
- Pyrexia
- Constitutional symptoms: malaise, fatigue, anorexia, weight loss
- Abdominal pain: splenic abscess
- Haematuria: renal embolic phenomenon
- Cardiac symptoms: Dyspnoea, chest pain, palpitations
b)
Heart
- New or worsening murmur (85%) - pansystolic murmur of mitral regurgitation or early diastolic murmur of aortic regurgitation
Eyes
- Roth spots: exudative, oedematous haemorrhage lesions of the retina with place centre due to septic emboli to the retina
- Petechiae
Hands and feet
- Clubbing
- Splinter haemorrhages: thin, reddish-brown lines of blood under the nails (micro emboli)
- Osler’s nodes: tender subcutaneous violaceous nodules mostly on the pads of finger and toes. Subacute > acute
- Janeway lesions: contender erythematous macula’s on the palms and soles (micro abscesses). Acute > subacute
Skin and mucosa
- Petechiae on extremities and buccal mucosa
Splenomegaly
The mnemonic to describe clinical features of IE is FROM JANE. What does this stand for?
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anaemia
Nail-bed haemorrhages
Emboli
Around 25% of patients with IE have evidence of embolic phenomenon at the time of diagnosis.
Describe the embolic phenomenons that can manifest
Hands and feet: Osler nodes and janeway lesions
Eyes (2%): Roth spots
Neurological (40%)l: cerebral abscess, intracerebral haemorrhage, embolic stroke, seizures
Septic emboli: splenic, renal, pulmonary abscesses, vertebral osteomyelitis, septic arthritis, psoas abscess
Immune reaction (ie., immune complex deposition): glomerulonephritis, synovitis
Describe the differential diagnosis of infective endocarditis and what is the key differential to be excluded?
May mimic rheumatological and autoimmune condition such as RhA and SLE int he subacute or chronic state
Must be differentiated from other causes of sepsis including pneumonia and abdominal sepsis in the acute setting
Describe the 1st line, 2nd lien and 3rd line investigations for IE, including the possible findings
1st line (diagnostic)
- Blood culture (microbiology)
- Echocardiography
2nd line
- blood tests: raised WCC, ESR/CRP
- urine dipstick: microscopic haematuria
- ECG: 10% develop conduction problem; heart block (prolonged PR) may be a sign of aortic root abscess
3rd line
- Thorax and abdominal imaging with CT/MRI: to look for pulmonary or splenic abscesses
- Cerebral imaging with CT/MRI: assesses for neurological complications
Describe how the blood culture must be taken for a microbial diagnosis of IE
- At least three set of blood cultures should be obtained
- Blood cultures taken at 30 mine intervals
- At last 10ml each sample from different peripheral sites using immaculate aseptic technique
a) When should an echocardiography be performed in IE?
b) Describe the different echocardiograms you worked use and the indications for their use
c) What is the hall mark finding on echocardiogram?
d) Give four other possible findings
a) Should be performed rapidly in all with moderate to high suspicion of IE
b)
- A TTE is performed in the first instance (but has lower sensitivty with a specificity of 99%)
- A TOE is performed following a positive TTE to look for local complications (e.g., valve perforations, abscess formation). Has a sensuosity of 90-100% and should e performed in most patients
c) Valvulare vegetation (oscillating irregular mass)
d)
- Abscess formation
- Pseudoaneurysms
- Valve perforations
- New dehiscence of a prosthetic valve
The modified duke criteria. It contains both major and minor criteria that are used to make a diagnosis of IE. It has an 80% sensitivity and specificity.
a) Describe the major criteria
b) Describe the minor criteria
a)
- Microbiological criteria (positive blood culture)
Two or more separate blood cultures for typical IE microorganisms:
- Streptococci viridians
- Other streptococci,
- S.auerus
OR
Persistently positive blood cultures
- Blood cultures drawn more than 12 hrs apart
- Coxiella burnetii
- Evidence of endocardial involvement
- Oscillating intracardiac mass OR abscess OR
- New parietal dehiscence of prosthetic valve
OR
New valvular regurgitation
- A change in pre-existing murmur is insufficient
b)
Predisposing factors
- predisposing heart disease
- IVDU
Symptoms
- Fever > 38
Vascular phenomenon
- Major arterial emboli
- Pulmonary emboli
- Mycotic aneurysms
- intracranial haemorrhage
- Janeway lesions
Immunological phenomenon
- Glomerulonephritis
- Osler’s nodes
- Roth spots
- Rheumatoid factor
Microbiological evidence
- Positive culture not meeting major criteria
Based on the modified duke criteria. IE can be divided into definite, possible and rejected
a) What is needed for IE to be definite?
b) What is needed for IE to be possible ?
c) What is needed for IE to be rejected?
a) 2 major criteria OR 1 major and 3 minor criteria or 5 minor criteria
b) 1 major and 1 minor criteria OR 3 minor criteria
c) Firm alternative diagnosis OR resolution of symptoms suggesting IE owning 4 days of antibiotics OR no pathological evidence of IE at surgery or autopsy within 4 days of antibiotics OR does not meet criteria for possible IE
Describe the management of IE
- Antibiotics
- Large doses of IV antibiotics recommended in all cases
- A Hickman line should be inserted to allow Lon-term administration of antibiotics
- Typical duration therapy is 4-6 weeks - Surgery
- Referral to IE team
a) Describe the regimen for methicillin-sensitive staph.A (MSSA) and methicillin-resistant staph A (MRSA) / penicillin allergy causing IE
b) What must be added in the presence of a prosthetic valve
a) MSSA - Flucloxacillin 12 g/day in 4-6 doses. Duration 4 -6 weeks
MRSA or penicillin allergy - vancomycin 30-60 mg/kg/day on 2-3 doses. Duration 4-6 weeks
b) Rifampicin and gentamicin should be added to both regimens and the duration should be ≥6 weeks.
a) Describe the standard four-week regimen for streptococcal species causing IE
a) Describe the standard two-week regimen for streptococcal species causing IE
c) a) Describe the standard regimen for streptococcal species causing IE in those who are penicillin allergic
a) penicillin G or amoxicillin or cetriaxone
b) penicillin G or amoxicillin or cetriaxone with gentamicin
d) vancomycin for four weeks
When IE is highly suspected, but the organism is not yet known, what can you do and what is the known as?
Give antibiotics following three sets of blood cultures. This known as empirical therapy.
What are in the indications for surgery in infective endocarditis?
- Heart failure
- Uncontrolled infection
- Prevention of embolization (e.g., large vegetations > 10mm)
- Difficult pathogens
- Prosthetic valve endocarditis
Who is involved in the endocarditis team?
- Cardiologist
- Cardiothoracic surgeon
- Microbiologist
- Nurse specialist
Describe the advice you should give to patients to prevent IE
Antibiotic prophylaxis
Maintain a good oral health
- high risk patients should be referred for dental assessment
Advise about risk of invasive procedures
- Such as tattooing or body piercing
IVDU-targeted health promotion
- Needle-change programme
- Education
- Addiction management
a) Prophylactic antibiotics may be given in high-risk or sub-group of high risk patients to prevent IE.
a) Give 4 examples of high risk patients
b) Give 2 examples of sub-groups of high risk patients
c) Give 3 instances when prophylactic antibiotics should not be given
a)
- Cardiac procedures
- Respiratory tract procedures
- Urological procedure
- Obstetric procesdures
b)
- Prosthetic heart valves or material used for cardiac valve repair
- Previous IE
- Congenital heart disease
c)
- Routine dental procedures
- Routine prophylaxis for non-dental procedures
- To cover IE if antimicrobial therapy has been instigated for a GI/GU procedure at a site where there is suspected infection
Describe the complications of IE
Cardiac (50%) - heart failure, preivalvular abscess, pericarditis, cardiac tamponade
Neurological (80% - may be silent) - stroke, abscess, meningitis, encephalitis, haemorrhage, seizures
Metastatic infection - mystic aneurysm, embolization, abscess formation
Embolization sequelae - stroke, blindness, ischaemic limb, splenic/renal infarct, PE, MI
Describe the prognosis of IE
Higher morbidity and mortality in the elderly and in S.auerus, gram-negative and fungal infections
- morbidity usually results from neurological complications (e.g., stroke)
Lower mortality in strep. viridan’s and enterococci
What is the key pathological process in IE
Formation of infected vegetation
Describe how endocardial injury can lead to IE
Endocardial injury leads to thrombus formation
Thrombus is initially sterile and known a s a non-bacterial vegetation
Bacterial invasion of the vegetation (collection of organisms and thrombus) occurs because of microbial component recognised adhesive molecules (MSCRAM)
The infected vegetative thrombus further enlarges secondary to aggregation of platelets and fibrin and is relatively immune fro, host defences
Once deposited on the endocardial surface, the organisms adhere and eventually lead to invasion and destruction of the valve leaflets
What is rheumatic fever?
It is a multi-system disorder that occurs because of an autoimmune reaction to group A streptococcal (GAS) infection
Describe the epidemiology of rheumatic fever
- Common in children aged 5-14 years, rare in those over age 30
- High incidence in developing countries, especially where there is overcrowding and poor access to health care
- Low incidence in developed countries. This is due to the use of antibiotics for bacterial pharyngitis, better hygiene and a declining rheuamtogenic strains of streptococcus
Describe the aetiology of rheumatic fever
- Rheumatogenic strains
- Genetic susceptibility]
- Associated factors e.g. poverty and overcrowded living
Describe the pathophysiology of rheumatic fever
Not completely understood
Describe the clinical features of rheumatic fever
- Typically presents 2-3 weeks after a sore throat from group A strep
- 50% have cardiac involvement
- Developmental heart disease is usually due to recurrent episodes
The diagnosis for acute rheumatic fever is aided using the revised Jones Criteria. It is composed of the major criteria and minor criteria
a) Describe the components of the major criteria
b) Describe the components of the minor criteria
a) CASES
Carditis (40% of patients)
- Breathlessness, palpitation, chest pain, syncope
- Murmurs - mitral regurgitation (most common), aortic regurgitation
- Carey Coombs murmur
- Pericardial rub
Arthritis (75% of patients)
- Acute, migratory polyarthritis
- Joints are red, swollen and tender
- Lasts between one day and four weeks
- Typically affects large joints (knees, ankles, elbows, wrists)
Subcutaneous nodules (10% of patients)
- Small, firm, painless nodules on extensor surface of bones and tendons
- Usually appear more Etna three weeks after onset of manifestations
Erythema marginatum
- Rash with red, raised edges and a clear centre
- Mainly on trunk and proximal extremities (thighs and arms)
Sydenham’s chorea (at least 3 months after acute episode)
- Late manifestation
- Emotional liability followed by involuntary, semi-purposeful movements of hands, feet, or face
- Explosive or halting speech
b) FRAPP
First degree AV block - prolonged PR interval (not if carditis is one of the major criteria)
Raised acute phase reactants - ESR/CRP/leucocytosis
Arthralgia (not if arthritis is one of the major criteria)
Previous rheumatic fever
Prolonged PR interval
How is a diagnosis of rheumatic fever made using the revised Jones Criteria?
- Two major criteria or one major and two minor
PLUS
- Evidence of preceding streptococcal infection
Give 4 differential diagnosis of rheumatic fever
- Infective endocarditis
- Septic arthritis
- Transient synovitis
- Juvenile idiopathic arthritis
- Chorea
Describe the first-lien and second-line investigations for rheumatic fever, including the findings
First line
- Throat swab culture: often negative
- Anti-streptococcal serology
- ECG: AV block, features of pericarditis
- Blood cultures: to exclude infective endocarditis
- Echocardiography: may reveal valvular involvement
Second line
- Systemic autoantibodies in SLE
- Copper and caeruloplasmin for Wilson’s disease
Describe the management of rheumatic fever
General measures
- Bed-chair rest reduces pain and cardiac workload
- Continue until temperature, CRP/ESR and leucocyte counts normalises
Eradication of group-A beta-haemolytic streptococcal infection (antimicrobial therapy)
- Single dose STAT IV benzylpenicillin or oral penicillin IV for 10 days
Suppression of inflammatory response (arthritis symptoms)
- Mostly for symptomatic relief of arthropathy
- Aspirin is firsline/NSAIDs
- Corticosteroids if response to salicylates, pericarditis, or heart failure
Management of heart failure in carditis
- Mainstay is bed rest and corticosteroids e.g., prednisolone
- In severe may require ACEi, digoxin and diuretics
Management of chorea
- Usually, self-limiting
- First-line is benzodiazepine (e.g., diazepam)
What is rheumatic heard disease?
A long-term consequence of rheumatic fever - an inflammatory condition involving heart, skin, and connective tissue usually in children and young adults
Rheumatic heart disease
a) Primordial prevention
b) Primary prevention
c) Secondary prevention
a) Improved living conditions (prevent spread of group A strep via droplets) and access to medical care
b) Penicillin for confirmed strep pharyngitis (to prevent chronic cardiac inflammation)
c) Extended antibiotics (years-lifelong)
What is mitral stenosis?
Narrowing of the mitral valve orifice that occurs a s a result of fusion of the leaflet commissures
What is the normal area of a valve compared to the are in mitral stenosis?
Normal MV is 4-6 cm2
MS valve area < 2cm2
a) What is the most common cause of mitral stenosis
b) What are other causes?
a) Rheumatic heart disease ( up to 95%)
b)
- Ageing: degenerative calcification of the leaflets
- congenital valve deformity
- Carcinoid syndrome
- Rheumatological disorders: rheumatoid arthritits, SLE
- Mitral annular calcification
- Radiation associated MS
- Fabry’s disease
Describe the pathophysiology of mitral stenosis
Recurrent inflammation causes valve damage over time
As the valve narrows, blood flow across the left atrium to the left ventricle is reduce
This increases pressure in the left atrium which causes left atrial dilatation (compensatory mechanism for chronically elevated atrial pressure)
This predisposes patient to AF and arterial thrombosis
Raised atrial pressure translates to raised pumonlary venous pressure and pulmonary hypertension which can eventually lead to right sided heart failure
a) Describe the symptoms of mitral stenosis
b) Signs of mitral stenos
a) (mimic those of heart failure)
- Exertional dyspnoea: most common
- Haemoptysis
- Chest pain
- Thromboembolism - may present with stroke
- Peripheral oedema/abdominal discomfort (hepatomegaly) - Palpitations due to AF
b)
- On auscultation: opening snap, rumbling mid-diastolic murmur. Loudest in expiration and heard best with patient lying on left and bell at apex in the left lateral position. It can radiate to axilla. Loud S1
- Low volume/pitch pulse
- AF
- Mitral facies (malar flush)
Pulmonary hypertension -> right ventricular heave, prominent a-wave
- Right heart failure -> raised JVP, peripheral oedema, hepatomegaly
Describe the 1st line and 2nd line investigation for mitral stenosis
1st line
- Echocardiography (TTE)
- ECG
- CXR
2nd line
- Echocardiography (TOE)
- Stress testing (Sometimes use in those who are asymptomatic or have minor symptoms as well as those whose symptoms are discordant with echo findings)
a) Describe the findings on ECG in mitral stenosis
b) Describe the findings on CXR in mitral stenosis
a)
- AF
- P-mitrale (bifid P waves) due to left atrial enlargement
- May present with right axis deviation if chronic disease
b)
- Left atrial enlargement: double right heart border, splayed trachea, prominence of the atrial appendage
- Pulmonary oedema
Severity of mitral stenosis based on echocardiogram findings with valve area (cm2) mean gradient (mmHg) and PA pressure (mmHg)
a) Mild
b) Moderate
c) Severe
a)
Valve area: >1.5
Mean gradient: <5
PA pressure: < 30
b)
Valve area: 1.0-1.5
Mean gradient: 5-10
PA pressure: 30-50
c)
Mild: <30
Moderate: 30-50
Severe: >50
Describe the management of mitral stenosis
Anticoagulation
- Warfarin should be given if in AF or previous embolic events
- AF treated
Symptomatic/treatment relief for right heart failure
- Beta-blockers, diuretics
Valve intervention
- Percutaneous mitral comissurotomoy (PMC) / percutaneous mitral valvotomy (PMV) / percutaneous mitral balloon valvuloplasty (PMBV) is 1st line
- Surgical repair, commissutrotomy or valve replacement if PMC fails or is unsuitable
What are 4 indications for valve intervention in mitral stenosis
- Symptomatic severe mitral stenosis (<1.5 cm2)
- Asymptomatic very severe mitral stenosis
- Pulmonary hypertension
- High risk of embolism or haemodynamic decompensation
a) Describe percutaneous mitral commissurotomy (PMC)
b) Give 6 contra-indications of PMC
a)
- Minimally invasive approach that uses a balloon delivered by a catheter which enters the right femoral vein
- This balloon is then inflated in various stages to help alleviate the stenosis
b)
- Valve area >1.5cm2
- Left atrial thrombus
- Absence of commissural fusion
- Severe or bi-commissural calcification
- More than mild mitral regurgitation
- Severe concomitant aortic stenosis requiring surgery
- Severe combine tricuspid regurgitation/stenosis requiring surgery
- Concomitant coronary artery disease requiring surgery
What is mitral regurgitation?
Refers to back-flow of blood from left ventricle into the left atrium due to the incompetence of the mitral valve
Aetiology of mitral regurgitation can be divide into acute and chronic causes
a) Give 4 acute causes of mitral regurgitation
b) Give primary and secondary causes of chronic mitral regurgitation
a)
- Papillary muscle infarction
- Ruptured chord tendineae
- Acute rheumatic fever
- Infective endocarditis
- Trauma
b)
Primary
- Degenerative valve disease (most common in developed countries)
Mitral valve prolapse
- Rheumatic heart disease (developing countries)
- Congenital anomalies
- Connective tissue disease (e.g., Ehlers-Danlos syndrome, Marfan’s syndrome)
- Infective endocarditis
- Medications (e.g., ergotamine, bromocriptine, pergolide)
Secondary (where left ventricular remodelling or dilatation distorts the valvular apparatus)
- Left ventricular remodelling -> coronary heart disease: ischaemic mitral regurgitation
- Left ventricular dilatation -> cardiomyopathy
Describe the pathophysiology of acute and chronic mitral regurgitation
Back flow into the left atrium causes a decrease in cardiac output. This results in an increase in left atrial pressure and left atrial dilatation over time, as wells volume loading of the left ventricle. Ventricular filling increases in the subsequent systole as regurgitant blood flows back to the left ventricle
Acute MR - a lack of physiological compensation (dilatation) means that increased left atrial pressure results in significant haemodynamic instability and pulmonary hypertension, which may lead to pulmonary oedema
Chronic MR - In chronic MR there is gradual worsening which allows for compensatory mechanisms to occur. The compensatory mechanisms are atrial dilatation (maintain atrial pressure) and ventricular hypertrophy (to maintain larger stroke volume). Eventually such changes cannot maintain normal cardiac function and leads to a decompensated state. The heart fails, ejection fraction falls and pulmonary pressure rises
Mitral regurgitation
a) Signs
b) Symptoms
a)
Acute
- Presents as an emergency
- Sudden onset severe dysponea
- Rapidly progressive pulmonary oedema
- Hypotension and cariogenic shock
Chronic
- Asymptomatic if mild or moderate
- Symptoms occur when left heart failure develops n severe mitral regurgitation -> dyspnoea on exertion, fatigue
- AF
- Risk of developing infective endocarditis
b)
- On auscultation: pan systolic murmur that may radiate to the axilla, S1 may be soft due to incomplete closure. Additional heart sound, S3, may be heard caused by rapid filling of a dilated ventricle
On palpitation: apex beat may be displaced laterally. A systolic thrill may be felt in severe disease
Signs of heart failure: peripheral oedema, auscultation may note bi-basal cracks, raised JVP
Give the first line and second line investigations of mitral stenosis
First-line
-TTE and doppler
- ECG
- CXR
second-line
- Cardiac catheterisation (- to check for coronary artery disease if severe chronic secondary mitral regurgitation, used for evaluation of the coronary vessels prior to valvular surgery, if echocardiogram is inconclusive)
- Cardiac MRI (if echocardiogram is inconclusive)
- Exercise testing
a) What is diagnostic of mitral regurgitation on a TOE?
b) What ECG changes will see in acute and chronic mitral regurgitation?
c) What Car changes will you see in acute and chronic mitral regurgitation?
a) Regirgitant blood flow
b)
Acute mr - may be entirely normal or reflect recent MI
Chronic MR - AF, P-mitrale (bifid P waves) due to atrial enlargement
c)
Acute MR - hear size is usually normal but shows pulmonary oedema
Chronic MR - cardiomegaly (enlarged left atrium)
Signs of congestive heart failure
a) Describe the management of acute mitral regurgitation
b) Describe the management of chronic mitral regurgitation
a)
1. Priority is medical stabilisation
- Inotropes and intra-aortic ballon pumps if life-threatening (hypotension)
- Sodium nitroprusside to reduce mitral regurgitation
- Surgery
- Mitral valve repair
b)
- Medical therapy
- Anticoagulant with warfarin if patient has AF or a previous embolic event. Target INR is 2.5
- In patients with HF - beta-blockers, ACEi and Mineralocorticoid receptor antagonists e.g., spironolactone may be considered
- Cardiac resynchronisation therapy (CRT) is used when appropriate - Surgical therapy
- Mitral valve repair ore replacement
Give 2 indications for mitral valve surgery in mitral regurgitation?
- Symptomatic mitral regurgitation and left ventricular ejection fraction > 30%
- Asymptomatic severe mitral regurgitation with pulmonary hypertension or new onset AF or left ventricular dysfunction
What is mitral valve prolapse?
Mitral valve prolapse refers to one or both mitral valve leaflets proposing and projecting into the left atrium
a) What is the most common cause of mitral valve prolapse?
b) Give 3 rarer causes
a) Myxomatous degeneration (accumulation of proteoglycans by an Unkown mechanism)
b)
- Connective tissues disease (e.g., Marfan’s syndrome, Ehlers-Danlos syndrome)
- Myocardial ischaemia
- Associated with cardiomyopathies and Turner’s syndrome
a) Describe the symptoms of mitral valve prolapse
b) Describe the signs of mitral valve prolapse
a)
- Asymptomatic (most people)
- Atypical chest pain
- Palpitations
- Rarely autonomic symptoms
b)
- Mid-systolic ‘click’ -> due to sudden tensing of the cord tendineae
- and/or systolic murmur may be heard if there is mitral regurgitation
What investigations for mitral valve prolapse?
Echocardiography is diagnostic
ECG and CXR is usually normal
Describe the management of mitral valve prolapse
- Reassurance for asymptomatic patient
- Lifestyle advice (reduce caffeine intake) for patients with palpitations
- Beta-blockers for patients with palpitation or chest pain
- If severe, treat mitral regurgitation
- Consider anticoagulation if there is a risk of cerebrovascular disease
Explain how t left ventricular volume is associated with the timing of the prolapse
A low left ventricular volume leads to an early click and murmur. A low LV volume can occur from reduced preload (e.g., standing, valsalva manoeuvre), increased contractility or reduced BP
A high left ventricular volume leads to a later click and murmur. A high LV volume can occur from increased preload (e.g., squatting), reduced contractility (e.g., beta blockers) and increased blood pressure
What is aortic stenosis?
Aortic stenosis refers to narrowing of the valve orifice leading to an obstruction of blood flow across the aortic valve
Give the 3 main causes of aortic stenosis
- Calcification (most common cause)
- Congenital bicuspid aortic valve
- Rheumatic heart disease
Calcification is the most common cause of aortic stenosis.
Give 4 risk factors of calcification
- Hypercholesterolaemia
- Hypertension
- Smoking
- Diabetes
(Similar risk factors to atherosclerosis as similar process)
Calcification is the most common cause of aortic stenosis.
Give 4 risk factors of calcification
- Hypercholesterolaemia
- Hypertension
- Smoking
- Diabetes
(Similar risk factors to atherosclerosis as similar process)
a) Congenital bicuspid aortic valves is a common cause of aortic stenosis. Explain why this is the case?
b) When does the stenosis appear?
a) Congenital bicuspid aortic valves are predisposed to becoming stenotic as they are unable to withstand the haemodynamic stresses as the normal 3 leaflet aortic valve. This leads to turbulent flow with subsequent fibrosis and calcification.
b) Stenosis tends to appear at a younger age (<65)
Describe the pathophysiology of aortic stenosis
Thickening of the aortic valve leads to narrowing of the valve orifice.
This leads to increased after load.
This causes left ventricular hypertrophy, which is initially adaptive, maintaining wall stress and allowing the heart to pump effectively
With time, this hypertrophic response decompensated, and patients transition to heart failure and the development of symptoms.
a) Describe the symptoms of aortic stenosis
b) Describe the signs of aortic stenosis
a) Triad of ‘SAD’ on exertion
Syncope
Angina
Dyspnoea
+ easy brushing and epistaxis
b)
- On auscultation: crescendo-descrescendo ejection systolic murmur, radiating to both carotids and loudest on expiration at right second intercostal space
- Soft S2 (a marker of severity, the aortic component of the second heart sound may become quieter in more severe disease as the valve leaflets fail to oppose each other forcefully, S4 (caused by the atria contracting against stiff, hypertrophied ventricles) and reversed splitting
- On palpitation: Heaving and sustained (non-displaced) apex beat
- Slow rising and delayed carotid pulse (as reduced rate of blood ejected into the aorta)
- Narrow pulse pressure (small difference between systolic and diastolic pressures)
Why does syncope occur in aortic stenosis?
Less blood flow to carotid arteries where baroreceptors are. Baroreceptors maintain blood pressure.
a) Why is there reduce myocardial O2 supply in aortic stenosis?
b) What symptom does this cause?
a)
- Coronary perfusion pressure (CPP) is the driving force pushing blood into the coronary arteries
- Coronary blood flow happens in diastole
- CPP = Aortic diastolic pressure - Left ventricular end diastolic pressure (LVEDP)
- In severe AS the stiff hypertrophies LV has a high LVEDP which leads to reduced CPP
What are the first-line and second-line investigations for aortic stenosis
First-line
1. Echocardiogram and doppler
2. ECG
3. CXR
Second-line
1. Cardiac MRI
2. Cardiac catheterisation (if echocardiography is inconclusive)
3. ECG exercise stress testing (may be used in asymptomatic patients)
a) What findings on an echocardiogram and doppler is diagnostic of aortic stenosis
b) What are the findings on ECG of aortic stenosis
c) What are the findings on CXR for aortic stenosis
a) A narrow aortic valve area is diagnostic
b)
- Left ventricular hypertrophy (deep S-waves in V1 and V2, tall r-waves in V5 and V6) with strain pattern (in severe disease), may show left axis deviation
- P-mitrale
- Left bundle branch block/complete AV block
c)
Typically demonstrates a small heart; cardiomegaly occurs if heart failure develops
Dilated ascending aorta
Aortic stenosis is classified by severity on echocardiogram according to its transaortic mean pressure gradient and valve area.
What is the transaortic mean pressure gradient and valve area in severe aortic stenosis.
Mean gradient: > 40mmHg
Aortic valve area: <1cm2
Describe the management of aortic stenosis
Medical therapy
- No medical therapy for AS has been shown to improve outcome
- CAD is common in AS patients, and atherosclerotic risk factor modification is recommended
- Onset of symptoms requires early valvular intervention. Medical therapy for symptoms is only a bridge for intervention or those unfit for surgery. ACE inhibitors, diuretics and digoxin may be considered
Surgical therapy
1. Valvotomy - percutanées ballon valotomy/open valvotomy
2. Valve replacement - mechanical/prosthetic valves
3. Transcatheter aortic valve replacement (TAVI) - for patients 75+ as no open heart surgery but does not last as long
What is aortic regurgitation?
Aortic regurgitation refers to the back flow of blood through the aortic valve during diastole from an incompetent aortic valve
Describe the epidemiology of aortic regurgitation
- The prevalence of aortic regurgitation increases with advancing age
- Not as common as aortic stenosis or mitral regurgitation
Causes of aortic regurgitation can be split into either primary disease of the aortic valve leaflets, or dilation of the aortic root.
Give 3 causes for valve leaflets and 3 for aortic root
Valve leaflets
- rheumatic heart disease
- Infective endocarditis
- Congenital and degenerative disease
Aortic root
- Aortic dissection
- Connective tissue disease
- Aortitis
Give 3 causes each for acute and chronic aortic regurgitation
Acute
- Infective endocarditis
- Rheumatic fever
- Aortic dissection
Chronic
- Rheumatic heart disease
- Arthritides
- Bicuspid valve
- Connective tissue disorders
Describe the pathophysiology of acute and chronic aortic regurgitation
Acute AR
- Medical emergency
- Valvular incompetence occurs so no time for compensatory mechanisms to occur
- This leads to an acute rise in atrial pressure which results in pulmonary oedema and cariogenic shock
- Regurgitation of blood during diastole causes and increase in the left ventricular end-diastolic volume (pre-load) and pressure. The effects are two-fold:
1. Reduced coronary flow - results in angina
2. Increased end-diastolic pressure - causes increased pulmonary pressures with resulting pulmonary oedema and dyspnoea. In severe cases, cardiogenic shock may occur
Chronic MR
- Valvular incompetence develops slowly, so patients may remain asymptomatic for may decades
- Regurgitation of blood during diastole causes an increase in the left ventricular end-diastolic volume (preload).
- This leads to systolic and diastolic dysfunction, left ventricular dilatation develops with eccentric hypertrophy
- The dilatation allows for an increased stroke volume compensating for regurgitant flow supported by ventricular hypertrophy. - These changes maintain ejection fraction, with a greater preload leading to greater contractility
- Eventually compensatory mechanisms fail and heart failure develops
why is there’d reduced myocardial oxygen in aortic regurgitation?
- Coronary perfusion pressure (CPP) is the driving force pushing blood into the coronary arteries
- Coronary blood flow happens in diastole
- CPP = Aortic diastolic pressure - Left ventricular end diastolic pressure (LVEDP)
- In severe AR the aortic diastolic pressure is low which leads to reduced CPP
a) What are the symptoms of aortic regurgitation?
b) What are the signs of aortic regurgitation?
a)
- Sudden dysponea
- Chest pain
- Bi-basa crackles
- Raised JVP
b)
- On auscultation: high pitched early diastolic murmur best heard with patient sitting forward over sternal border, laterally displaced apex, soft S1 and S2
- Palpitations
- Angina
- Dyspnoea
- Water hammer (collapsing) pulse
- Wide pulse pressure
Eponymous signs (medical signs that are named after a person or persons) are associated with aortic regurgitation (often asked about in examinations, the relevance of these signs in clinical practise today is questionable).
Give 4 eponymous signs of AR
De mussels sign
- Head nodding with heartbeat
Quincke’s sign
- Pulsation of nail beds
Traube’s sign
- ‘pistol shot’ femoral pulses
Duroziez’s sign
- to and fro murmur heard when stethoscope compresses femoral vessels
Müller’s sign
- Pulsation of uvula
What is the 1st line and 2nd line management of aortic regurgitation
First-line
1. Echocardiogram and doppler
2. ECG
3. CXR
Second-line
1. Cardiac catheterisation
2. Angiography - In patients with chronic AR undergoing surgery, pre-operative angiography is indicated. Typically, this is in the form of coronary angiography to assess for concomitant coronary artery disease that require bypass
a) What is diagnostic of aortic regurgitation on echocardiogram and doppler?
b) What ECG changes are seen in AR?
c) What CXR changes are seen in AR?
a) A regurgitant jet is diagnostic
b) Left ventricular hypertrophy
c)
- Cardiomegaly characteristic of chronic AR
- Signs of heart failure in acute AR
- Dilated ascending aorta
- Pulmonary oedema
a) Describe the management of acute AR
b) Describe the management of chronic AR
a)
- Immediate aortic valve replacement or repair should be performed ASAP
- Haemodynamic support may be necessary (inotropes and nitrates) before surgery
b)
Medical therapy
- Treatment of hypertension is recommended in all
- Symptomatic patients require surgery, ad medical therapy is not a substitute. Therapy with ACEi and beta-blockers may be considered in severe AR when surgery is contraindicated
Surgical intervention
- Definitive treatment of chronic AR is with aortic valve replacement
- Mechanical valve
- Biprosthetic valve
- Tavi for > 75 years old
What are the indications for aortic valve replacement in an aortic regurgitation
- Symptomatic severe AR
- Asymptomatic AR and LVEF < 50%
- Patients with advanced left ventricular dilatation
- Patients with severe AR undergoing cardiac surgery for other indication
Describe the management, lifespan and suitability of mechanical valve replacement compared to biprosthetic valve replacement
Mechanical valve
- Requires long-term anticoagulation with vitamin K antagonist (warfarin), long lifespan reducing the need for a second operation. Suited to younger patients
Biprosthetic valve
- No need for long-term anticoagulation, limited life span (around 10 years) and a repeat operation is more likely. Suited to older patients
At what age is a TAVI for aortic stenosisi/regurgitation recommended in?
> 75 years
Tricuspid stenosis
a) Aetiology
b) Symptoms
c) Signs
d) Investigation
e) Management
a) Rheumatic fever is most common cause. Other causes include infective endocarditis and congenital anomalies
b)
- Fatigue
- Ascites (the build-up of fluid in the space between the lining of the abdomen and abdominal organs)
- Peripheral oedema
c) Opening snap and early diastolic murmur
d) Echocardiogram
e) Diuretics and surgical repair
Tricuspid regurgitation
a) Aetiology
b) Symptoms
c) Signs
d) Investigations
e) Management
a)
- Right ventricular dilatation
- Rheumatic fever
- Infective endocarditis
- Carcinoid syndrome
- Congenital anomalies
- Certain drugs (e.g., fenfluramine, peroglide)
b)
- Fatigue
- Right upper quadrant pain on exertion
- Oedema
- Dyspnoea
- Orthopnoea
c)
- Giant V waves in JVP
- Right ventricular heave
- Pulsatile liver
- Pansystolic murmur
d) Echocardiogram
e)
- Treat heart failure with diuretics, digoxin, and ACE inhibitors
- Surgical valve replacement is indicated in severe cases
Pulmonary stenosis
a) Aetiology
b) Symptoms
c) Signs
d) Investigation
e) Management
a)
- Most commonly occurs as a congenital defect
- May be acquired after rheumatic fever or in carcinoid syndrome
b)
- Dyspnoea
- Fatigue
- Oedema
- Ascites
c)
- Ejection systolic murmur that radiates to the eft shoulder
- Widely split second heart sound
- Right ventricle heave may be elicited
d) Echocardiogram
e) Surgical repair is indicated
Pulmonary regurgitation
a) Aetiology
b) Signs
c) Investigation
d) Management
a) General caused by pulmonary hypertension
b) Decrescendo murmur in early diastolic. This is called graham Steell murmur if associated with mitral stenosis and pulmonary hypertension.
c) Echocardiogram
d) Surgical valve replacement
Modifiable biomedical and lifestyle/behavioural risk factors of coronary artery disease?
Biomedical
- Diabetes
- High blood cholesterol
- Hypertension
Lifestyle/behavioural
- Smoking
- Sedentary lifestyke
- Obesity
- Diet
- Alcohol
- Stress
Non-modifiable risk factors of coronary artery disease
- Family history
- Gender
- Ethnicity
- Age
Describe how ethnicity and geography relates to coronary artery disease
- High incidence in Southeast Asia
- Low in Japan
- High in USA and UK
Name 3 risk calculators for primary prevention of coronary artery disease
Framingham risk score
QRISK3 CVD
HeartScore
Describe secondary prevention of coronary artery disease including lifestyle and pharmocological
Lifestyle
- Smoking cessation
- Reduce alcohol consumption to recommended amount for men and women ( no more than 14 units a week) physical activity
- Physical activity/weight loss
Psychological factors
Cardiac rehabilitation
Pharmacological
- Anti-platelets
- Beta-blockers/Ivabradine
- Statin
- ACEi
Describe lifestyle modifications to treat hypertension
- Weight loss
- Mediterranean diet
- Reduced salt intake
- Physical activity
- Moderate alcohol
What is the first line therapy for all patients with CVD and type II diabetes?
High dose of simvastatin or atorvastatin (80mg)
What is the recommended amount of physical activity for adults
150-300 min a week of moderate-intensity or 75-150 min a week of vigorous-intensity aerobic vigorous activity
What is recommended for adults who cannot perform 150 min of moderate intensity a week?
Recommended that they should stay as active as their abilities and health condition allows
What is obesity associated with?
- Raised BP
- Raised LDL and triglycerides
- Low HDL
- Impaired glucose tolerance
- Increased insulin resistance
- Endothelial dysfunction
- Prothrombosis
- Proinflammatory
- Dyslipidaemia and in particular an atherogenic lipoprotein phenotype
a) What is cardiac rehabilitation?
b) What is their role?
c) What are the benefits
a) Long-term programs involving medical evaluation, prescribed exercise, cardiac risk factor modification, education, and counselling
b)
- To limit the physiologic and psychological effects of cardiac illness
- Reduce the risk for sudden death or re-infarction
- Control cardiac symptoms
- Stabilise or reverse atherosclerotic process
- Enhance the psychosis and vocational status of selected patients
c)
- Reduces all cause mortality, cardiac mortality, morbidity and unplanned admissions
- Improves QoL, functional capacity
- Supports early return to work and the development of self-management skills
Modern cardiac rehabilitation is menu-based, and patient centred, and provides pathway across the 7 stages from diagnosis to long term management.
What are the 7 stages
Stage 0 - Identify and refer patient
Stage 1 - Manage referral and recruit patient
Stage 2 - Assess patient
Stage 3 - Develop patient care plan
Stage 4 - Deliver comprehensive CR programme
Stage 5 - Conduct final CR assessment
Stage 6 - Discharge and transition to long term management
What are the recommendations when it comes to fat intake
- Fat should be MUFA/PUFA in nature
- Fat should not be replaced with simple sugars and refine carbohydrate (white starches) as they are likely to increase risk of CVD, diabetes etc
What is the recommended amount of free sugars (i.e., simple sugars from lactose)?
5% or less
a) What is the Mediterranean diet?
b) What are the benefits
a) A diet that involves more bread, fruit, vegetable, and fish; less meat’ and replace butter and cheese with products based on plant oils
b) Reduces risk of CHD
a) What does the ‘Diet approaches to stop hypertension (DASH)’ diet emphasis?
b) What are the benefits?
a)
- Reduced sodium intake (up to 2.3g in standard DASH)
- Fruits and vegetables,
- Fat-free/low-fat dairy,
- Whole grains, nuts, and legumes,
- Limits saturated fat, cholesterol, red and processed meats, sweets, added sugars, salt and sugar-sweetened beverages
b) Associated with decreased incidence of CVD, CHD, stroke and diabetes
What are the advantages of taking omega-3 fatty acids (EPA + DHA) ?
Reduce CVD risk
