Week 5 Flashcards
Aetiology of Aortic Regurgitagtion (AR)
Results from either primary disease of the aortic valve leaflets or secondary dilation of the aortic root. The condition can present acutely or chronically
Acute AR aetiology
- Infective endocarditis (leading to leaflet destruction)
- Aortic dissection (damaging leaflet support or causing prolapse of dissection flap)
- Chest trauma (causing leaflet rupture)
- Congenital cusp rupture
- Iatrogenic injury (e.g., after surgery on aortic valve)
chronic AR aetiology
- Bicuspid aortic valve
- Chronic aortic root dilation (e.g., Marfan syndrome, syphilis)
- Degenerative or calcific disease
- Rheumatic heart disease (RHD)
- Prosthetic valve failure—either mechanical or bioprosthetic—can also result in acute or chronic AR
Aortic Stenosis AS aetiology
AS is the most common cause of LV outflow obstruction in adults.
* Degenerative calcific AS is the leading cause in older adults, due to progressive leaflet stiffening and calcification.
* Congenital bicuspid aortic valve is the most common cause in younger adults.
* Rheumatic AS
Epidemiology of AVD
Low- and middle-income countries (LMICs)
- Rheumatic Heart Disease (RHD) remains the dominant cause of aortic valve disease
- Commonly affects young people, often leading to early valve damage.
- Endemic in regions such as sub-Saharan Africa, South Asia, Oceania and among Indigenous populations in high-income countries (e.g., Australia, New Zealand)
High income countries (HICs)
- Degenerative calcific aortic stenosis (AS) is the most prevalent form.
- Affects older populations (>80yo) often alongside comorbidities.
- Driven by population ageing and atherosclerotic risk factors (e.g., hypertension, high cholesterol, smoking)
Pathogenesis of AR
- Acute AR: The non-compliant LV is unable to accommodate sudden regurgitant volume, causing elevated LV end-diastolic pressure, decreased cardiac output, and pulmonary edema. The rapid pressure rise may cause premature mitral valve closure and cardiogenic shock.
- Chronic AR: The LV adapts through eccentric hypertrophy and dilation, preserving forward flow for years. Eventually, increased wall stress and subendocardial ischemia lead to systolic dysfunction and heart failure
Pathogenesis of AS
AS imposes pressure overload on the LV due to a fixed obstruction at the valve. The LV undergoes concentric hypertrophy to maintain cardiac output despite increased afterload.
* Diastolic dysfunction develops early due to reduced compliance
* Over time, myocardial fibrosis and impaired coronary reserve may lead to angina, syncope, or heart failure
* In advanced cases, LV systolic dysfunction occurs, reducing ejection fraction
clinical manifestations of AS
Dyspnoea on exertion: due to diastolic dysfunction and inability to increase output
- Exertional syncope from fixed outflow and vasodilation
- Exertional angina due to increased demand and impaired subendocardial perfusion
- Classic triad (dyspnoea, syncope, angina) signals advanced disease
- Harsh, crescendo-decrescendo systolic murmur at aortic area, radiating to carotids
- Single or paradoxically split second heart sound
- Development of heart failure (often late)
- Atrial fibrillation, especially in elderly or those with severe hypertrophy
- Sudden cardiac death, particularly in untreated symptomatic AS
Clinical manifestations of AR
Acute AR:
Sudden onset dyspnoea, orthopnoea, and hypotension
* Signs of cardiogenic shock: cool extremities, tachycardia, and poor perfusion
* Low-pitched early diastolic murmur
* Pulmonary oedema on auscultation and chest radiograph
Chronic AR:
* Often asymptomatic for years
* When symptoms appear: exertional dyspnoea, palpitations or angina
* High-pitched diastolic murmur at left sternal border
Aetiology of Mitral valve dysfunction
MVP is a primary (organic) disease of the mitral valve, most commonly due to:
- Degenerative MV disease: Myxomatous degeneration (common in younger patients) or fibroelastic deficiency (more common in older adults)
- Genetic predisposition (autosomal dominant)
- Connective tissue disorders (e.g., Marfan, Ehlers-Danlos)
- Rheumatic heart disease
- Infective endocarditis
- Trauma
Epidemiology of MVP
- MVP is the most common structural cause of primary mitral regurgitation.
- Based on large cohort studies (e.g. Framingham in the USA), the prevalence of MVP is about 2–3% in the general population. MVP is more common in women, but men with MVP are more likely to develop complications such as severe MR, atrial fibrillation, and heart failure
Pathophysiology of MVP
- Leaflet Degeneration:
leaflets become thickened, redundant, and floppy due to accumulation of proteoglycans and disruption of the normal collagen-elastin structure.
this weakens the structural integrity of the valve.
- Elongated or Ruptured Chordae Tendineae:
the chordae tendineae (thin strings anchoring the leaflets to the papillary muscles) may stretch excessively, reducing tension needed to keep the valve shut or rupture, causing a flail leaflet.
this allows the leaflet(s) to bulge or “prolapse” ≥2 mm into the left atrium
this may be silent or lead to mitral regurgitation due to incomplete coaptation
clinical manifestations of MVP
- Asymptomatic in majority
- When symptomatic: Atypical chest pain, palpitations ± arrhythmias (e.g., PVCs, AF), fatigue, dyspnoea (with MR), autonomic symptoms (e.g., dizziness)
- Complications: MR (most common), infective endocarditis, AF, cerebrovascular embolism (stroke), sudden cardiac death (rare)
Mitral regurgitation MR, aetiology
Primary (Organic) - due to structural abnormalities of the valve
Degenerative – most common in developed countries
Rheumatic heart disease – globally significant
Infective endocarditis – leaflet perforation or chordal rupture
Trauma – e.g., blunt chest trauma, deceleration injuries
Congenital – cleft mitral leaflet
Drug-induced
Cardiac amyloidosis – valve thickening, MR
Mitral annular calcification – in elderly
Secondary functional MR aetiology
Ischaemic heart disease – post-MI, papillary muscle dysfunction
Dilated cardiomyopathy – annular dilation and leaflet tethering
Right ventricular pacing – dyssynchrony → MR
Atrial functional MR – annular dilation in atrial fibrillation or HFpEF
epidemiology of MR
Mitral Regurgitation (MR) is the most common specific type of heart valve disease in Australia.
Prevalence: 1–2% in people aged <60 years, 9–11% in people aged >70 years. Of those with MR, 30% have moderate-severe forms, many of whom will require intervention.
MR is more common in men than women and is strongly associated with cardiovascular risk factors and ageing
pathogenesis of MR
Primary MR
- Valve leaflet/chordal degeneration → incomplete closure → retrograde flow into LA
- Over time: LA and LV volume overload, compensatory dilation, eccentric hypertrophy
- Chronic overload → LV dysfunction and elevated LA pressure
Secondary MR
- Normal leaflets, but abnormal ventricular geometry causes:
- Papillary muscle displacement
- Annular dilation
- Impaired coaptation (“tenting”)
- MR severity may fluctuate with haemodynamic conditions (e.g., during exertion)
clinical manifestations of MR
Asymptomatic phase (common); mild MR remains silent for years; moderate/severe MR may be asymptomatic initially due to compensatory remodelling
Symptomatic MR:
- Exertional dyspnoea; fatigue – due to reduced effective forward stroke volume; palpitations – atrial fibrillation common
- Paroxysmal nocturnal dyspnoea, orthopnoea (in more advanced stages)
- Pulmonary oedema – particularly with acute MR or exercise-induced MR
- Right-sided HF signs – in advanced chronic cases
- Sudden worsening – with chordal rupture (flail leaflet)
Primary Tricuspid Regurgitation Aetiology
- Congenital anomalies: Ebstein anomaly (most common congenital cause; apical displacement of the septal leaflet, leading to atrialisation of RV)
- Fibrosis (e.g., from rheumatic disease, radiation, or carcinoid syndrome)
- Leaflet destruction from infective endocarditis
- Device-related: leaflet damage from pacemaker or ICD lead
- Prolapse or flail (e.g., myxomatous degeneration)
- Chordal rupture (e.g., trauma or endocarditis)
- Papillary muscle infarction or fibrosis (in ischaemic heart disease)
- Valve Perforation or Impingement: pacemaker/ICD leads may perforate or entangle leaflets or chordae
- Direct trauma (blunt chest injury or iatrogenic)
Secondary TR Aetiology
Mechanisms are either:
1. Ventricular STR due to RV dilation due to:
- Left sided heart disease
- Pulmonary hypertension
- RV infraction or cardiomyopathy
2. Atrial STR due to atrial fibrillation and right atrial enlargement
3. Cardiac implantable electronic device related STR: due to lead impingement or induced desynchrony
Primary TR Pathophysiology
- Results from direct pathology of tricuspid valve or subvalvular apparatus, such as leaflet destruction, prolapse or congenital malformation.
- Unlike secondary TR, where the valve is anatomically normal but fails due to chamber remodelling, in PTR the valve itself is diseased
Secondary TR Pathophysiology
- Annular Dilation is central to secondary TR and occurs due to RA or RV enlargement (e.g., in AF or pulmonary hypertension)
- Tricuspid annulus is non-planar and dynamic — it loses its sphincter-like contraction as it dilates
- Leaflet Tethering and Malcoaptation is more common in ventricular-type secondary TR and results from papillary muscle displacement and RV dilation causing tenting of the leaflets. Leaflets cannot coapt in systole, even if structurally normal
TR Epidemiology
TR is a common valvular abnormality, especially in the elderly
- Mild TR is seen in ~75–80% of adults on echocardiography
- Moderate to severe TR affects ~4–5% of Australians over 75 - similar to aortic stenosis and mitral regurgitation
- TR remains underdiagnosed and undertreated - often detected late, when right-sided heart failure is already established
- TR is especially common in the elderly with comorbid AF and heart failure, particularly among women
- Although TR is less common than aortic and mitral valve dysfunction in Australia, and it is usually secondary to other cardiac or valvular diseases, its significant form is associated with adverse outcomes.
- Mortality risk with moderate-severe TR is comparable to untreated aortic stenosis, with 40–79% mortality reported within 1–4 years
TR Pathogenesis
TR results in systolic backflow of blood into the right atrium, leading to:
- Right atrial pressure overload
- Chronic venous congestion
- Progressive right ventricular (RV) dilation and dysfunction
Initially, TR may be well tolerated due to the compliance of the right atrium and venous system. Over time, chronic volume overload causes:
- RV systolic dysfunction
- Decreased forward output
- Symptoms of right-sided heart failure (e.g., peripheral oedema, ascites)
Increased central venous pressure can impair renal perfusion and hepatic congestion, contributing to cardiorenal and cardiohepatic syndromes
