Aortic Valve
Stenosis Insufficiency / Regurgitation Stenosis
Definition Aortic valve occlusion/narrowing Incomplete closure of aortic valve → reflux of blood Mitral valve occlusion/nar
Etiology - Senile Calficic / Degenerative (60-80 y.o.) - most common in 1st world Primary valvular causes ● Rheumatic - Most common
countries - Bicuspid aortic valve ○ Recurrent rheumatic fever attacks
- Bicuspid valve → presents before (50-70 y.o.) - Infective endocarditis → valve perforation ● Congenital - rare
- 1-2% of people, M > W - Rheumatic heart disease ● Acquired - Very rare
- Rheumatic disease - most common cause worldwide Aortic root disease → age-related degenerative aortic dilation, ○ SLE, rheumatoid arthritis, malignant carc
- Associated with MS & AR aortic aneurysms, aortic dissection. Whipple disease, drugs, calcification (old
Epidemiology - Risk factors for senile AS → aterogenic risk factors Acute AR → infective endocarditis, trauma, aortic dissection ● Higher incidence in developing countries
- Bicuspid valve associated w/ aortic pathology Chronic AR → bicuspid valve, rheumatic heart disease, ● ⅔ of pxs → females
- Prevalence ↑ with age connective tissue disorders → aortic root dilation ● Onset 10 years after disease
Pathophysiology Preload ↑ ↑↑↑ Normal or ↓
Afterload ↑↑↑ Normal RV (↑), otherwise NOR
Contractility ↑ Normal Normal
Pressure-
volume loop
↑Afterload → LV concentric hypertrophy →↓wall stress but ↓ ventricular Regurgitant volume → ↑↑↑ preload - Normal valve area → 4-6 cm2
compliance → ↑LVEDP & LHF → ↑↑↑ wall stress & work → Acute AR → sudden ↑↑↑ in EDV → LVEDP → ↑LAP → ↑wedge - ↓Valve area → ↑Resistance to blood flow →
- ↑O2 demand → ↑ risk of ischemia → myocardial fibrosis pressure → pulmonary edema & congestion. between left atrium & ventricle → ↑LAP
- Eventually leads to ventricular dilation → contractile dysfunction → ↓↓↓ SV → cardiogenic shock & MI → MEDICAL EMERGENCY → left atrial enlargement & remodeling →
→ ↑ velocity of blood ejection → aortic root dilation Chronic AR → ↑SV due to Frank-Starling mechanism → LV thrombosis
Late in disease → ↑ LA pressure → ↑ wedge pressure → pulmonary HTN & eccentric hypertrophy (dilation) → preserved LAP → ↑pulmonary vascular tone → pulmonary
congestion → RHF & symptoms Later on → Physiologic limit of FSM → systolic failure → ↓CO → → ↑ RVP & hypertrophy → right sided failur
*Left atrial contraction significantly contributes to ventricular filling in these decompensation → ↑LVEDP & LAP → pulmonary congestion
pxs → Afib → significant worsening of symptoms - ↓ aortic DP + ↑ demand → ↑risk of ischemia ***Normal left ventricular function - !!!
Clinical Features Murmurs & 1. Early systolic ejection click (valve stops opening abruptly) - Decrescendo early diastolic murmur 1. Loud S1 (normalizes in late stages)
sounds 2. Late systolic crescendo-descendo systolic murmur - ↓S1 due
to ↑LV volume → premature mitral closure 2. Opening snap after S2 (the earlier, the more
3. Soft S2 (due to ↓aortic valve mobility) - Austin Flint murmur: m id-diastolic murmur ← regurgitant jet 3. Mid-diastolic decrescendo murmur - starts a
4. S4 (non-compliant ventricle) displaces mitral valve leaflet → Presystolic accentuation (atrial contraction
Signs & Asymptomatic if valve area >1 cm2 (normal aortic valve area → 3-4 cm2) - Dyspnea on exertion & ↓ exercise tolerance Symptoms begin when valve area 2-2.5 cm2 (no
Symptoms Triad: Angina, syncope, & left heart failure - Fatigue - Only w/ exertion → ↑LA pressure & heart rate
- Palpitations - Sensation of forceful heartbeat Valve area <1.5 cm2 → symptoms even at rest
- Fatigue - Angina - Dyspnea & pulmonary congestion
- Exertional dyspnea - ↑LV volume + ↓ aortic DP → Widened pulse pressure - Right-sided HF → systemic congestion
- Pulsus et tardus: low amplitude pulse w/ delayed peak - Water hammer pulse / Corrigan pulse - Afib & ↑ risk of thrombosis
- ↓ pulse pressure ← ↓ SV - Quincke sing: visible capillary pulse - Ortner Syndrome: hoarseness due to r. lary
- Reverse splitting (delayed A2) → severe - Corrigan sign: Prominent carotid pulsations - Malar flush
- Palpable systolic thrill in carotids - De Musset sign: head bobbing w/ heart beat Lutembacher syndrome → MVS + Atrial septal
Stenosis Insufficiency / Regurgitation Stenosis
Definition Aortic valve occlusion/narrowing Incomplete closure of aortic valve → reflux of blood Mitral valve occlusion/nar
Etiology - Senile Calficic / Degenerative (60-80 y.o.) - most common in 1st world Primary valvular causes ● Rheumatic - Most common
countries - Bicuspid aortic valve ○ Recurrent rheumatic fever attacks
- Bicuspid valve → presents before (50-70 y.o.) - Infective endocarditis → valve perforation ● Congenital - rare
- 1-2% of people, M > W - Rheumatic heart disease ● Acquired - Very rare
- Rheumatic disease - most common cause worldwide Aortic root disease → age-related degenerative aortic dilation, ○ SLE, rheumatoid arthritis, malignant carc
- Associated with MS & AR aortic aneurysms, aortic dissection. Whipple disease, drugs, calcification (old
Epidemiology - Risk factors for senile AS → aterogenic risk factors Acute AR → infective endocarditis, trauma, aortic dissection ● Higher incidence in developing countries
- Bicuspid valve associated w/ aortic pathology Chronic AR → bicuspid valve, rheumatic heart disease, ● ⅔ of pxs → females
- Prevalence ↑ with age connective tissue disorders → aortic root dilation ● Onset 10 years after disease
Pathophysiology Preload ↑ ↑↑↑ Normal or ↓
Afterload ↑↑↑ Normal RV (↑), otherwise NOR
Contractility ↑ Normal Normal
Pressure-
volume loop
↑Afterload → LV concentric hypertrophy →↓wall stress but ↓ ventricular Regurgitant volume → ↑↑↑ preload - Normal valve area → 4-6 cm2
compliance → ↑LVEDP & LHF → ↑↑↑ wall stress & work → Acute AR → sudden ↑↑↑ in EDV → LVEDP → ↑LAP → ↑wedge - ↓Valve area → ↑Resistance to blood flow →
- ↑O2 demand → ↑ risk of ischemia → myocardial fibrosis pressure → pulmonary edema & congestion. between left atrium & ventricle → ↑LAP
- Eventually leads to ventricular dilation → contractile dysfunction → ↓↓↓ SV → cardiogenic shock & MI → MEDICAL EMERGENCY → left atrial enlargement & remodeling →
→ ↑ velocity of blood ejection → aortic root dilation Chronic AR → ↑SV due to Frank-Starling mechanism → LV thrombosis
Late in disease → ↑ LA pressure → ↑ wedge pressure → pulmonary HTN & eccentric hypertrophy (dilation) → preserved LAP → ↑pulmonary vascular tone → pulmonary
congestion → RHF & symptoms Later on → Physiologic limit of FSM → systolic failure → ↓CO → → ↑ RVP & hypertrophy → right sided failur
*Left atrial contraction significantly contributes to ventricular filling in these decompensation → ↑LVEDP & LAP → pulmonary congestion
pxs → Afib → significant worsening of symptoms - ↓ aortic DP + ↑ demand → ↑risk of ischemia ***Normal left ventricular function - !!!
Clinical Features Murmurs & 1. Early systolic ejection click (valve stops opening abruptly) - Decrescendo early diastolic murmur 1. Loud S1 (normalizes in late stages)
sounds 2. Late systolic crescendo-descendo systolic murmur - ↓S1 due
to ↑LV volume → premature mitral closure 2. Opening snap after S2 (the earlier, the more
3. Soft S2 (due to ↓aortic valve mobility) - Austin Flint murmur: m id-diastolic murmur ← regurgitant jet 3. Mid-diastolic decrescendo murmur - starts a
4. S4 (non-compliant ventricle) displaces mitral valve leaflet → Presystolic accentuation (atrial contraction
Signs & Asymptomatic if valve area >1 cm2 (normal aortic valve area → 3-4 cm2) - Dyspnea on exertion & ↓ exercise tolerance Symptoms begin when valve area 2-2.5 cm2 (no
Symptoms Triad: Angina, syncope, & left heart failure - Fatigue - Only w/ exertion → ↑LA pressure & heart rate
- Palpitations - Sensation of forceful heartbeat Valve area <1.5 cm2 → symptoms even at rest
- Fatigue - Angina - Dyspnea & pulmonary congestion
- Exertional dyspnea - ↑LV volume + ↓ aortic DP → Widened pulse pressure - Right-sided HF → systemic congestion
- Pulsus et tardus: low amplitude pulse w/ delayed peak - Water hammer pulse / Corrigan pulse - Afib & ↑ risk of thrombosis
- ↓ pulse pressure ← ↓ SV - Quincke sing: visible capillary pulse - Ortner Syndrome: hoarseness due to r. lary
- Reverse splitting (delayed A2) → severe - Corrigan sign: Prominent carotid pulsations - Malar flush
- Palpable systolic thrill in carotids - De Musset sign: head bobbing w/ heart beat Lutembacher syndrome → MVS + Atrial septal
