Case 9: Terrance K. - Aortic Stenosis + Regurgitation

SL Valves Anatomy: Leaflets

Attach to annulus fibrosus (fibrous ring) connecting to cardiac skeleton (connective tissue)

3 in aortic (L) and pulmonary (R)

SL Valves Anatomy: Annulus

Thinner than AV

SL Valves Anatomy: Aortic Root

Proximal segment of ascending aorta

• Include annulus, sinuses of Valsalva, sinotubular junction

SL Valve Histology: Leaflets

Covered by single endothelial cell layer

Contain valve interstitial cells

3 layers

1. Fibrosa: Great artery side

• Contain: Collagen

• Provide tensile strength

2. Spongiosa: Middle layer

• Contain: Proteoglycans

• Increase compressibility

• Absorb shock

3. Ventricularis: Ventricle side

• Contain: Elastin fibres

• For elasticity → Rapid recoil + coaptation

SL Valves Physiology: Leaflets

Separate ventricles from great arteries (pulmonary artery and aorta)

Diastole: Closed = Prevent regurg

• Great artery elastic recoil = Blood back to heart = Distend leaflets together

Systole: Open = Blood flow through

SL Valves Physiology: Aortic Root

Connect LV and systemic circulation (ascending aorta)

Maintain valve structure for coaptation

Accommodate pressure and volume changes during systole and diastole

• For coronary artery perfusion

Aortic Stenosis (AS): Description

Aortic valve narrowing with leaflet thickening and fibro-calcific remodelling

Evolve to obstruction = Restrict CO

AS: Epidemiology

Risk factors:

• Older age

• Metabolic syndrome

• High von Willebrand factor in valve tissues (increase calcification)

Athersclerotic risk factors

• Male

• Smoking

• Hypertension

• Hypercholesterolemia

AS: Etiology

Aortic Valve Sclerosis: Leaflet calcification and fibrosis (most common)

Bicuspid Aortic Valve: Leaflet fusion in utero (congenital)

Rheumatic Fever: Common in low-income

AS: Types

Depend on echo findings

Normal:

• Aortic valve area (AVA) = 3-4 cm²

• Mean transvalvular pressure (MTP) < 5 mmHg

High-Gradient:

• AVA ≤ 1 cm²

• MTP ≥ 40 mmHg

Low-Flow Low-Gradient with Reduced LVEF:

• AVA ≤ 1 cm²

• MTP < 40 mmHg

• LVEF < 50%

• Stroke Volume Index (SVI) ≤ 35 mL/m²

Low-Flow Low-Gradient with Preserved LVEF:

• AVA ≤ 1 cm²

• MTP < 40 mmHg

• LVEF ≥ 50%

• SVI < 35 mL/m²

Normal-Flow Low-Gradient with Preserved LVEF:

• AVA ≤ 1 cm²

• MTP < 40 mmHg

• LVEF ≥ 50%

• SVI > 35 mL/m²

AS: Pathogenesis

1. Lipid accumulation, inflammation, calcification (interstitial cells → Osteoblasts) of aortic valve = Stiffening

2. Fibro-calcific leaflet remodelling over time

• Response to injury

3. Narrow aortic valve orifice = Increase LV load

• Increased systolic pressure = LV concentric hypertrophy

• Decrease coronary flow = Unable to match O2 demand

AS: Investigations

Echo (TTE and transesophageal/TEE)

CXR

Cardiac catheterization

AS: Echo

Assess aortic valve structure, function, and stenosis severity

Assess LV

AS: CXR

Determine presence of pulmonary edema

Calcifications in aortic valve = More severe

LV hypertrophy

AS: Cardiac Catheterization

Evaluate aortic valve area, CO, and MAP gradient

AS: Clinical Presentation

Mostly asymptomatic

Dyspnea

Angina

Dizziness and syncope

Physical:

• Low BP

• Weak and delayed distal pulse

Auscultation:

• Crescendo-decrescendo late systolic ejection murmur → Bilateral radiation to carotids

• Soft S2

• S4

AS: Treatment/Mangement

Surgery: Surgical aortic valve replacement (AVR)

Transcatheter AVR

• Wedge replacement valve into old valve

Percutaneous balloon valvuloplasty

• Inflate balloon in valve = Stretch open stenotic valve

Aortic Regurg (AR): Description

Blood regurg through aortic valve into LV during diastole

AR: Epidemiology

Risk factors:

• Older age

• Appetite suppressants

AR: Etiology

Acute:

• Malcoaptation from leaflet abnormality (infective endocarditis, LV dilation)

• Aortic annulus or root abnormality (aortic dissection)

Chronic:

• Malcoaptation from leaflet abnormality (calcific aortic valve, bicuspid aortic valve, rheumatic disease)

• Aortic annulus or aortic root abnormality (dilation)

AR: Pathogenesis

1. Aortic valve dysfunction = Regurg from aorta → LV

2. Chronic AR = LV dilation + eccentric hypertrophy = Compensatory SV increase

AR: Investigations

Echo (TTE)

CXR

AR: Echo

Assess aortic valve structure, function, regurg severity

• Abnormal leaflets

• Anterior mitral valve leaflets fluttering

• Aorta dilation

Visualize LV

• Dilation

• Hypertrophy

AR: CXR

Assess pulmonary edema

Large aortic root/arch

Chronic: Large cardiac silhouette

AR: Clinical Presentation

Acute:

• Sudden severe dyspnea

• Pulmonary edema

Chronic:

• Palpitations

• High pulse pressure (diff between systolic and diastolic)

  • Water Hammer Pulse: Rapid upstroke then vessel collapse (bounding)

• LHF symptoms

  • Exertional dyspnea

  • Angina

  • Orthopnea

  • Fatigue

  • Syncope

• Auscultation:

  • S3

  • High-pitched decrescendo early diastolic murmur

  • Austin Flint murmur (low-pitched mid-diastolic murmur at apex)

AR: Treatment/Management

Surgery: Aortic valve replacement

Pharmacological: Treat HF symptoms

Pressure Changes in AS

High afterload = Decrease blood flow across aortic valve in systole = Increase LV systolic pressure

• Systolic pressure gradient between LV and aorta

LV concentric hypertrophy over time = Decrease wall stress + compliance

• Increase LV diastolic pressure = LA hypertrophy (overcome high LV pressure)

Volume Changes in AS

High afterload = Decease blood flow across aortic valve in systole = Increase LV ESV

LV dilation over time = Increase compliance

• Accommodate increased blood volume

AS: P-V Loop Changes

Increased ESV

• Low blood emptying from LV → Aorta

Decreased EDV

• Hypertrophy = Decrease compliance (blood entering)

Decreased SV

• LV cannot compensate for increased afterload (stiff aortic valve) = Decrease blood outflow

• Increase systolic ejection pressure