Cardiac Valve Opening and Closing Mechanism
Heart valves open and close primarily through inertial flow forces rather than simple pressure gradients, with valve leaflet motion being a dynamic, continuous process throughout the cardiac cycle—not occurring during discrete "isovolumic" periods as traditionally taught.
Fundamental Mechanism
The traditional Wiggers Diagram concept of valve function based solely on pressure differences has been challenged by recent evidence. Valves open and close in response to inertial flow through the valves themselves, not just instantaneous pressure transmission through incompressible blood 1. This represents a paradigm shift from the century-old teaching that pressure gradients alone control valve motion.
Key Findings on Valve Timing
Recent in vivo data demonstrates that:
- No consistent isovolumic periods exist during the cardiac cycle
- The mitral valve closes at variable points during the rising phase of left ventricular pressure (not at a fixed pressure crossover point)
- Aortic valve closure and mitral valve opening occur simultaneously at the end of systolic pressure drop 1
Structural Basis of Valve Function
Aortic Valve Anatomy
The aortic valve consists of three semi-lunar leaflets attached to a crown-like 3D structure (not a simple ring). The cusps are:
- Mobile and free at the commissures
- Symmetrical in normal valves
- Attached to a fibrous sleeve that connects to the aorta above and left ventricular outflow tract below
- Dynamically changing in size throughout the cardiac cycle in response to inner pressure 2
Mitral Valve Dynamics
The mitral valve demonstrates complex dimensional changes:
- Maximal opening occurs in late diastole, with the annular diameter reaching 29.3 ± 3.5 mm and area of 962.8 ± 149.3 mm²
- Maximal valve opening angles (anterior: 68.3° ± 5.6°, posterior: 55.9° ± 5.4°) also occur in late diastole
- Minimal opening occurs in mid-systole, with annular diameter of 9.8 ± 1.7 mm and area of 76.2 ± 27.3 mm² 3
Role of Papillary Muscles
The papillary muscles play an active role in valve function beyond simple tethering:
- Papillary muscle shortening throughout isovolumic relaxation suggests active participation in opening the mitral valve
- Maximal papillary muscle elongation occurs 25 ± 2 ms after onset of ejection
- Papillary muscle shortens by 14 ± 4% during the cycle
- 39 ± 7% of papillary muscle shortening occurs after the aortic incisura, indicating continued active function during early diastole
- Elongation in late diastole is necessary to permit proper leaflet closure 4
Clinical Classification of Valve Motion
When assessing valve dysfunction, leaflet motion is classified using Carpentier's system 2:
- Type I: Normal leaflet motion (regurgitation due to annular dilatation or leaflet perforation)
- Type II: Excessive motion (prolapse)
- Type III: Restrictive motion (limited opening or closing)
Important Clinical Caveats
Prosthetic Valve Assessment
For mechanical valves, fluoroscopy or cine-CT is essential to assess leaflet motion because echocardiographic imaging is obscured by strong reflections from the mechanical components. Opening and closing angles must be measured from side views and compared to expected values for that valve type 5.
Bioprosthetic Valve Considerations
Bioprosthetic valve stenosis may result from:
- Structural valve deterioration
- Reversible valve thrombosis (thin thrombus layer responsive to oral anticoagulation)
- Pannus formation
- 3D TEE or 4D CT imaging is useful to distinguish thrombosis from other causes 5
Secondary Valve Dysfunction
In secondary tricuspid or mitral regurgitation, increased leaflet tethering (measured as tenting area >1.0 cm² or coaptation distance >0.76 cm) predicts severity and residual regurgitation after surgical repair 2.