Left Ventricular End-Diastolic Pressure in Severe Aortic Stenosis
In severe aortic stenosis, left ventricular end-diastolic pressure (LVEDP) is typically elevated, not low, due to increased left ventricular wall thickness and diastolic dysfunction that develops as a compensatory mechanism to pressure overload. 1
Pathophysiology of LVEDP in Aortic Stenosis
Severe aortic stenosis creates a pressure overload on the left ventricle, triggering a series of compensatory mechanisms:
- Left ventricular hypertrophy (LVH): The left ventricle adapts to systolic pressure overload through a hypertrophic process, resulting in increased LV wall thickness while maintaining normal chamber volume 1
- Diastolic dysfunction: The hypertrophied heart exhibits:
- Impaired relaxation in early diastole
- Decreased compliance in mid to late diastole
- Reduced LV filling 1
- Elevated filling pressures: As a direct consequence of diastolic dysfunction, LVEDP increases 1
Evidence for Elevated LVEDP in Severe AS
Research clearly demonstrates that patients with severe aortic stenosis typically have elevated LVEDP:
- A study of patients with severe symptomatic AS and preserved ejection fraction showed that decompensated LVH was characterized by increased LVEDP (>15 mmHg) 2
- Another study examining patients undergoing transcatheter aortic valve implantation found that elevated post-procedural LVEDP (>12 mmHg) was present in 70% of patients with severe AS 3
- In patients with severe AS undergoing balloon aortic valvuloplasty, elevated LVEDP was common and associated with worse outcomes 4
Clinical Implications
The elevated LVEDP in severe AS has important clinical implications:
- Marker of disease progression: As AS progresses from compensated to decompensated LVH, LVEDP increases 2
- Predictor of outcomes: Higher LVEDP is associated with:
Special Considerations
- Atrial contribution: A forceful atrial contraction contributes to elevated end-diastolic pressure and plays an important role in ventricular filling 1
- Loss of atrial contraction: Atrial fibrillation often leads to clinical deterioration in AS patients due to loss of this atrial contribution 1
- Relationship to afterload: Patients with severe AS who have inappropriately decreased stroke volume relative to afterload tend to have higher LVEDP, suggesting failed hemodynamic adaptation 6
Summary
Severe aortic stenosis leads to left ventricular hypertrophy and diastolic dysfunction, which results in elevated—not low—left ventricular end-diastolic pressure. This elevated LVEDP is a marker of disease progression and a predictor of worse clinical outcomes in patients with severe aortic stenosis.