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Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
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Wall stress and patterns of hypertrophy in the human left ventricle
The Journal of Clinical Investigation
|July 1, 1975
Summary
Chronic left ventricular pressure overload causes concentric hypertrophy by increasing wall thickness to normalize systolic stress. Volume overload leads to eccentric hypertrophy, normalizing systolic but not diastolic wall stress.
Area of Science:
- Cardiology
- Physiology
- Biomedical Engineering
Background:
- Chronic left ventricular (LV) pressure overload typically causes concentric hypertrophy (wall thickening).
- Chronic LV volume overload typically causes eccentric hypertrophy (chamber enlargement).
- The hemodynamic factors driving these distinct hypertrophy patterns require elucidation.
Purpose of the Study:
- To investigate the role of hemodynamic factors in differential LV hypertrophy patterns.
- To measure LV wall stresses throughout the cardiac cycle in patients with pressure overload, volume overload, and controls.
Main Methods:
- Cardiac catheterization in 30 patients (6 pressure overload, 18 volume overload, 6 controls).
- Measurement of LV pressure, meridional wall stress (sigman), wall thickness (h), and radius (R) throughout the cardiac cycle.
- Calculation of the wall thickness to radius (h/R) ratio.
Main Results:
- Pressure overload normalized peak systolic wall stress due to increased wall thickness (concentric hypertrophy, increased h/R ratio).
- Volume overload did not normalize end-diastolic wall stress (eccentric hypertrophy, normal h/R ratio).
- Systolic wall stress was normalized in both overload conditions.
Conclusions:
- Hypertrophy may develop to normalize systolic wall stress but not diastolic wall stress.
- Increased systolic tension leads to myocardial fiber thickening.
- Increased diastolic tension may lead to fiber elongation, improving chamber efficiency without normalizing diastolic stress.
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