Cardiac hypertrophy and left ventricular end-diastolic stress
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Left ventricular wall stress, crucial for hypertrophy, was assessed in patients with heart conditions. Results indicate that muscle fiber stress is a key factor in left ventricular hypertrophy development.
Area of Science:
- Cardiology
- Biomedical Engineering
- Physiology
Background:
- Left ventricular hypertrophy (LVH) is a significant cardiac adaptation.
- Understanding the determinants of LVH is crucial for managing heart disease.
- Wall stress is a proposed mechanical stimulus for cardiac hypertrophy.
Purpose of the Study:
- To calculate equatorial and longitudinal left ventricular wall stress at end-diastole.
- To investigate the relationship between wall stress and different left ventricular pathologies.
- To test the hypothesis that muscle fiber stress is a determinant of LVH.
Main Methods:
- Calculated end-diastolic left ventricular wall stress in 66 patients and 4 controls.
- Utilized a thick-walled ellipsoid model for stress calculations.
- Grouped patients based on conditions: volume overload (aortic/mitral incompetence), pressure overload (aortic stenosis), and congestive cardiomyopathy.
Main Results:
- In volume overload and cardiomyopathy, ventricular dilation was matched by increased wall thickness, maintaining a normal stress conversion factor.
- Absolute stress in these conditions correlated with end-diastolic pressure.
- In pressure overload (aortic stenosis), increased wall mass normalized absolute fiber stress by reducing the stress conversion factor.
Conclusions:
- Muscle fiber stress appears to be a critical determinant of left ventricular hypertrophy.
- The heart adapts wall thickness to normalize stress in response to volume or pressure overload.
- These findings support mechanical factors in the pathogenesis of cardiac hypertrophy.
Abstract:
Equatorial and longitudinal left ventricular wall stress were calculated at end-diastole in a group of 66 patients in sinus rhythm. Thirty-one patients had volume overload of the left ventricle: six with acute and 21 with chronic aortic incompetence, and four with chronic mitral incompetence. Another six patients had aortic stenosis and 25 had congestive cardiomyopathy. Four patients served as controls. Stress was calculated using a thick-walled ellipsoid model. In patients with volume overload and congestive cardiomyopathy, ventricular dilatation was accompanied by an appropriate increase in wall thickness so that the "stress conversion factor" (the factor relating pressure to stress) was normal and absolute stress depended on end-diastolic pressure. In pressure overload of the left ventricle (aortic stenosis), the increase in wall mass reduced the stress conversion factor so that aboslute fiber stress was normal. These data support the hypothesis that muscle fiber stress may be an important determinant of left ventricular hypertrophy.