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Cited by 2,403Cardiovascular Function and Risk FactorsCardiomyopathy and Myosin StudiesCardiac Fibrosis and Remodeling

Wall stress and patterns of hypertrophy in the human left ventricle.

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Grossman, W, Jones, D, McLaurin, L P·1975·Journal of Clinical Investigation
DOI 10.1172/jci108079PMC PMC436555
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Abstract

It is generally recognized that chronic left ventricular (LV) pressure overload results primarily in wall thickening and concentric hypertrophy, while chronic LV volume overload is characterized by chamber enlargement and an eccentric pattern of hypertrophy. To assess the potential role of the hemodynamic factors which might account for these different patterns of hypertrophy, we measured LV wall stresses throughout the cardiac cycle in 30 patients studied at the time of cardiac catheterization. The study group consisted of 6 subjects with LV pressure overload, 18 with LV volume overload, and 6 with no evidence of heart disease (control). LV pressure, meridional wall stress (sigman), wall thickness (h), and radius (R) were measured in each patient throughout the cardiac cycle. For patients with pressure overload, LV peak systolic and end diastolic pressures were significantly increased (220 plus or minus 6/23 plus or minus 3 mm Hg) compared to control (117 plus or minus 7/10 plus or minus 1 mm Hg, P less than 0.01 for each). However, peak systolic and end diastolic (sigman) were normal (161 plus or minus 24/23 plus or minus 3 times 10-3 dyn/cm-2) compared to control (151 plus or minus 14/17 plus or minus 2 times 10-3 dyn/cm-2, NS), reflecting the fact that the pressure overload was exactly counterbalanced by increased wall thickness (1.5 plus or minus 0.1 cm for pressure overload vs. 0.8 plus or minus 0.1 cm for control, P less than 0.01). For patients with volume overload, peak systolic (sigman) was not significantly different from control, but end diastolic (sigmam) was consistently higher than normal (41 plus or minus 3 times 10-3 dyn/cm-2 for volume overload, 17 plus or minus 2 times 10-3 dyn/cm-2 for control, P less than 0.01). LV pressure overload was associated with concentric hypertrophy, and an increased value for the ratio of wall thickness to radius (h/R ratio). In contrast, LV volume overload was associated with eccentric hypertrophy, and a normal h/R ratio. These data suggest the hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress. We propose that increased systolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolic stress (force per unit cross-sectional area) to normal. In contrast, increased resting or diastolic tension appears to result in gradual fiber elongation or lengthening which improves efficiency of the ventricular chamber but cannot normalize the diastolic wall stress.

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  • Pressure overload typically causes a concentric pattern of hypertrophy.

    “Typically, we think of pressure overload as causing a concentric pattern of hypertrophy (120).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [120]

  • Chronic volume overload or high output failure is classically felt to produce an eccentric form of cardiac hypertrophy with enlarged cardiac chambers, but normal wall thickness.

    “Chronic volume overload or high output failure is classically felt to produce an eccentric form of cardiac hypertrophy with enlarged cardiac chambers, but normal wall thickness (120).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [120]

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Research works printed but not linked: 3

  1. [2]2. Alpert, N. R. 1971. Preface. Cardiac Hypertrophy. N. R. Alpert, editor. Academic Press, Inc. New York. XVXVI.
  2. [25]25. Walker, M. L., Jr., E. W. Hawthorne, and H. Sandler. 1971. Methods for assessing performance for the intact hypertrophied heart. In Cardiac Hypertrophy. N. R. Alpert, editor. Academic Press, Inc., New York. 387405.
  3. [30]30. Hood, W. P., Jr. 1971. Dynamics of hypertrophy in the left ventricular wall of man. In Cardiac Hypertrophy. - N. R. Alpert, editor. Academic Press, Inc., New York. 445-452.

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Authors
Grossman, W., Jones, D., & McLaurin, L. P.
Affiliations
University of North Carolina at Chapel Hill (US)
ORCID
Jones, D
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1975-07-01
Volume
56
Issue
1
Pages
56-64
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci108079
PMC
PMC436555
OpenAlex
W2104475665
Cited by
2,403
References
33
Citations by year
2026: 32 · 2025: 45 · 2024: 38 · 2023: 36 · 2022: 49 · 2021: 59 · 2020: 69 · 2019: 59 · 2018: 49 · 2017: 64 · 2016: 57 · 2015: 72 · 2014: 74 · 2013: 81 · 2012: 69
FWCI
7.38
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
left ventricular hypertrophy, wall stress, concentric hypertrophy, eccentric hypertrophy, left ventricular pressure overload, left ventricular volume overload, wall thickness, diastolic wall stress, systolic wall stress, cardiac cycle, myocardial fibers, hemodynamics
MeSH terms
Adolescent, Adult, Angiocardiography, Cardiac Output, Electrocardiography, Female, Cardiac Catheterization, Cardiomegaly, Heart Ventricles, Hemodynamics, Humans, Male, Middle Aged, Myocardial Contraction, Pressure, Stress, Mechanical, Ultrasonography

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