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Changes in nonmyocyte tissue composition associated with pressure overload of hypertrophic human hearts
J A Huysman1, H W Vliegen, A Van der Laarse
1Department of Pathology, University Hospital Leiden, The Netherlands.
Insights
Pressure overload increases nonmyocyte tissue in the left ventricle endocardium, correlating with heart weight. This change is more pronounced in hypertension and aortic stenosis, especially with coronary artery disease.
Area of Science:
- Cardiovascular Pathology
- Cardiac Remodeling
- Myocardial Tissue Composition
Background:
- Left ventricular hypertrophy (LVH) due to pressure overload is a significant cardiovascular condition.
- Understanding changes in myocardial tissue composition is crucial for assessing LVH.
- Subendocardial (ENDO) and subepicardial (EPI) layers may respond differently to pressure overload.
Purpose of the Study:
- To investigate alterations in nonmyocyte tissue volume in ENDO and EPI layers of the left ventricle.
- To determine if these changes are associated with pressure-overloaded conditions like hypertension and aortic stenosis.
- To explore the impact of concomitant coronary artery disease on myocardial tissue composition.
Main Methods:
- Post-mortem analysis of 41 human hearts (19 normal, 17 hypertension, 5 aortic stenosis).
- Grid-point method used to quantify volume percentages of nonmyocyte tissue in ENDO and EPI.
- Correlation analysis between nonmyocyte tissue volume and heart weight index.
Main Results:
- Nonmyocyte tissue volume fraction increased in ENDO with higher heart weight index across all pressure-overload groups (r = 0.59, P < 0.001).
- Hypertension led to increased scar fibrosis in ENDO, amplified by coronary artery disease.
- Aortic stenosis showed increased diffuse interstitial tissue in both ENDO and EPI.
Conclusions:
- The volume fraction of nonmyocyte tissue in the left ventricular endocardium increases with heart weight, irrespective of the pressure-overload cause.
- This increase in nonmyocyte tissue is also observed in the epicardium in aortic stenosis.
- Myocardial tissue composition changes significantly in response to pressure overload and associated conditions.
Abstract:
To investigate whether pressure-overloaded left ventricular hypertrophy is associated with changes in tissue composition of left ventricular subendocardial (ENDO) and subepicardial (EPI) myocardium, we studied post-mortem 19 normal hearts, 17 hearts of patients with systemic hypertension, and 5 hearts of patients with aortic stenosis. Coronary artery disease was present in 9 hearts of the hypertension group and all 5 hearts of the aortic stenosis group. By means of a grid-point method, volume percentages of nonmyocyte tissue were measured. In ENDO and EPI, nonmyocyte tissue contributed to 27 +/- 8% and 27 +/- 12% for normal hearts, 35 +/- 7% and 32 +/- 7% for hearts in the hypertension group without coronary disease, 40 +/- 10% and 29 +/- 8% for hearts in the hypertension group with coronary artery disease, and 38 +/- 9% and 40 +/- 7% for hearts with aortic stenosis, respectively. For the total group of 41 hearts the volume percentage of nonmyocyte tissue correlated with heart weight index in ENDO (r = 0.59: P less than 0.001), but not in EPI (r = 0.10; not significant). Hearts from patients with hypertension showed a significant increase in microscopical scar fibrosis in ENDO compared to normal, and this increase was amplified by the presence of coronary artery disease. Hearts from patients with aortic stenosis showed an increase in diffuse, non-scar interstitial tissue compared to normal, and occurred in ENDO and EPI. We conclude that the volume fraction of nonmyocyte tissue in ENDO increases as heart weight increases, independent of the type of pressure-overload. Only in the aortic stenosis group this increase of nonmyocyte tissue fraction was observed in EPI as well.