Changes in nonmyocyte tissue composition associated with pressure overload of hypertrophic human hearts.

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.