Author + information
- Received July 15, 1993
- Revision received December 23, 1993
- Accepted January 28, 1994
- Published online July 1, 1994.
- ↵∗Address for correspondence: Dr. Piero Anversa, Department of Mediane, Vosburgh Pavilion, Room 302, New York Medical College, Valhalla, New York 10595.
Objectives. The present investigation was designed to evaluate the growth reserve capacity of the aged and senescent myocardium.
Background. Aging affects the ability of the heart to sustain alterations in ventricular loading, and this phenomenon may be coupled with attenuation of the hypertrophic reaction of the myocardium. However, because myocyte cellular hyperplasia has been documented experimentally in the old heart, a similar adaptation may also occur in humans and play a role in this process.
Methods. The changes in number and size of ventricular myocytes were measured quantitatively in pathologic hearts of elderly subjects. Morphometric methodologies were applied to the analysis of 13 hypertrophic hearts obtained at autopsy from patients 80 ± 4 (mean ± SD) years old. An identical number of nonhypertrophic hearts collected from subjects 76 ± 7 years old were used as control hearts.
Results. A 71% increase in left ventricular weight was associated with a 33% increase in average myocyte cell volume per nucleus and a 36% augmentation in the total number of myocyte nuclei in the ventricular myocardium. However, a 55% increase in right ventricular weight was the result of a 59% increase in the aggregate number of myocyte nuclei, with no change in myocyte cell volume. These cellular processes were associated with a 95% and 83% enlargement of the myocardial interstitium in the left and right ventricle, respectively.
Conclusions. Myocyte nuclear and possibly cellular hyperplasia appear to be the prevailing growth mechanism of the overloaded aging myocardium. Proliferation of myocyte nuclei and connective tissue accumulation are the major determinants of ventricular remodeling in the hypertrophic senescent heart.
☆ This work was supported by Grants HL-38132, HL39902, HL-40561 and program project Grant HL-37412, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
- Received July 15, 1993.
- Revision received December 23, 1993.
- Accepted January 28, 1994.