Morphometry of human coronary capillaries during normal growth and the effect of age in left ventricular pressure-overload hypertrophy

In adults, acquired pressure-overload left ventricular hypertrophy can result in myocardial ischemia, which may be due in part to insufficient capillary growth during development of hypertrophy. The coronary microvascular response to congenital pressure-overload hypertrophy in children has not been previously characterized.

Average capillary density and heterogeneity of capillary spacing were measured in 63 postmortem human hearts with left ventricular hypertrophy and control hearts without heart disease. Pathology specimens were chosen that had left ventricular hypertrophy caused by 1) congenital isolated aortic valve stenosis in infants less than 1 year old at death, children 9-14 years old, and adults 15-30 years old; 2) congenital isolated coarctation of the aorta in adults 15-39 years old; and 3) acquired aortic stenosis in adults 51-86 years old. Major findings of the study were: 1) Human left ventricular capillary density and heterogeneity of capillary spacing are similar to other mammalian species. 2) Capillary density is higher in infants (3,315 +/- 85 capillaries per square millimeter), decreases with increasing heart weight during normal growth in early childhood (children, 2,388 +/- 75 capillaries per square millimeter, p less than 0.05), and thereafter remains relatively constant. 3) Capillary density with left ventricular hypertrophy is dependent on the age of onset. Congenital aortic stenosis and coarctation are characterized by an increase in capillary supply proportional to myocyte volume, maintaining capillary density similar to control hearts. Adults with acquired aortic stenosis have decreased capillary density (1,671 +/- 66 capillaries per square millimeter, p less than 0.01 versus control).

Pressure-overload left ventricular hypertrophy in children demonstrates proportional capillary angiogenesis, whereas in adults, hypertrophy appears to be associated with failure of compensatory angiogenesis.