Hyperplasia of coronary intima in young males in relation to development of coronary heart disease in adults

The aim of the investigation was to study structural features of coronary arteries in young males which may influence the development of stenosing coronary atherosclerosis in older age. We studied the coronary arteries from 84 males, 10-39 years old, who died from accidents in Moscow, Malmo and Riga, and 98 males aged 40 and above from Moscow who died from coronary heart disease (71 cases) or other diseases (27 cases). In children and young males from all three cities, musculo-elastic hyperplasia of the coronary intima took place constantly but with different degrees of expression; a strict relationship of the intimal thickness and age was observed. Histometric investigations of the right coronary artery showed that in young males of Riga, in comparison with those of Malmo, the intima was significantly thicker both outside (69.6+/-2.8 and 58. 2+/-2.5 microm) and within the area of cushion like thickening (118. 8+/-4.0 and 101.9+/-3.8 microm), they had more extended cushion-like thickening of intima (42.6+/-3.0 and 30.8+/-3.3% to the length of the artery circumference) and destroyed parts of the internal elastic lamina (28.3+/-1.9 and 19.1+/-1.7% of its length). In males older than 40 years, severe coronary atherosclerosis and stenosis was also significantly more common in Riga than in Malmo. Our data indicate that with age the intimal musculo-elastic hyperplasia in the coronary arteries is transformed to a fibro-elastic layer. The thickness of this layer in the presence of stenosing plaques (>75% of arterial lumen) was much greater than in the presence of plaques with stenoses less than 50% (188.1+/- 7.3 and 69.8+/-4.5 microm, respectively). CONCLUSION: The development of stenosing coronary atherosclerosis is closely related to the degree of musculo-elastic intimal hyperplasia in childhood and young age. The formation of a fibro-elastic layer in the coronary intima decreases the ability of the artery to dilate during the development of atherosclerosis.