Purpose: Myocardial tissue ischemia may be mitigated by a well-developed coronary collateral circulation. Only few detailed 3D data are available of the entire human coronary arterial tree. Here, high-resolution reconstructions of the coronary vasculature of two human hearts were quantitatively analyzed.
Methods: Two hearts became available through autopsy: heart #1 (64 years, 595 g) with left ventricular hypertrophy and a scar on the inferior wall, indicating an old infarction and heart #2 (84 years, 330 g) without prior cardiovascular events. The coronary arteries were cannulated, flushed with saline solution and thereafter filled with fluorescent replica material at 100 mmHg. After cast polymerization, the hearts were frozen and then alternately cut and en-face imaged using an imaging cryomicrotome, resulting in a complete 3D reconstruction (voxel size 32 μm). From the reconstructions, arterial segment length, diameter, and collateral presence were determined.
Results: In heart #1, about 1300 collaterals were detected and evenly distributed over the myocardium. The scar tissue showed a lower vascular density compared to the rest of the myocardium. Bridging collaterals were most prevalent between LCX and LAD and between LAD and RCA. Collateral vessels connecting through the border zone of the scar tissue ran in multiple parallel pathways. In heart #2, about 4300 collaterals were found throughout the entire myocardium, but predominantly in the subendocardium. Bridging collaterals were mainly present between LCX and LAD territories. Although the total number of collaterals in heart #1 was lower than in heart #2, the mean collateral diameter in heart #1 was significantly higher (90.6 μm, SEM 1.30 vs. 66.8 μm, SEM 0.53. P<0.05).
Conclusions: In the aged, but healthy heart, abundant collaterals were distributed throughout the entire myocardium providing the substrate for outward remodeling. In the hypertrophied heart with an old infarction, fewer but larger collaterals were found than in the healthy heart. These findings suggest that collateral development between perfusion territories differs distinctly between healthy and hypertrophied human hearts.