Mitochondria in aneurysms and dissections of the human ascending aorta

Factors causing the weakness that underlies thoracic aorta aneurysms and dissections are not well known. Based on the findings of apoptosis and ischemic-like necrosis, we hypothesized a possible role for mitochondrial disturbances in the pathogenesis of these diseases. To evaluate if mitochondria at the aortic medial layer are damaged, samples of ascending aortas with aneurysms (n = 6), acute dissections (n = 5), and hypertensive (n = 9) and normotensive controls (n = 7) were analyzed by transmission electron microscopy. Number of mitochondria, areas of cytoplasm, and areas of mitochondria were measured, and area percentage of the cytoplasm corresponding to mitochondria, their number by unit of area, and their mean area were calculated in randomly taken photographs. Data were compared using one-way analysis of variance or Kruskal-Wallis tests. Significant differences (P ≤ 0.05) were found in the number of mitochondria and their mean area, showing opposite results: the number increased and the mean area decreased from normotensive controls to hypertensive controls to acute dissections to aneurysms, although post hoc tests showed that only the differences between the aneurysms and either both controls (number of mitochondria/mm²: 10.37 in normotensive controls, 15.61 in hypertensive controls, and 43.67 in aneurysms) or normotensive controls only (mean area: 2800.15 in normotensive controls vs 894.91 μm² in aneurysms) were significant. In conclusion, there are more, smaller mitochondria in ascending aorta aneurysms. This pattern possibly corresponds to dysfunctional mitochondria, indicating that alterations in the dynamics of these organelles may play a role in the pathogenesis of thoracic aorta aneurysms and dissections.