Dans ce travail, In this work, we aimed to establish the structural differences between the aortic root and the pulmonary artery root in fetuses and adults through microscopic counting, allowing us to evaluate the number of elastic laminae and smooth muscle cells in each arterial wall. We did not find any published articles in the literature regarding the number or percentage of these elastic laminae and smooth muscle cells in the wall of the aorta or pulmonary artery in either fetuses or adults. Likewise, we did not find any studies comparing the number or percentage of different cells in the walls of these two large vessels (aortic root and pulmonary artery root) in fetuses and adults. Some authors [9] have studied the normal anatomy of the aortic root, including the valvular leaflets, the nodules of Arantius, the fibrous trigones, and the coronary orifices, without focusing on the histology of the aortic root wall. Other authors [10] have limited their studies to describing the morphology of smooth muscle cells and elastic laminae in the pulmonary artery wall without quantifying or comparing these elements. In our current study, we found a statistically significant difference in fetuses between the mean number of elastic laminae and the mean number of smooth muscle cells in the wall of the aortic root (p < 0.001). The same difference was observed between the mean number of elastic laminae and the mean number of smooth muscle cells in the wall of the pulmonary artery root (p < 0.001).

However, we did not find a statistically significant difference between the mean number of elastic laminae in the aortic root and the mean number of elastic laminae in the pulmonary artery root (p = 0.2675). We also did not find a statistically significant difference between the mean number of smooth muscle cells in the aortic root and the mean number of elastic laminae in the pulmonary artery root (p = 0.6914).

In adults, we found a statistically significant difference between the mean number of elastic laminae and the mean number of smooth muscle cells in the wall of the aortic root (p < 0.001). The same difference was observed between the mean number of elastic laminae and the mean number of smooth muscle cells in the wall of the pulmonary artery root (p < 0.001).

Contrary to the fetus, we found a statistically significant difference between the mean number of elastic laminae in the aortic root and the mean number of elastic laminae in the pulmonary artery root (p < 0.001). There was also a statistically significant difference between the mean number of smooth muscle cells in the aortic root and the mean number of elastic laminae in the pulmonary artery root (p < 0.001). Similarly, in this study, we found a statistically significant difference between the thickness of the wall of the aortic root and that of the pulmonary artery root (p < 0.001). The wall of the aortic root is twice as thick as the wall of the pulmonary artery. Our work shows that there is a similarity between the structure of the wall of the aortic root in the embryo and that of the aortic root in adults, or between the structure of the wall of the pulmonary artery root in the embryo and that of the pulmonary artery root in adults, with variability in the number of elastic laminae and smooth muscle cells. Our sample size is relatively small due to the rarity of available human fetal specimens for the study. We aimed to maximize representativity by including specimens covering a wide range of gestational ages. We also selected only young adults whose ages are eligible for the ROSS procedure. This limitation in our sample size could affect the generalizability of our results.

Some authors have also reported that the medial layer of the aorta has a greater number of elastic laminae, more organized with a denser weave [11,12,13]. The pulmonary autograft undergoes a significant environmental change following the Ross procedure due to differences in hemodynamic conditions. The arterial pressure in the aorta is approximately 120/80 mm Hg at rest, whereas in the pulmonary artery, it is around 25/10 mm Hg [14]. In the healthy pulmonary and aortic roots, blood flow is laminar with sinusoidal swirls behind the leaflets, acting as low-pressure zones to facilitate smooth opening and closure [15, 16]. The acceleration of blood flow and the maximum velocity in the aorta are approximately double that of the pulmonary root [17]. Additionally, powerful left ventricular contractions subject the aortic root to cyclic elongation and torsional deformation [18]. Adequate aortic distensibility is necessary to reduce cardiac workload and ensure diastolic coronary flow [19]. The cyclic volume expansion of the aortic root is nearly twice that of the pulmonary root. Both arterial walls exhibit nonlinear mechanical behavior and are more compliant within their physiological pressure ranges, as their smooth muscle cell components are deposited and interconnected at pressure and transmural stretch levels specific to vessels. During physiological arterial pulsatility, the mechanical load is primarily borne by elastic fibers. With increasing distension, collagen fibers are recruited, causing arterial stiffening [20, 21]. Since pulmonary sinuses are more compliant within the transmural pressure range of 0 to 30 mm Hg, the most significant diameter changes are observed in this range. Beyond 30 mm Hg, proportionally less distension is observed with increasing pressures as the wall stiffens [22, 23]. Therefore, once exposed to systemic pressures after the Ross procedure and before any remodeling, the pulmonary autograft wall will behave significantly more rigidly than the aorta [19, 20, 24, 25].

Experiments conducted on porcine subjects [26], have demonstrated that the pulmonary autograft expands when exposed to systemic arterial pressures. This dilation is not accompanied by degeneration or necrosis of the pulmonary arterial wall; it remains viable, but its wall does not seem to adapt well to high pressures. These experimental findings are supported by numerous series of operated patients, with most teams observing a significant dilation of the aortic sinus [27,28,29,30].

These same teams also note a significant dilation of the sinotubular junction. Extrinsic factors that may contribute to the dilation of the aortic root have been described, including the patient’s young age [27], male gender [27, 31], aortic bicuspidity [30], the absence of suture reinforcement, and the duration of follow-up [27, 30].

Authors [32] have reported that patients with aortic bicuspidity more frequently exhibit histological lesions in the aortic wall and also in the wall of the pulmonary artery. These patients thus have a more fragile pulmonary artery and are even more exposed to the risk of dilation of the pulmonary autograft.

Our study has several limitations, including the small sample size (20 fetuses and 4 adults) and the scarcity of available specimens. Additionally, the dependence on the anatomy lab and the pathology cytology service for the preparation or reading of slides could introduce selection bias when all slides are not read and reread by the same two practitioners (the first reading and the second rereading for control). Future studies with larger samples are needed to confirm our results and extend their generalization.