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Review
. 2021 May 31:8:649855.
doi: 10.3389/fcvm.2021.649855. eCollection 2021.

Coronary Arteries: Normal Anatomy With Historical Notes and Embryology of Main Stems

Affiliations
Review

Coronary Arteries: Normal Anatomy With Historical Notes and Embryology of Main Stems

Gaetano Thiene et al. Front Cardiovasc Med. .

Abstract

Anatomy of subepicardial coronary arteries became a topic of investigation at autopsy in Florence (Italy) by Banchi in the early twentieth century, with the discovery of dominant and balanced patterns. Thereafter, in the 60's of the same century Baroldi in Milan did post-mortem injection with spectacular three-dimensional casts. Later Sones at the Cleveland Clinic introduced selective coronary arteriography for in vivo visualization of coronary arteries. In the present chapter we show these patterns, as well as normal variants of origin and course with questionable risk of ischemia, like myocardial bridge as well as origin of the left circumflex coronary artery from the right sinus with retroaortic course. As far as embryology, the coronary arteries and veins are epicardial in origin and finally connect the former with the aorta, and the latter with the sinus venosus. At the time of spongy myocardium, intramural blood supply derives directly by the ventricular cavities, whereas later, at the time of myocardial compaction, vascularization originates from the subepicardial network. The connection of the subepicardial plexus with the aorta occurs with prongs of the peritruncal ring, which penetrate the facing aortic sinuses. Septation of truncus arteriosus is not responsible for the final position of the coronary orifices. Infact in transposition of the great arteries coronary ostia are regularly located within facing sinuses of the anterior aorta.

Keywords: anatomy; coronary arteries; embriology; history; normal variants.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The original drawings of coronary artery dominant patterns, from Banchi (2). (a,b) Right dominance and (c,d) left dominance.
Figure 2
Figure 2
Postmortem casts of coronary arteries. From Baroldi and Scomazzoni (3). (a) Left coronary artery anatomy, (b) dominant right pattern, (c) dominant left pattern, and (d) balanced pattern.
Figure 3
Figure 3
The topographical variability of coronary artery orifices in normal hearts. From Muriago et al. (5).
Figure 4
Figure 4
(a) The right coronary artery orifice (arrow) is just above (2 mm) the sinotubular junction, within normal limits. (b) The right coronary orifice (arrow) is well above the sinotubular junction (10 mm), over the threshold of normal limits.
Figure 5
Figure 5
The coronary arteries arise from the facing aortic sinuses, perpendicular to the aortic wall, and the pulmonary root does not interfere with their proximal course. Note the left stem dividing into the left anterior descending (LAD) and the left circumflex (LC) branches. From Roberts (6).
Figure 6
Figure 6
The blood flow of the ventricular septum is supported by perforating branches, originating from the anterior and posterior descending coronary arteries. From Baroldi and Scomazzoni (3).
Figure 7
Figure 7
A double left anterior descending coronary artery (arrows). From Baroldi and Scomazzoni (3).
Figure 8
Figure 8
(a) Diagram with origin of the left circumflex artery from the right coronary artery and retroaortic course. From Roberts (6). (b) Gross view of the aortic root. Arrow indicates the retroaortic course of the anomalous left circumflex artery.
Figure 9
Figure 9
The first historical description of myocardial bridge made in 1834 by Leopoldo and Floriano Caldani, Professors of Anatomy at the University of Padua. From Caldani et al. (8).
Figure 10
Figure 10
Myocardial bridge with deep intramural course: the coronary segment is completely surrounded by a myocardial sleeve. Gross (a) and histological views (b). Azan Mallory stain.
Figure 11
Figure 11
Origin of the left anterior descending coronary artery from the right coronary artery. Note the anomalous proximal course in front of the pulmonary infundibular. From Roberts (6).
Figure 12
Figure 12
Embryology of the myocardium. (a) Spongy myocardium from a mature fog with blood supply deriving directly from the endocardium of the ventricular cavities. (b) The myocardium of a fetal chick heart becomes compact, with blood supply deriving from the subepicardial vasculature. From de la Cruz et al. (13).
Figure 13
Figure 13
Origin of coronary arterial stems from the peritruncal epicardial ring. (a) From Bogers et al. (17). (b) From de la Cruz et al. (13).
Figure 14
Figure 14
The hypothesis according to which sprouts or buds arise from the facing aortic sinuses and make contact with the subepicardial coronary vasculature. From Angelini (18).
Figure 15
Figure 15
Embryology of coronary artery orifices and main stems. (A) Formation of the coronary ostia and stems is initiated when the capillary ring that encircles the aortic root expands and attaches as a vascular plexus (in response to CXCL12 + CXR4). The sites of ostial formation are adjacent to an epicardial cusp (Epi-cus), a thickened portion of the subepicardium that contains epicardium-derived cells (EPDCs) that are rich in Vascular endothelial growth factor (VEGF) receptors and erythroblasts [red blood cells (RBCs)]. Cardiomyocytes guide the attachment of the vascular plexus. Fibroblast growth factors (FGFs) from the myocardium promote Sonic hedgehog (Shh) signaling, which, together with hypoxia inducible factor-1 (Hif-1), stimulates VEGFs and angiopoietin (Ang) 2, thus facilitating angiogenesis of the vascular plexus. (B) Myocardium-derived cardiomyocytes and neural crest cells facilitate the entry of the vascular plexus into an opening in the aortic wall, created by apoptosis. An endothelial ingrowth demarcates the pathway of the ostium formation. (C) The onset of coronary flow and shear stress is key to the remodeling of the vascular plexus. Differentiation, migration, and attachment of vascular smooth muscle cells (VSMCs) are influenced by (1) platelet-derived growth factor (PDGF)-BB activation in endothelial cells and the ligand's interaction with PDGFR-β in VSMC progenitors; and (2) the influence of VEGFs and fibroblast growth factors (FGFs). From Tomanek and Angelini (20).

References

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