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Jornal Vascular Brasileiro

versão impressa ISSN 1677-5449

J. vasc. bras. vol.9 no.2 Porto Alegre jun. 2010 



Rupture of vasa vasorum and intramural hematoma of the aorta: a changing paradigm



Adamastor Humberto Pereira

Departamento de Cirurgia, Hospital de Clínicas de Porto Alegre, Faculdade de Medicina da Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil




Rupture of vasa varorum has been recognized as one cause of intramural hematoma of the aorta for 90 years. This brief revision presents systematically, the physiology of these vessels and its role in the physiopathology of the alterations in the aortic wall secondary to hypertension, arteriosclerosis and in Acute Aortic Syndrome. The hypothesis is that rupture of vasa vasorum is a secondary phenomenon and not one causal factor in the physiopathology of intramural hematoma.

Keywords: Aortic intramural hematoma, vasa vasorum, aortic dissection.


A ruptura dos vasa vasorum tem sido reconhecida como uma das causas do hematoma intramural da aorta há 90 anos. Esta breve revisão apresenta sistematicamente a fisiologia desses vasos e o seu papel na fisiopatologia das alterações parietais da aorta que ocorrem na hipertensão arterial, na arteriosclerose e na síndrome aórtica aguda. A hipótese defendida aqui é a de que a ruptura dos vasa vasorum ocorre como um fenômeno secundário e não como um dos fatores causais na fisiopatologia do hematoma intramural.

Palavras-chave: Hematoma intramural da aorta, vasa vasorum, dissecção da aorta.




Vasa vasorum (VV) are small arteries which penetrate the arterial wall both through the luminal surface (vasa vasorum internae) and the adventitia (vasa vasorum externae). Adventitial VV ramify into smaller vessels supplying the outer media layers. Venous VV are more numerous and also supply mainly the outer media. In humans, arteries containing less than 29 cellular layers or less than 0.5 mm diameter do not present VV.1,2

Thanks to microcomputerized tomography, tridimensional study of these vessels became possible,3,4 as well as microarteriography have enabled a more thorough understanding of their anatomy and distribution5 through the injection of a silicone polymer (Microfil®; Flow Tech, U.S.).

VV seem to play a fundamental role in the physiopathology of the three acute aortic syndrome entities: aortic dissection, intramural hematoma (IMH), and penetrating ulcer.

VV reactivity

Anatomically VV are characterized by the presence of endothelial cells, smooth muscle cells and by being externally covered with connective tissue. These features are similar to those encountered in small coronary arteries, indicating that VV can regulate their own tone and consequently arterial wall perfusion.6-8 Isolated porcine aortic VV responded to endothelium-dependent vasodilator substance P and to bradykinin similarly to the native artery, confirming the afore mentioned autoregulating aspect.9,10

VV hemodynamics

VV's anatomic localization and ramification characteristics prevent the blood flow from reaching the inner media due to the compressive stress inside the arterial wall, as described by the Lamé's formula (Figure 1). This formula indicates that the compression stress in the arterial wall's interior equals the luminal pressure in subendothelial region, but decreases toward the adventitia.



Consequently, no wall perfusion may occur near the artery's lumen in the wall's site where tissue pressure exceeds vasa vasorum's pressure (determined mainly by pressure drop throughout the vasa vasorum, as described in Poiseulle's law).11

Flow resistance in the VV is high because its radius is considerably smaller than arterial lumen, especially in large arteries as the aorta. In the inner media the compression stresses are higher than VV's luminal pressure. However, these comments are related to a static condition, without considering the dynamics of systole and diastole. Systolic impulsion in the VV progresses throughout its rami and reaches the terminal rami with some delay if compared to the systolic pressure inside the native artery. Therefore, perfusion may be slightly higher than expected in a static state.11

Adventitial VV are connected through a plexus, but behave as terminal arteries; VV's microembolization reduces the density of these vessels in that point and increases the number of ramifications in areas of low blood suppliance.11 This characteristic may impact on spatial distribution of perfusion and arterial wall drainage. The fact that the highest concentration of atheroma plaques in the several arterial segments coincides anatomically with lower perfusion by the VV may be a direct evidence of the role these vessels play in atherosclerotic disease.1,2,11

The reason for pulmonary arteries and veins not developing atherosclerosis may be related to the decreased flow of solutes toward the wall's interior due to the lower intraluminal pressure. In these vessels, the VV are not compressed during the whole cardiac cycle, keeping the media's perfusion stable. On the other hand, VV plexus in large veins is more numerous than in arteries because, contrarily to what happens in the latter, transendothelial diffusion from the lumen does not supply the inner media with oxygen and nutrients.11

Interestingly, VV in humans are less numerous in abdominal aorta and is probably one reason for a greater chance in developing aneurysms. In other species, like dogs, VV are numerous in the abdominal aorta; characteristically, they do not develop aneurysms.12

Vasa vasorum and aortic dissection

For more than 4 decades it has been known that adventitia excision and, consequently, that of VV, leads to ischemia of the outer media.13 In 2000, Angouras et al.14 published a neat study in swine submitted to adventitia excision associated to intercostal ligature. After adventitia excision, the aorta was wrapped in non-porous material (polyvinyl chloride) to prevent periaortic fibrosis and neovascularization. After 15 days the pigs were sacrificed, and the material was sent to microscopy and in vitro mechanical analysis. VV flow interruption resulted in ischemic necrosis of the outer media, with complete loss of smooth muscle cells and elastin and collagen fibers' architecture. In several sections, features of wall dissection were present. In vitro mechanical analysis evidenced arterial wall stiffening, which was, in some specimens, four times higher than in control animals.

Hypertension, the chief condition associated with dissection, is accompanied by hypertrophy and hyperplasia of smooth muscle cells and increase in oxygen consumption. Chronic hypertension is associated with VV occlusion and neovascularization, increased arterial thickness and accelerated atherosclerosis. In hypertensive crisis, ischemia of the media may be aggravated by VV constriction. The inner media remains nourished by diffusion from the arterial lumen.15-22 These factors result in two regions with distinct characteristics in the media: a more elastic inner region and a stiffer outer region. Due to the differences in the two regions' elastic moduli, an increased shear stress occurs in this interface.

Vasa vasorum and intramural hematoma

IMH is the cause of 5-20% cases of acute aortic syndrome.23-25 The relation between VV rupture and intramural hematoma was first established in 1920 by Krukenberg et al.;26 since then, IMH has been accepted as a possible cause. IMH is by definition distinguished from acute dissection and hematoma secondary to penetrating ulcer due to the absence of an intimal rupture site. IMH without penetrating ulcer is usually more extensive, sometimes impairing the ascending aorta, arch and descending aorta. Most publications accept this cause-effect relationship between VV rupture and HI, but evidence is scarce, as observed by Sundt27 in a recent literature review. It seems difficult to explain how these small vessels with low intraluminal pressure may dissect big portions of the aorta and often lead to arterial wall rupture. This mechanism also does not explain why in penetrating ulcer the hematoma tends to be more restricted even when there is a direct communication between the lumen and the media. On the other hand, Park et al.28 have observed a 73% frequency of intimal rupture in patients with type A IMH (ascending aorta) who had been submitted to surgery with no preoperative defect detected by tomography. In other words, more than 70% of type A IMH patients were erroneously diagnosed, once intimal rupture was present.

In 2008, Grimm et al.29 suggested that small atheroma plaques was another mechanism for IMH development, affecting the whole thoracic aorta in eight of their treated patients; the authors related the plaques position with the greater or lesser extension of the lesion.

Despite the huge advances in imaging technology, as 128-multidetector computed tomography, IMH diagnosis is still controversial, since it is necessary to demonstrate the absence of intimal rupture to perform this diagnosis. In this context, the quality of the images is crucial. Distinguishing acute dissection with thrombosis of the false lumen from IMH is difficult, some authors prefer to define the lesion as dissection without reentry orifice.30-32

Discussion on pathophysiological causes of IMH may seem more philosophical than actually helpful for clinical practice, as stated by Reuthebuch,33 since most cases of type A IMH would be treated by open surgery, and type B IMH, observed with clinical treatment. Knowledge about pathophysiological mechanisms involved in the IMH genesis is notwithstanding desirable and may imply a change in some paradigms in prognosis and treatment in an age of rapid advances of methods and images.



As already established, IMH occurs in older patients, generally hypertensive. Complex structural and metabolic alterations of the aortic wall related with ischemia of the media are a substratum for the division of layers of this tunica, as observed above. VV rupture is probably a secondary phenomenon and occurs in other arterial territories, not accompanied by arterial wall lamination. Lower blood supply by the VV is probably involved in the pathophysiology of the three entities of acute aortic syndrome, but its importance in each of them is yet to be defined.



1. Wolinsky H, Glagov S. Nature of species differences in the medial distribution of aortic vasa vasorum in mammals. Cir Res. 1967;20:409-21.         [ Links ]

2. Okuyama K, Yagimuna G, Takahashi T, Sasaki H, Mori S. The development of vasa vasorum of the human aorta in various conditions. A morphometric study. Arch Pathol Lab Medicine. 1988;112:721-5.         [ Links ]

3. Barger AC, Beeuwkes R 3rd, Lainey LL, Silverman KJ. Hypothesis: vasa vasorum and neovascularization of human coronary arteries. A possible role in the pathophysiology of atherosclerosis. N Engl J Med. 1984;310:175-7.         [ Links ]

4. Gössl M, Malyar NM, Rosol M, Beighley PE, Ritman EL. Impact of coronary vasa vasorum functional structure on coronary vessel wall perfusion distribution. Am J Physiol Heart Circ Physiol. 2003;285:H2019-26.         [ Links ]

5. Den Hartog JP. Strength of Materials. New York: Dover Publications; 1949. p. 323.         [ Links ]

6. Scotland RS, Vallance PJ, Ahluwalia A. Endogenous factors involved in regulation of tone of arterial vasa vasorum: implications for conduit vessel physiology. Cardiovasc Res. 2000;46:403-11.         [ Links ]

7. Heistad D, Marcus M, Martin J. Effects of neural stimuli on blood flow through vasa vasorum in dogs. Circ Res. 1979;45:615-20.         [ Links ]

8. Heistad D, Marcus ML. Role of vasa vasorum in nourishment of the aorta. Blood Vessels. 1979;16:225-38.         [ Links ]

9. Nikol S, Pelisek J, Engelmann MG, et al. Vascular endothelial growth factor (VEGF165) and its influence on angiogenesis versus arteriogenesis in different vascular beds. J Endovasc Ther. 2002;9:842-54.         [ Links ]

10. Nikol S, Engelmann MG, Pelisek J, et al. Local perivascular application of low amounts of a plasmid encoding for vascular endothelial growth factor (VEGF165) is efficient for therapeutic angiogenesis in pigs. Acta Physiol Scand. 2002;176:151-9.         [ Links ]

11. Erik L, Ritman EL, Lerman A. The Dynamic Vasa Vasorum. Cardiovasc Res. 2007;75:649-58.         [ Links ]

12. Gössl M, Rosol M, Malyar NM, et al. Functional anatomy and hemodynamic characteristics of vasa vasorum in the walls of porcine coronary arteries. Anat Rec A Discov Mol Cell Evol Biol. 2003;272:526-37        [ Links ]

13. Wilens SL, Malcolm JA, Vazquez JM. Experimental infarction (medial necrosis) of the dog's aorta. Am J Pathol 1965;47:695-711.         [ Links ]

14. Angouras D, Sokolis DP, Dosios T, et al. Karayannacosa: Effect of impaired vasa vasorum flow on the structure and mechanics of the thoracic aorta: implications for the pathogenesis of aortic dissection. Eur J Cardiothorac Surg. 2000;17:468-73.         [ Links ]

15. Heistad DD, Marcus ML, Law EG, Armstrong ML, Ehrhardt JC, Abboud FM. Regulation of blood flow to the aortic media in dogs. J Clin Invest. 1978;62:133-40.         [ Links ]

16. Marcus ML, Heistad DD, Law EG, Armstrong ML, Abboud FM. Effects of chronic hypertension on vasa vasorum in the thoracic aorta. Cardiovasc Res. 1985;19:777-81        [ Links ]

17. Ohhira A, Ohhashi T. Effects of aortic pressure and vasoactive agents on the vascular resistance of the vasa vasorum in canine isolated thoracic aorta. J Physiol (Lond). 1992;453:233-45        [ Links ]

18. Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol. 1984;53:849-55.         [ Links ]

19. Roberts WC. Aortic dissection: anatomy, consequences and causes. Am Heart J. 1981;101:195-214.         [ Links ]

20. Olivetti G, Melissari M, Marchetti G, Anversa P. Quantitative structural changes of the rat thoracic aorta in early spontaneous hypertension. Tissue composition, and hypertrophy and hyperplasia of smooth muscle cells. Circ Res. 1982;51:19-26.         [ Links ]

21. Kosan RL, Burton AC. Oxygen consumption of arterial smooth muscle as a function of active tone and passive stretch. Circ Res. 1966;18:79-88.         [ Links ]

22. Jones RM. Mechanics of composite materials. Washington: Scripta Book Company; 1975. p. 210-22.         [ Links ]

23. Evangelista A, Mukherjee D, Mehta RH, et al. Acute intramural hematoma of the aorta: a mystery in evolution. Circulation. 2005;111:1063-70.         [ Links ]

24. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis, Circulation. 2002;106:342-8.         [ Links ]

25. Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: Part I. From etiology to diagnostic strategies. Circulation. 2003;108:628-35.         [ Links ]

26. Krukenberg E. Beitrage zur frage des aneurysma dissecans. Beitr Pathol Anat Allg Pathol. 1920;67:329-51.         [ Links ]

27. Sundt TM. Intramural hematoma and penetrating atherosclerotic ulcer of the aorta. Ann Thorac Surg. 2007;83:S835-41.         [ Links ]

28. Park KH, Lim C. Choi JO, et al. Prevalence of aortic intimal defect in surgically treated acute type A intramural hematoma. Ann Thorac Surg. 2008;86:1494-500.         [ Links ]

29. Grimm M, Loewe C, Gottardi R, et al. Novel insights into the mechanisms and treatment of intramural hematoma affecting the entire thoracic aorta. Ann Thorac Surg. 2008;86:453-56.         [ Links ]

30. Matsuo H. The thrombosed type of aortic dissection-its clinical features and diagnosis. Int J Angiol. 1998;7:329-34.         [ Links ]

31. Matsuo H. Recognition and management of thrombosed type of aortic dissection with long-term follow-up results. Int J Angiol. 2000;9:27-30.         [ Links ]

32. Takagi H, Manabe H, Kawai N, Goto S, Umemoto T. Thrombosed-type acute aortic dissection. Ann Thorac Surg. 2009;88:1389.         [ Links ]

33. Reuthebuch O. Invited commentary. Ann Thorac Surg. 2008;86:1501.         [ Links ]



Adamastor Humberto Pereira

Manuscript received Jan 11 2010, accepted for publication Feb 04 2010.



No conflicts of interest declared concerning the publication of this article.

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