J Thorac Cardiovasc Surg 2006;131:1421-1422
© 2006 The American Association for Thoracic Surgery
Reply to the Editor
George Koullias, MD,
Raj Modak, MD,
Paul Barash, MD,
John A. Elefteriades, MD
Section of Cardiovascular Surgery and Department of Anesthesia, Yale University School of Medicine, 333 Cedar St (121 FMB), New Haven, CT 06510
(Email: john.elefteriades{at}yale.edu).
Our team wishes to thank Dr Sundt for his extremely kind comments regarding our scientific investigations at the Center for Thoracic Aortic Disease at Yale University. We agree entirely with Dr Sundt that "residual strain" represents yet another facet of the complex mechanical behavior and measurable properties of the aortic wall. He and his colleagues, in the important work they cite in their letter, have measured this phenomenon in human aortas. From an engineering standpoint, residual strain is considered more important in thick-walled tubes (ratio of wall thickness to vessel diameter >1:10). The aneurysmal aorta is often thin-walled (thickness of 2-3 mm in a vessel with a diameter 
5 cm) and often becomes even more so as the aneurysmal process advances (Figure 1). Thus the effect of residual strain, although an important inherent design characteristic of the human aorta, might diminish as the aneurysmal state advances.
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Figure 1. The opened wall of a large ascending aortic aneurysm. Note that the wall of the aorta has become so thin that the markings on a ruler can be read right through the aortic wall.
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We also have observed regional differences in stress distribution and resultant strain. In our echocardiographic studies on normal and aneurysmal ascending aortas, we have consistently found that the anterior wall of the aorta (the "greater curve," so to speak) expands more than the posterior wall. These data were recently presented at the American Society of Anesthesiologists meeting in Las Vegas (October 23-27, 2004). This finding agrees with the mechanical concept that an unsupported tissue layer (the anterior wall) experiences more stress compared with a supported layer (the posterior wall, which is supported by the pulmonary artery and the associated central mediastinal fibrous tissues). These findings validate and support the importance of regional variations in mechanical properties of the aorta that Dr Sundt and colleagues have detected.
We share Dr Sundt's skepticism regarding ruptured vasa vasorum as the cause of intramural hematoma. In fact, prompted by an insightful observation by Dr Kouchoukos some years ago, we have scrutinized the internal lining of the widely opened aorta during deep hypothermic arrest in cases of intramural hematoma. In most, but not all, cases one can find an intimal tear that was not appreciated even on high-quality preoperative radiographic images. In a small minority of cases, no intimal tear exists. It is specifically to explain such no-tear intramural hematomas that the concept of rupture of the vasa vasorum has been postulated. Also, our echocardiographic measurements have confirmed Dr Sundt's hypothesis that stress on the adventitia is greater than stress on the media. We agree with Dr Sundt that uneven distribution of wall stress across the layers of the aortic wall might play a role in the genesis of intramural hematoma. This thesis awaits scientific confirmation.
