Surgical versus endovascular treatment of acute thoracic aortic rupture: a single-center experience

Doss, Mirko; Balzer, J. O.; Martens, Sven; Wood, Jeffrey P.; Wimmer‐Greinecker, Gerhard; Fieguth, Hans‐Gerd; Moritz, Anton

doi:10.1016/s0003-4975(03)00877-4

Cited by 108 publications

(87 citation statements)

References 16 publications

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“…Whereas emergency surgery can be life saving for aneurysm patients (6), there is no cure for emphysema (7). These diseases are caused by various changes in the extracellular matrix (ECM) that lead to a weakening of ECM.…”

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confidence: 99%

A zipper network model of the failure mechanics of extracellular matrices

Ritter

Jesudason²,

Majumdar³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Mechanical failure of soft tissues is characteristic of life-threatening diseases, including capillary stress failure, pulmonary emphysema, and vessel wall aneurysms. Failure occurs when mechanical forces are sufficiently high to rupture the enzymatically weakened extracellular matrix (ECM). Elastin, an important structural ECM protein, is known to stretch beyond 200% strain before failing. However, ECM constructs and native vessel walls composed primarily of elastin and proteoglycans (PGs) have been found to fail at much lower strains. In this study, we hypothesized that PGs significantly contribute to tissue failure. To test this, we developed a zipper network model (ZNM), in which springs representing elastin are organized into long wavy fibers in a zipper-like formation and placed within a network of springs mimicking PGs. Elastin and PG springs possessed distinct mechanical and failure properties. Simulations using the ZNM showed that the failure of PGs alone reduces the global failure strain of the ECM well below that of elastin, and hence, digestion of elastin does not influence the failure strain. Network analysis suggested that whereas PGs drive the failure process and define the failure strain, elastin determines the peak and failure stresses. Predictions of the ZNM were experimentally confirmed by measuring the failure properties of engineered elastin-rich ECM constructs before and after digestion with trypsin, which cleaves the core protein of PGs without affecting elastin. This study reveals a role for PGs in the failure properties of engineered and native ECM with implications for the design of engineered tissues.elastin ͉ strain ͉ stress ͉ trypsin T issue failure is characteristic of several life-threatening diseases, including capillary stress failure in the lung (1), pulmonary emphysema (2), vessel wall aneurysms (3, 4), and prosthetic heart valve failure (5). Whereas emergency surgery can be life saving for aneurysm patients (6), there is no cure for emphysema (7). These diseases are caused by various changes in the extracellular matrix (ECM) that lead to a weakening of ECM. A better understanding of the structure of the ECM, and how its components contribute to functional behavior (8), is necessary to provide insight into the development and progression of these diseases and will also be important if future tissue-engineered constructs are to be implanted in the body.Elastin, collagen, and proteoglycans (PGs) are the principle components that form the complex structural network of the ECM that is necessary for tissues to function properly (9). Elastin and collagen are fibrous proteins capable of carrying loads and resisting tension (10, 11). PGs make up the gel in which elastin and collagen fibers are embedded and are necessary for the stability of the ECM (12). Varying the structure and composition of the ECM has major effects on its mechanical (9, 13-15) and failure properties (3,(16)(17)(18)(19)(20)(21).Independently, 2 groups have obtained similar surprising results related to failure of t...

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mentioning

confidence: 99%

A zipper network model of the failure mechanics of extracellular matrices

Ritter

Jesudason²,

Majumdar³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Since then, several authors have reported successful endovascular treatment of both chronic and acute lesions of the thoracic aorta (Dake, 2001;Kato et al, 1997;Fujikawa et al, 2001;Lachat et al, 2002;Czermak et al, 2002;Amabile et al, 2004;Dunham et al, 2004;Hoornweg et al, 2006;Alsac et al, 2008;Kaya et al, 2009). Despite advances in surgical techniques, surgery for acute thoracic aortic rupture is associated with high morbidity and mortality rates (Doss et al, 2003;Dake et al, 1994). Open thoracic aortic repair carries the risk of severe complications affecting the heart, lungs, kidneys, and nervous system (spinal cord ischemia), with frequencies as high as 50% (Lachat et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Endovascular Repair of Thoracic Aortic Emergencies

Ribé¹,

Portero²,

Solis³

et al. 2011

Diagnosis and Treatment of Abdominal and Thoracic Aortic Aneurysms Including the Ascending Aorta and the Aortic Arch

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“…Nevertheless, even when cases of rupture are included, the mortality rates are equivalent or better than those for the surgical repair of stable patients (15-40%). [21][22][23][24] One of the limitations of this study, as with other studies on this topic, is the inability to gauge the prevalence of PTAU in the general population or in the context of patients presenting with thoracic aortic pathologies. Similarly, we are unable to comment on the natural history of asymptomatic or incidental PTAU.…”

Section: Discussionmentioning

confidence: 99%

Short series of emergency stent-graft repair of symptomatic penetrating thoracic aortic ulcers (PTAU)

et al. 2009

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Acute penetrating thoracic aortic ulcers (PTAU) are associated with vessel rupture, particularly when intramural haematoma (IMH) is present. Although surgical repair is the treatment of choice for PTAU in the aortic arch, definitive treatment of PTAU in other locations of the thoracic aorta remains controversial, particularly in this frail cohort of patients. Recent series of elective and semi-elective endovascular stent-graft repair of PTAU of the descending thoracic aorta show comparable results with the previously advocated best medical management. We report our results from a retrospective, observational study of acute stent-graft repair of symptomatic PTAU. Between 2000 and 2005, 11 patients (seven male, four female; median age 71 years) presented with acute PTAU. CT scans demonstrated an associated IMH in six, a contained leak in three or rupture in four unstable patients. All were covered by a single endovascular stent [Gore (5), Talent (5), Zenith (1); 10 inserted via the groin and one via iliac conduit within 1 week of presentation (five < 24 h). Technical success was 90.90% (10/11) and 3/11 (27%) died within 30 days (two ARDS, one a persistent leak and rupture at 48 h). One patient developed transient paraplegia; three haemothoraces required chest drains, one of which subsequently required empyema drainage. In survivors, CT scans were satisfactory, with no further intervention required at 32.5 (6-66) months of median follow-up. In conclusion, endovascular management of acute PTAU appears effective and durable with mortality rates that are likely to be better than for open surgery. However, haemodynamic compromise at presentation remains a robust denominator of over-all survival.

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Surgical versus endovascular treatment of acute thoracic aortic rupture: a single-center experience

Cited by 108 publications

References 16 publications

A zipper network model of the failure mechanics of extracellular matrices

A zipper network model of the failure mechanics of extracellular matrices

Endovascular Repair of Thoracic Aortic Emergencies

Short series of emergency stent-graft repair of symptomatic penetrating thoracic aortic ulcers (PTAU)

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