Controversies in Aortic Dissection and Aneurysmal Disease by Robert S. Bonser, Domenico Pagano, Axel Haverich, Jorge

By Robert S. Bonser, Domenico Pagano, Axel Haverich, Jorge Mascaro

In this booklet the authors evaluation the surgical administration of sufferers with aortic affliction. This frequently arguable region of administration finds many ideas open to cardiovascular expert. This reference stories each one controversy and gives useful solutions to the cardiac health care provider and should aid them demonstrate the spectrum of issues and their management.

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Life expectancy in the Marfan syndrome. Am J Cardiol. 1995;75:157–60. 13 12. Milewicz DM, Dietz HC, Miller DC. Treatment of aortic disease in patients with Marfan syndrome. Circulation. 2005;111:e150–7. 13. Neptune ER, Frischmeyer PA, Arking DE, et al. Dysregulation of TGF-beta activation contributes to pathogenesis in Marfan syndrome. Nat Genet. 2003;33: 407–11. 14. Habashi JP, Judge DP, Holm TM, et al. Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome. Science.

2) [92, 93, 95]. Some surgeons express the law of Laplace as the simple clinical rule that “gradual, continuous dilatation is the sine qua non of aortic dissection” [92], or even simpler, “that a balloon blown up to its limit of elasticity would pop” [1]. Indeed, many studies were performed to establish a “size-­ rupture correlation” [49, 96–100]. Finally, based on their analysis of 54 patients with ascending aortic aneurysms, Coady et al. 1 percentage points [49]. 5 cm of the ascending aorta in idiopathic aneurysm is based on this “hinge- point” finding in 54 TAAD patients [101].

46. Dasouki M, Markova D, Garola R, et al. Compound heterozygous mutations in fibulin-4 causing neonatal lethal pulmonary artery occlusion, aortic aneurysm, arachnodactyly, and mild cutis laxa. Am J Med Genet A. 2007;143A:2635–41. 47. Renard M, Holm T, Veith R, et al. Altered TGFbeta signaling and cardiovascular manifestations in patients with autosomal recessive cutis laxa type I caused by fibulin-4 deficiency. Eur J Hum Genet. 2010;18:895–901. 48. Braverman AC, Guven H, Beardslee MA, Makan M, Kates AM, Moon MR.

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