John A Elefteriades1. 1. Division of Cardiothoracic Surgery, Yale University Medical Center, 333 Cedar Street, Room 121 FMB, New Haven, Connecticut 06510, USA. john.elefteriades@yale.edu
Abstract
BACKGROUND: The purpose of the present study was to use the clinical database at the Yale University Center for Thoracic Aortic Disease to shed light on the pathophysiology of thoracic aortic aneurysm (TAA), the clinical behavior of thoracic aortic aneurysm, and the optimal clinical management. MATERIALS AND METHODS: The Yale database contains information on 3,000 patients with thoracic aortic aneurysm, with 9,000 patient-years of follow-up and 9,000 imaging studies. Advanced statistical techniques were applied to this information. RESULTS: Analysis provided the following observations: (1) TAA is a genetic disease with a predominantly autosomal dominant mode of inheritance, (2) matrix metalloproteinase (MMP) enzymes are activated in the pathogenesis of TAA, (3) wall tension in TAA approaches the tensile limits of aortic tissue at a diameter of 6 cm, (4) by the time a TAA reaches a clinical diameter of 6 cm, 34% of affected patients have suffered dissection or rupture, (5) extreme physical exertion or severe emotion often precipitate acute dissection, and (6) single nucleotide polymorphisms (SNPs) are being identified which predispose a patient to TAA. CONCLUSIONS: The "playbook" of TAA is gradually being read, with the help of scientific investigations, positioning practitioners to combat this lethal disease more effectively than ever before.
BACKGROUND: The purpose of the present study was to use the clinical database at the Yale University Center for Thoracic Aortic Disease to shed light on the pathophysiology of thoracic aortic aneurysm (TAA), the clinical behavior of thoracic aortic aneurysm, and the optimal clinical management. MATERIALS AND METHODS: The Yale database contains information on 3,000 patients with thoracic aortic aneurysm, with 9,000 patient-years of follow-up and 9,000 imaging studies. Advanced statistical techniques were applied to this information. RESULTS: Analysis provided the following observations: (1) TAA is a genetic disease with a predominantly autosomal dominant mode of inheritance, (2) matrix metalloproteinase (MMP) enzymes are activated in the pathogenesis of TAA, (3) wall tension in TAA approaches the tensile limits of aortic tissue at a diameter of 6 cm, (4) by the time a TAA reaches a clinical diameter of 6 cm, 34% of affected patients have suffered dissection or rupture, (5) extreme physical exertion or severe emotion often precipitate acute dissection, and (6) single nucleotide polymorphisms (SNPs) are being identified which predispose a patient to TAA. CONCLUSIONS: The "playbook" of TAA is gradually being read, with the help of scientific investigations, positioning practitioners to combat this lethal disease more effectively than ever before.
Authors: Ryan R Davies; Amy Gallo; Michael A Coady; George Tellides; Donald M Botta; Brendan Burke; Marcus P Coe; Gary S Kopf; John A Elefteriades Journal: Ann Thorac Surg Date: 2006-01 Impact factor: 4.330
Authors: J A Elefteriades; J Hartleroad; R J Gusberg; A M Salazar; H R Black; G S Kopf; J C Baldwin; G L Hammond Journal: Ann Thorac Surg Date: 1992-01 Impact factor: 4.330
Authors: T Juvonen; M A Ergin; J D Galla; S L Lansman; J N McCullough; K Nguyen; C A Bodian; M P Ehrlich; D Spielvogel; J J Klein; R B Griepp Journal: J Thorac Cardiovasc Surg Date: 1999-04 Impact factor: 5.209
Authors: M A Coady; J A Rizzo; G L Hammond; D Mandapati; U Darr; G S Kopf; J A Elefteriades Journal: J Thorac Cardiovasc Surg Date: 1997-03 Impact factor: 5.209
Authors: Ryan R Davies; Lee J Goldstein; Michael A Coady; Shawn L Tittle; John A Rizzo; Gary S Kopf; John A Elefteriades Journal: Ann Thorac Surg Date: 2002-01 Impact factor: 4.330
Authors: Alik Farber; Willis H Wagner; David V Cossman; J Louis Cohen; Daniel B Walsh; Mark F Fillinger; Jack L Cronenwett; Stephen R Lauterbach; Phillip M Levin Journal: J Vasc Surg Date: 2002-08 Impact factor: 4.268