Download PDF
Int J Angiol 2014; 23(03): 177-182
DOI: 10.1055/s-0034-1382288
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Ascending Thoracic Aortic Aneurysms Protect Against Myocardial Infarctions

Katherine Chau
1   Aortic Institute at Yale-New Haven, Yale University, School of Medicine, New Haven, Connecticut
,
John A. Elefteriades
1   Aortic Institute at Yale-New Haven, Yale University, School of Medicine, New Haven, Connecticut
› Author Affiliations
Further Information

Publication History

Publication Date:
28 August 2014 (online)

    Permissions and Reprints

Abstract

There has been increasing evidence that ascending thoracic aortic aneurysms (TAAs) protect against atherosclerosis. However, there have been no studies examining the relationship between ascending TAAs and clinical endpoints of atherosclerosis, such as stroke or peripheral arterial disease. In this study, we aim to characterize the relationship between TAAs and a specific clinical endpoint of atherosclerosis, myocardial infarction (MI). We compared prevalence of coronary artery disease (CAD) and MIs in 487 patients who underwent surgical repair for ascending TAAs to 500 control patients who did not have an ascending TAA. Multivariate binary logistic regression was used to calculate the odds of having MI if a patient had an ascending TAA versus any of several MI risk factors. There was a significantly lower prevalence of CAD and MI in the ascending TAA group than in the control TAA group. The odds of having a MI if a patient had a MI risk factor were all > 1 (more likely to have a MI), with the lowest statistically significant odds ratio being 1.54 (age; p = 0.001) and the highest being 14.9 (family history of MI; p < 0.001). The odds ratio of having a MI if a patient had an ascending TAA, however, was near 0 at 0.05 (p < 0.001). This study provides evidence that ascending TAAs protect against MIs, adding further support to the hypothesis that ascending TAAs protect against atherosclerotic disease.

Keywords

atherosclerosis - cardiovascular risk factors - coronary artery - myocardial infarction - aneurysm - acute coronary syndrome - infarction
 

  • References

  • 1 Ramanath VS, Oh JK, Sundt III TM, Eagle KA. Acute aortic syndromes and thoracic aortic aneurysm. Mayo Clin Proc 2009; 84 (5) 465-481
    CrossrefPubMedGoogle Scholar
  • 2 Kuzmik GA, Sang AX, Elefteriades JA. Natural history of thoracic aortic aneurysms. J Vasc Surg 2012; 56 (2) 565-571
    CrossrefPubMedGoogle Scholar
  • 3 Buxton DB. Molecular imaging of aortic aneurysms. Circ Cardiovasc Imaging 2012; 5 (3) 392-399
    CrossrefPubMedGoogle Scholar
  • 4 Cornuz J, Sidoti Pinto C, Tevaearai H, Egger M. Risk factors for asymptomatic abdominal aortic aneurysm: systematic review and meta-analysis of population-based screening studies. Eur J Public Health 2004; 14 (4) 343-349
    CrossrefPubMedGoogle Scholar
  • 5 Johnsen SH, Forsdahl SH, Singh K, Jacobsen BK. Atherosclerosis in abdominal aortic aneurysms: a causal event or a process running in parallel? The Tromsø study. Arterioscler Thromb Vasc Biol 2010; 30 (6) 1263-1268
    CrossrefPubMedGoogle Scholar
  • 6 Kaschina E, Scholz H, Steckelings UM , et al. Transition from atherosclerosis to aortic aneurysm in humans coincides with an increased expression of RAS components. Atherosclerosis 2009; 205 (2) 396-403
    CrossrefPubMedGoogle Scholar
  • 7 Nakashima Y, Kurozumi T, Sueishi K, Tanaka K. Dissecting aneurysm: a clinicopathologic and histopathologic study of 111 autopsied cases. Hum Pathol 1990; 21 (3) 291-296
    CrossrefPubMedGoogle Scholar
  • 8 Agmon Y, Khandheria BK, Meissner I , et al. Is aortic dilatation an atherosclerosis-related process? Clinical, laboratory, and transesophageal echocardiographic correlates of thoracic aortic dimensions in the population with implications for thoracic aortic aneurysm formation. J Am Coll Cardiol 2003; 42 (6) 1076-1083
    CrossrefPubMedGoogle Scholar
  • 9 Kojima S, Suwa S, Fujiwara Y , et al. Incidence and severity of coronary artery disease in patients with acute aortic dissection: comparison with abdominal aortic aneurysm and arteriosclerosis obliterans [in Japanese]. J Cardiol 2001; 37 (3) 165-171
    PubMedGoogle Scholar
  • 10 Islamoğlu F, Atay Y, Can L , et al. Diagnosis and treatment of concomitant aortic and coronary disease: a retrospective study and brief review. Tex Heart Inst J 1999; 26 (3) 182-188
    PubMedGoogle Scholar
  • 11 Ayyash B, Tranquilli M, Elefteriades JA. Femoral artery cannulation for thoracic aortic surgery: safe under transesophageal echocardiographic control. J Thorac Cardiovasc Surg 2011; 142 (6) 1478-1481
    CrossrefPubMedGoogle Scholar
  • 12 Achneck H, Modi B, Shaw C , et al. Ascending thoracic aneurysms are associated with decreased systemic atherosclerosis. Chest 2005; 128 (3) 1580-1586
    CrossrefPubMedGoogle Scholar
  • 13 Hung A, Zafar M, Mukherjee S, Tranquilli M, Scoutt LM, Elefteriades JA. Carotid intima-media thickness provides evidence that ascending aortic aneurysm protects against systemic atherosclerosis. Cardiology 2012; 123 (2) 71-77
    CrossrefPubMedGoogle Scholar
  • 14 Grainger DJ. Transforming growth factor β and atherosclerosis: so far, so good for the protective cytokine hypothesis. Arterioscler Thromb Vasc Biol 2004; 24 (3) 399-404
    CrossrefPubMedGoogle Scholar
  • 15 Nataatmadja M, West J, West M. Overexpression of transforming growth factor-β is associated with increased hyaluronan content and impairment of repair in Marfan syndrome aortic aneurysm. Circulation 2006; 114 (1, Suppl): I371-I377
    CrossrefPubMedGoogle Scholar
  • 16 Neptune ER, Frischmeyer PA, Arking DE , et al. Dysregulation of TGF-beta activation contributes to pathogenesis in Marfan syndrome. Nat Genet 2003; 33 (3) 407-411
    CrossrefPubMedGoogle Scholar
  • 17 McCaffrey TA. TGF-betas and TGF-β receptors in atherosclerosis. Cytokine Growth Factor Rev 2000; 11 (1-2) 103-114
    CrossrefPubMedGoogle Scholar
  • 18 Silence J, Collen D, Lijnen HR. Reduced atherosclerotic plaque but enhanced aneurysm formation in mice with inactivation of the tissue inhibitor of metalloproteinase-1 (TIMP-1) gene. Circ Res 2002; 90 (8) 897-903
    CrossrefPubMedGoogle Scholar
  • 19 Lemaître V, O'Byrne TK, Borczuk AC, Okada Y, Tall AR, D'Armiento J. ApoE knockout mice expressing human matrix metalloproteinase-1 in macrophages have less advanced atherosclerosis. J Clin Invest 2001; 107 (10) 1227-1234
    CrossrefPubMedGoogle Scholar
  • 20 Koullias GJ, Ravichandran P, Korkolis DP, Rimm DL, Elefteriades JA. Increased tissue microarray matrix metalloproteinase expression favors proteolysis in thoracic aortic aneurysms and dissections. Ann Thorac Surg 2004; 78 (6) 2106-2110 , discussion 2110–2111
    CrossrefPubMedGoogle Scholar
  • 21 Silence J, Lupu F, Collen D, Lijnen HR. Persistence of atherosclerotic plaque but reduced aneurysm formation in mice with stromelysin-1 (MMP-3) gene inactivation. Arterioscler Thromb Vasc Biol 2001; 21 (9) 1440-1445
    CrossrefPubMedGoogle Scholar
  • 22 McCaffrey TA, Consigli S, Du B , et al. Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1. J Clin Invest 1995; 96 (6) 2667-2675
    CrossrefPubMedGoogle Scholar
  • 23 Mallat Z, Gojova A, Marchiol-Fournigault C , et al. Inhibition of transforming growth factor-beta signaling accelerates atherosclerosis and induces an unstable plaque phenotype in mice. Circ Res 2001; 89 (10) 930-934
    CrossrefPubMedGoogle Scholar
  • 24 Lutgens E, Gijbels M, Smook M , et al. Transforming growth factor-beta mediates balance between inflammation and fibrosis during plaque progression. Arterioscler Thromb Vasc Biol 2002; 22 (6) 975-982
    CrossrefPubMedGoogle Scholar
  • 25 Ye S, Eriksson P, Hamsten A, Kurkinen M, Humphries SE, Henney AM. Progression of coronary atherosclerosis is associated with a common genetic variant of the human stromelysin-1 promoter which results in reduced gene expression. J Biol Chem 1996; 271 (22) 13055-13060
    CrossrefPubMedGoogle Scholar
  • 26 Vaughan CJ, Casey M, He J , et al. Identification of a chromosome 11q23.2-q24 locus for familial aortic aneurysm disease, a genetically heterogeneous disorder. Circulation 2001; 103 (20) 2469-2475
    CrossrefPubMedGoogle Scholar
  • 27 Humphries SE, Luong LA, Talmud PJ , et al. The 5A/6A polymorphism in the promoter of the stromelysin-1 (MMP-3) gene predicts progression of angiographically determined coronary artery disease in men in the LOCAT gemfibrozil study. Lopid Coronary Angiography Trial. Atherosclerosis 1998; 139 (1) 49-56
    CrossrefPubMedGoogle Scholar
  • 28 Andreotti F, Porto I, Crea F, Maseri A. Inflammatory gene polymorphisms and ischaemic heart disease: review of population association studies. Heart 2002; 87 (2) 107-112
    CrossrefPubMedGoogle Scholar
  • 29 Kempf K, Haltern G, Füth R , et al. Increased TNF-alpha and decreased TGF-beta expression in peripheral blood leukocytes after acute myocardial infarction. Horm Metab Res 2006; 38 (5) 346-351
    Article in Thieme ConnectPubMedGoogle Scholar
  • 30 Yokota M, Ichihara S, Lin TL, Nakashima N, Yamada Y. Association of a T29—>C polymorphism of the transforming growth factor-beta1 gene with genetic susceptibility to myocardial infarction in Japanese. Circulation 2000; 101 (24) 2783-2787
    CrossrefPubMedGoogle Scholar
  • 31 Koch W, Hoppmann P, Mueller JC, Schömig A, Kastrati A. Association of transforming growth factor-beta1 gene polymorphisms with myocardial infarction in patients with angiographically proven coronary heart disease. Arterioscler Thromb Vasc Biol 2006; 26 (5) 1114-1119
    CrossrefPubMedGoogle Scholar
  • 32 Grainger DJ, Metcalfe JC. Tamoxifen: teaching an old drug new tricks? . Nat Med 1996; 2 (4) 381-385
    CrossrefPubMedGoogle Scholar
  • 33 Saitta A, Morabito N, Frisina N , et al. Cardiovascular effects of raloxifene hydrochloride. Cardiovasc Drug Rev 2001; 19 (1) 57-74
    PubMedGoogle Scholar