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Age-dependent aortic elongation: a new predictor for type A aortic dissection?
  1. Ibrahim Akin1,2,
  2. Christoph A Nienaber3
  1. 2 DZHK, DZHK (Deutsches Zentrum für Herz-Kreislaufforschung), Mannheim, Germany
  2. 1 Cardiology, Universitätsmedizin Mannheim, Mannheim, Germany
  3. 3 Cardiology and Aortic Centre, Royal Brompton Hospital and Harefield Trust, London, UK
  1. Correspondence to Professor Ibrahim Akin; Ibrahim.Akin{at}

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Aortic dissection is a relatively rare condition with catastrophic outcomes if left untreated. The classification of this pathology is essentially based on its anatomical location or acuity. Data from the International Registry for Acute Aortic Dissection (IRAD) revealed that in the absence of immediate surgical repair, acute type A aortic dissection (ATAAD) is associated with a 24% mortality in the first 24 hours, 29% at 48 hours, 44% at day 7 and 50% after 2 weeks. Despite major advances in diagnostic yield, the early clinical diagnosis of aortic dissection remains elusive in up to 38% of patients. Furthermore, in 28% of cases the correct diagnosis was ascertained only after postmortem examination.1

The most common risk factor associated with aortic dissection is systemic hypertension, with up to 72%. Particularly in the elderly, other major risk factors include atherosclerosis, prior cardiac surgery and known aortic aneurysms. With younger age (<40 years), hereditary conditions of aortopathology (eg, Marfan syndrome and other genetic factors) constitute a significant fraction of cases of aortic dissection.1

Despite recent advances in identifying structural and biomechanical properties of the aorta in vivo, a variety of determinants for the evolution to an aortic dissection are still unclear. The common denominator is a weakening of the aortic tunica media, which predisposes to dissection by splitting the cohesive layers of the aortic wall. This weakening of the tunica media could be due to either a derangement or possibly a loss of structural elements in the media layer, including elastin, collagen, non-fibrous matrix and smooth muscle cells.

Aortic diameter is currently the best-evaluated predictor for aortic dissection with specific ‘hinge points’ at which rupture or dissection is increasingly likely to occur. These hinge points are set at around 6 cm for the ascending aorta and 7 cm for the descending aorta,2 with current recommendations for preventive treatment when the diameter exceeds 5.5 cm regardless of location. For patients with Marfan syndrome or other hereditary conditions, bicuspid aortic valve or family history of aortic dissection, the threshold is set lower at 4.5 cm2 or 5.0 cm3. Interestingly, a substantial number of patients dissect at an aortic diameter less than 5.5 cm. The IRAD registry showed nearly 60% of patients with type A dissection had an aortic diameter <5.5 cm and almost 40% had diameters <5.0 cm,4 suggesting that aortic diameter alone is an insufficient marker to predict the risk of dissection, and highlighting the need for better predictors.

A detailed discussion on aortic dimensions and geometry in healthy individuals and in patients with ATAAD was presented in the Heart paper. The first article evaluated the aortic length of 210 consecutive routine non-dissected patients with contemporary CT. The length of the thoracic aorta was significantly related to age (r=0.54; p<0.001), with an increase of 59 mm in men and 66 mm in women noticed between the ages of 20 and 80 years, reflecting a longitudinal growth to approximately 125%. Such correlation was found for the ascending aorta, arch and proximal part of the descending aorta, while the distal part of the descending thoracic aorta failed to show such a relationship between age and length (p=0.178). Elongation was most prominent in the proximal part of the descending thoracic aorta (247%), followed by the arch (169%) and the ascending thoracic aorta (142%). Additionally, a change in geometry was noticed by a distalward shift in the aortic apex from type I to type II aorta.5

A separate back-to-back publication compared the control group with 40 patients with ATAAD and adjusted the data to predissection dimensions. Elongation of the ascending aorta and diameter proved both to be independent predictors of dissection (OR=5.3, CI 2.5 to 11.4, p<0.001; OR=8.6, CI 2.4 to 31.0, p=0.001, respectively). The ascending aorta was longer and more dilated in patients with ATAAD compared with healthy controls (78.6±8.8 mm vs 68.9±7.2 mm, p<0.001; 34.4±3.2 mm vs 39.4±5.7 mm, p<0.001, respectively). Meanwhile, longitudinal elongation in both the aortic arch and the descending aorta was not predictive.6

Current guidelines regarding replacement of ascending aorta are based on diameters only. Interestingly, of the 343 patients who had undergone CT angiography <2 years before and within 12 hours after aortic dissection onset, 334 (97%) patients had an ascending aorta diameter of <5.5 cm and 315 (92%) patients had a diameter <5 cm before dissection.7 Similar to the IRAD experience,4 more than 60% of women and 70% of men had a non-dilated ascending aorta before the onset of a type A dissection,8 corroborating a need for more powerful aortic event predictors.

This could be elongation of the ascending aorta as suggested and emphasised by the Maastricht group. It is generally believed that the aorta and large elastic arteries become tortuous with ageing. In this regard, the cross-sectional, propensity-matched study of non-cardiovascular patients was helpful in evaluating the geometric change during the ageing process dominated by lifelong exposure to pulsatile strain resulting in fracture and breakdown of elastin. Besides elongation and dilatation, this theory explains the age-related vascular stiffening as the reduction of elastin content impairs vessel compliance. Elastin content is highest in the aortic arch and proximal descending aorta. Furthermore, the mobile proximal aortic segments can move relatively free in the longitudinal direction as compared with the fixed distal parts. As circumferential strain values are comparable throughout the entire thoracic aorta, this provides a plausible explanation for an increasing diameter in the distal aorta but more elongation in the proximal aorta and arch.

This observation is supported by independent finite element stress analysis with peak wall stress present both above the sinotubular junction, and distal to the left subclavian artery, thereby setting a local stage for aortic dissection.9

Progressive ascending aortic growth in women, and the observation that both genders have similar absolute diameters at an older age, could provide the basis for the observation that aortic dissection is more predominant among men at younger age than women, while this difference between genders evens out with older age.10

Thus both the dynamic diameter and the length of the aorta play an important role in the pathophysiology of aortic dissection. Nevertheless, it should be emphasised that aortic dissection is triggered by multiple other factors. Previous guidelines recommended treatment based on hinge points in aortic diameter as a sole criterion, which however is insufficient. While the group in Maastricht effectively examined the influence of aortic elongation by geometric analysis as one new risk predictor, even the development of some global risk score with cut-off values is unlikely to cover all aspects of this disease entity. In addition to the classical comorbidities, haemodynamic and anatomical conditions, genetics, traumatic, iatrogenic and inflammatory factors certainly play an important role and should eventually be taken into consideration in the future.


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  • Contributors Both authors contributed to this editorial.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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