Aortic Size and Aortic Dissection

Variability is the law of life.

William Osler

In this issue of Cardiology, Mansour et al. [1], from the Aortic Institute at Yale-New Haven Hospital, Yale University School of Medicine, New Haven, CT, USA, have suggested that the aortic diameter increases substantially at the time of aortic dissection due to the dissection itself. They studied 55 patients with aortic dissection (29 of type A and 26 of type B, according to the Stanford classification) and compared them to a control group consisting of patients with aortic aneurysm without dissection.

Patients underwent imaging and aortic diameters were determined prior to dissection (average time 1.7 ± 1.9 years) and at the time of dissection. The control group had at least 2 images of the aorta; the time interval between obtaining the last 2 images was 1.9 ± 2.0 years. Mean diameter of the ascending aorta was 54.2 ± 7.0 mm at dissection and 45.1 ± 5.7 mm at predissection, and that of the descending thoracic aorta was 47.1 ± 13.8 mm and 39.5 ± 13.1 mm, respectively. After controlling for aneurysm growth, gender, and age, multivariate analysis revealed that the diameter of the ascending aorta increased by 7.65 mm, due solely to type A dissection, and the diameter of the descending thoracic aorta increased by 6.38 mm, due solely to type B dissection. Rylski et al. [2] reported similar findings; however, among others, they did not correct aortic diameter for aneurysmal growth at the time of aortic dissection, as did Mansour et al. [1]. This observation, even though it was made in a small number of patients, may obviously have important clinical implications, because indications for interventional therapy (surgical or percutaneous) are mostly based on the size of the aorta at the time of dissection, with only limited information being available for the size of the aorta just prior to this catastrophic event [3^,4^,5^,6^,7^,8^,9^,10^,11^,12]. However, it appears that, at least in certain patients, the diameter of the aorta prior to dissection is smaller than the size in clinical practice guidelines that recommend therapeutic intervention [2]. Importantly, the progression of the aortic diameter over time, also taken into consideration for clinical decisions about therapeutic intervention, is not always linear. It is quite plausible that the size of the aorta changes in a linear fashion up to a certain diameter, followed by an acceleration of aortic dilatation in a nonlinear fashion [10^,11].

Factors Determining Aortic Dilatation and Rupture

Structure and Function of the Aortic Wall

There are several factors contributing to instability of the aorta that may lead to dissection. The aorta is a dynamic organ, the function and size of which are largely related to the structure of its wall and also hemodynamic factors; the latter (among other effects) may also alter its wall structure. The normal aortic wall in mammals contains smooth muscle cells, elastin, and collagen. There is normally more elastin than collagen in the wall of the thoracic aorta and more collagen than elastin in that of the abdominal aorta. In patients with heritable disorders of connective tissue prone to aortic dilatation, dissection, and rupture, such as Marfan syndrome, Ehlers-Danlos syndromes, adult polycystic kidney disease, and others, the structure of the aortic wall is mostly genetically determined. Furthermore, approximately 20% of patients with a thoracic aortic aneurysm not related to a heritable connective tissue disorder have an affective family member suggesting that genetic predisposition is present in these patients [13^,14^,15]. Recently, Brownstein et al. [15] published a state of the art article, reporting known gene abnormalities related to aortic dilatation, dissection, and rupture.

There is also a vasa-vasorum (V-V) network with multiple anastomoses among the arterioles in the aortic wall, which plays an important role in aortic structure and function. In the ascending aorta, the V-V originate from the coronary arteries. In the aortic arch, they originate from the great vessels of the neck and their proximal branches, while those of the descending thoracic aorta originate from the intercostal arteries [13^,14]. The flow through the V-V, which provides a large amount of blood to the outer part of the aortic wall, is subject to active neurohumoral regulation. An acute decrease of blood supply to the aortic wall is associated with aortic dysfunction. The senile changes of the media are most frequently seen in places where there is the least V-V supply, and is most likely related to a decrease in nutrition to these areas [13^,14^,16^,17]. Studies with experimental animal models indicate that the removal of V-V from the thoracic aorta affects the structure of the outer part, but not the inner part of the aortic wall; these structural changes are also associated with reduced aortic distensibility [18^,19]. The dissimilar structure of the inner and outer part of the aortic wall may predispose and/or precipitate aortic dissection [20]. V-V flow decreases with age especially when arterial hypertension is present. Patients with coronary artery disease also have reduced aortic distensibility of the ascending aorta compared to matching controls; this phenomenon is at least partially related to a diminished V-V flow [21]. Importantly, it should be mentioned that during open-heart surgery, a certain number of V-V might be destroyed during the procedure. The effects of this surgery on V-V flow, aortic function, and progression of aortic size are not yet well defined. More recently, it has been shown that in certain heritable diseases associated with aortic aneurysm, V-V flow may be defective [14^,15].

The aortic wall structure also changes with age. In addition to changes in the V-V flow and the accumulative effect in the elderly of risk factors that may also affect aortic wall structure, significant changes in the wall of the aorta occur regardless of other risk factors [22]. The proximal aorta in young individuals expands by approximately 10% during left ventricular systole. Due to repetitive stretch of the aortic wall over time, fatigue and fracture of the elastic lamellae occur. This results in an increase in the collagen content and a decrease in the elastic properties of the aortic wall. This is in addition to and independent of, the changes that occur due to risk factors and the atherosclerotic process [23]. Furthermore, in certain diseases, and especially in the elderly, an inflammatory process may be present in the wall of the aorta that also contributes to its structural and functional abnormalities [24^,25^,26]. All these alterations of the aortic wall over time can eventually lead to aortic dilatation, dissection, and rupture (Fig. 1) [23].

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The Timing of Surgery in Patients with Aortic Dilatation

Life is short, the art long, opportunity fleeting, experience fallacious, judgment difficult.

Hippocrates

How often a relatively small size aorta dissects or ruptures in relation to the entire patient population with aortic dissection/rupture is not well known. Based on the information available, therefore, what approach should be used today for patients with aortic dilatation prone to aortic dissection or rupture? In the past, most of the recognizable aortic diseases were diagnosed at end-stage or at autopsy, with the result that therapeutic interventions were limited.

A series of events propelled the aorta into clinical consciousness. The imaging revolution, including molecular imaging in cardiovascular medicine, has had a profound effect on diagnostic precision in aortic disease states. In addition, innovative surgical techniques and percutaneous approaches have changed the prognosis for many patients who were previously considered untreatable [14]. At present, a mosaic approach is necessary since the population in which aortic dissection occurs is nonhomogeneous, and so several parameters have to be taken into consideration. To make a rational clinical decision, the size at which the aorta dissects has to be defined in each subgroup in which dissections commonly occur, and the indications for therapeutic intervention should be based on this information [15^,29]. Family history, arterial survey, arterial hypertension, aortic size and progression of aortic size, aortic function, inflammatory processes of the aortic wall that play an important role in the progression of aortic size, gene mutations, genetic biomarkers, V-V flow, hemodynamic factors, and triggers of aortic dissection must all be considered for each individual patient, as it is obvious that one aortic size does not apply to all (Fig. 2) [14^,15^,29].

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Future advances in the understanding of aortic aneurysm formation and the natural history of the disease will assist in better management of patients and result in better outcomes. Clinical investigators, pathologists, surgeons, imagers, and geneticists should be involved in this process by developing new approaches to genotype-phenotype correlations in clinical practice. At present, the approach should be based on current knowledge, common sense, and good clinical judgment. Recommendations and advice should be balanced in order to avoid early and unnecessary surgery, but also to prevent aortic dissection.

Since antiquity, physicians have had to make important decisions about the well-being of their patients, often based on incomplete information and under conditions of uncertainty [30]. The father of medicine, Hippocrates (460-370 B.C.), stated this nicely: “Life is short, the art long, opportunity fleeting, experience fallacious, judgment difficult.”

Conflict of Interest

There were no conflicts of interest.