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Adult Bicuspid Aortic Valve
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Despite the younger age of the BAV patients at surgery, no significant difference was
found in terms of in-hospital mortality between BAV and TAV IE patients, the two groups
thereafter showing similar age-adjusted postoperative 1-year and 5-year mortality [83, 84].
Further studies are needed to evaluate clinical features and surgical outcomes of IE among
BAV and TAV patients, in order to identify high-risk subgroups earlier, thus improving
surgical results [84].
BAV AORTOPATHY
Besides valve dysfunction or infection, the most common complications of BAV include
dilation or dissection of the ascending aorta [91]. BAV-associated aortopathy, thought to
occur in 30 to 80% of BAV patients, is a heterogeneous disease, both in terms of natural
history and anatomo-clinical forms of the disease [18, 58]. The natural course can vary,
ranging from indolent aortic diameter growth to rapid progression or earlier occurrence of
life-threatening complications [91]. The velocity of growth of the aorta in BAV patients can
be in absolute terms similar to the one observed in Marfan syndrome patients at the level of
the Valsalva sinuses, although the segment experiencing the fastest growth rate in BAV is the
tubular ascending [92].
Two main phenotypes of aortic dilatation can be observed: the most common one is the
“ascending phenotype” - predominant dilatation located at the tubular tract, distal to the
sinotubular junction -, encountered in 60-70% of dilated BAV aortas and usually associated
with aortic stenosis (AS) and advanced age [58]. The rarer “root phenotype” - a dilated aorta
with diameter at Valsalva sinuses exceeding the diameter of the tubular tract - represents the
20-25% of BAV aneurysms. It is uniquely associated with male sex, aortic regurgitation
(AR), RL-BAV and younger age at presentation: this type of dilatation, occurring earlier in
life and independently of hemodynamics, has been suggested to be a phenotypic marker of
more diffuse and more severe disease of the whole ascending aorta [56].
Pathogenetic Hypotheses
Historically, two hypotheses on the pathogenesis of BAV aortopathy have been
juxtaposed against each other: the genetic one and the hemodynamic one.
Arguments in favor of the first have included: aortic diameters being greater in BAV than
in age-matched TAV subjects already in childhood, especially at the ascending tubular tract
[93]; BAV patients with the same degree of AS having greater aortic diameters than TAV
counterparts [94]; progressive dilatation after isolated AVR in BAV patients with normal
aortic dimensions at the time of surgery [95]; non-BAV first degree relatives of aortic dilation
BAV patients exhibiting aneurismal aortic disease [96]. Genes associated so far with BAV
(with or without its complications) include the NOTCH1 (encoding for a heterodimeric
transmembrane receptor involved into development of the cardiac outflow tract), ACTA2
(smooth muscle actin alpha 2), GATA5 (encoding for a mediator of nitric oxide synthase
activation and endocardial cell differentiation), NKX2.5 (involved in cardiovascular
morphogenesis and modulation of vascular wall homeostasis), SMAD6 (that negatively
Alessandro Della Corte and Federica Lo Presti
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regulates both the bone morphogenetic protein pathway and the transforming growth factorβ1 signaling) and ROBO4 (encoding for a protein expressed in endothelial cells of the normal
ascending aorta). Although these pathways could be relevant in the pathogenesis of the
disease, to date, no major gene explaining a high rate of BAV/TAA cases has emerged.
Possible obstacles to progress in this field of research include: extreme locus heterogeneity;
incomplete penetrance; sex bias; environmental and/or epigenetic modifications of the clinical
course of the disease [97, 98].
Arguments forwarded by other Authors in favor of the hemodynamic theory included: the
evidence of altered flow patterns distal to the BAV even with normal echocardiographic
function [22, 99]; the striking correlation between site of dilatation of the aorta and location
of the highest wall stresses with different BAV morphologies (RL vs RL) [19]; the typical
asymmetric expression of aortic wall alterations (more severe at the convexity, or greater
curvature of the ascending aorta, where the skewed flow-jet from the malformed valve
impinges on the vessel wall, than at the concavity, or lesser curvature) [58, 100, 101, 102].
Indeed, outward vascular remodeling is known to be a well conserved adaptive mechanism, in
response to increased wall shear stress (WSS), aimed at bringing it back to physiological
levels [103]. Histological analysis of aortic wall samples harvested during surgery in BAV
patients subjected to pre-operative 4D flow MRI for WSS mapping showed more pronounced
elastic fiber loss and disarray in regions of aortic wall exposed to elevated WSS compared
with those subjected to normal WSS within the same aorta [101].
There is mounting evidence supporting that both pathogenic factors (gene variants and
hemodynamic derangements) can be considered as culprits in the onset and progression of
bicuspid aortopathy and the respective predominance of either factor in the determinism of
the disease can vary across the different anatomo-clinical forms of the disease [14]. Clinical
heterogeneity may be subtended by diverse combinations of coexisting genetic and
hemodynamic causative factors: the ascending phenotype may be a form of disease in whom
hemodynamic factors are predominant in determining aortic wall abnormalities and dilation;
the root phenotype is suggested to be the form in whom the role of some genetic defect
trumps the hemodynamic derangements [58, 104, 105].
Indications to Treatment: Wavering Guidelines
Elective surgery on BAV dilated aortas is performed in order to prevent life-threatening
complications such as aortic rupture or dissection, whose age-adjusted relative risk in BAV
subjects is almost 8-fold higher than in the general population [91]. From 1998 to 2017, 11
international official guidelines documents have been issued on thoracic aortic aneurysms
[106]: the thresholds for elective repair of BAV aortas ranged from the initial 5.5 cm to a
more aggressive nadir of 4.0 to 4.5 cm reached in 2010 [107], to return back to a conservative
cut-off of 5.5 cm since 2012 [108].
The wavering of recommendations reflected shifting perspectives in the etiology of BAV
aortopathy [109]. Aggressive approaches (both in terms of timing and extension of resection)
derived by the old assumption that in BAV patients an inherited frailty involves potentially
the entire aorta exposing it to life-long risk of dilatation and rupture. This widespread belief
led ten years ago to surgical indications similar to those for Marfan syndrome patients [104],
including BAV among connective tissue disorders [107]. On the other hand, the only two
Adult Bicuspid Aortic Valve
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natural history studies performed on the BAV population showed a much lower risk of acute
aortic events than in Marfan syndrome [24, 79]. On these bases, more conservative
approaches were suggested [108, 110], considering that not all BAV patients are exposed to
an equally high risk of aortic complications [109]. An interesting survey of 100 Canadian
cardiac surgeons [111] revealed that in real-world practice the operative approaches to BAV
aortopathy are highly variable both in terms of thresholds diameters and extent of the
resection. Finally in 2018, an American Association for Thoracic Surgery (AATS) consensus
document addressed uniquely BAV aortopathy [105]: repair of the ascending aorta/root was
recommended for an aortic diameter:
≥55 mm in patients without risk factors;
≥50 mm in patients with risk factors (e.g., root phenotype or predominant AR,
uncontrolled hypertension, family history of aortic dissection/sudden death,
coarctation, aortic growth >3 mm/year);
≥50 mm when the patients are at low surgical risk and operated on by an experienced
aortic team in a center with established surgical results;
≥45 mm in patients undergoing concomitant cardiac surgery.
The Risk of Aortic Dissection
Traditionally, aortic dissection has been interpreted as the result of mechanical aortic wall
failure, exclusively related to dilatation. The risk of dissection was cumulated with the risk of
rupture in old studies [112], and a critical diameter of 60 mm was found to represent the
“hinge point” at which this risk increased abruptly, therefore a diameter of 55 mm was
reasonable for elective surgery to prevent such acute complications of aortopathies. However,
data from a retrospective analysis from the International Registry of Acute Aortic Dissections
(IRAD) undermined the value of the aortic diameter as a predictor of acute aortic dissection,
since this complication occurred at diameters less than 50 mm in about 40% of affected
patients [113]. In BAV patients, in particular, the degree of medial degeneration in the aortic
wall seemed independent from the vessel diameter [114] and less severe than in diametermatched TAV controls [115]. Notably, when the phenotypic heterogeneity of BAV
aortopathy was accounted for in analyses, studies suggested a greater risk of dissection with
the root phenotype dilatation compared to the more frequent ascending phenotype [116] and
the “hinge point” of the risk of dissection at presentation was at 50 mm for the root and 53
mm for the ascending tract in a large study from the Cleveland Clinic [117]. Several reports
consistently found significantly greater diameters at the time of acute dissection in BAV than
in TAV patients [118, 119, 120]: this finding, apparently in contrast with the evidence of
greater risk of dissection in BAV subjects, moreover at a younger mean age, remains
unexplained and yet it stresses the idea that the risk of dissection in general is only in part
related to the size of the aorta [121].
Certainly, there is a critical need to develop individualized risk assessment beyond size
and growth criteria, with an approach involving precision medicine. This could include
quantification of wall remodeling phenomena by assessment of circulating biomarkers [102],
estimation of wall biomechanical properties including stiffness and distensibility by
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techniques of functional imaging [122], measurement of flow patterns and creation of WSS
maps by 4D flow MRI [11] and identification of genetic alterations by specific tests [98].
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