Revised Ghent nosology.
\r\n\tWith this goal in mind, together with the US Prof. John M. Ballato and the InechOpen publishing house since 2011 we have published in 2011, 2013, 2015 and 2017 4 books of our serial “Optoelectronics” and the book “Excitons”, edited in 2018 by Prof. Sergei L. Pyshkin. Publishing the new book “Luminescence” we are pleased to note the growing number of countries participating in this undertaking as well as for a long time fruitfully cooperating scientists from the United States and the Republic of Moldova.
\r\n\tSpecialists from all over the world have published in edited by us books their works in the field of research of the luminescent properties of various materials suitable for use in optoelectronic devices, the development of new structures and the results of their application in practice.
The size and shape of the dendritic arbor is a key factor in determining the connective potential of a neuron. While programs intrinsic to the neuron itself can instruct the general morphology of the dendritic arbor [1], it has long been recognized that the form dendrites take as they mature is under significant influence from extrinsic factors [2, 3]. The complexity of extrinsic influences, and the collective impact they have upon dendritic architecture, is evident when one compares the spatial patterning of dendritic arbors that have developed in situ, or within a tissue context, against those that form in vitro, largely deprived of patterned contact with other cells (e.g., see Figure 1). Although the importance of identifying and understanding how such extrinsic influences work has been recognized by neuroscientists for decades, relating specific influences to specific aspects of dendritic morphogenesis has proven challenging.
\nComparing hippocampal pyramidal neurons grown under different conditions can help distinguish intrinsically determined features of the dendritic arbor from those under extracellular control. (A) Camera lucida drawing of the dendritic arbors of pyramidal neurons of the CA fields of the hippocampus and granule cells of the dentate gyrus, based on Golgi-Cox impregnation of an adult rat (modified from [4]). The dendritic arbor has pronounced apical and basilar domains that are physically segregated and oriented in opposite directions. (B) A hippocampal neuron labeled by biolistic transfection of eGFP in an organotypic slice culture from rat. (C) Dissociated hippocampal neurons growing in primary culture, immunostained with MAP2 to reveal the dendritic arbors of the neurons present in the field of view. (D) An individual cultured neuron, labeled by transfection with eGFP, from within a similarly dense field of neurons (unstained) as in (C). Based on the shape of the soma, and orientation of the primary dendrites, the major dendrite that points toward the upper left of the frame might be a candidate “apical” dendrite.
But while fundamental questions remain, new tools are being brought to bear in this area of active investigation, and a series of insights have unfolded over the last decade. For example, interactions within, and between, neurons are one important source of cues involved in ontogenesis of the dendritic arbor. The mechanism of “self-avoidance” between dendrites within a given arbor can help establish appropriate spacing of branches (for review, see [5]). Similarly, segregation of branch territories has also been recognized as important in understanding how the dendritic arbors of a single type, or class, of neuron within a brain region are arranged in a territorial configuration. Such an arrangement optimizes dendritic capture of incoming afferents and is now understood at a mechanistic level [6, 7]. It is hard to envision how these homotypic mechanisms contribute to the cases where branching pattern and density vary stereotypically along a single primary stalk of the arbor, however.
\nThe hypothesis that astrocytes might also shape dendrites has received less attention. In 2010, Procko and Shaham proposed that glial cells might play such a role, although, at that time, direct evidence in vertebrate systems was lacking [8]. Mounting evidence, however, demonstrated that interactions between neurons and astroglia were crucial to other aspects of dendritic development [9, 10, 11]. Astroglia secrete factors that facilitate synapse formation, both in terms of the onset [12, 13, 14, 15, 16] and of rate [17, 18]. Because immature dendrites are not receptive to innervation [19], these synaptogenic effects could imply an astroglial contribution to dendrite maturation. In addition, astroglia produce factors that modulate synaptic efficacy [20] and regulate synapse pruning [21]. Moreover, a number of growth factors have been identified that selectively alter dendritic, but not axonal growth, of forebrain neurons, e.g., [22, 23] and these factors may be produced, or regulated by astroglia [24, 25]. Collectively, these findings point toward mechanisms whereby astroglia could influence the competence, or developmental state, of the dendrite. It is therefore becoming increasingly important to characterize these effects in more detail so as to determine the roles of astroglia as regulators of synapse formation versus sculptors of dendritic arbor size and shape.
\nIn this regard, data from two human neurodevelopmental disorders, Rett Syndrome and Fragile X mental retardation, implicate astroglia as a regulatory influence on the growth of dendrites [26, 27]. In Rett Syndrome, single-gene mutations in the X-linked transcription factor methyl-CpG-binding protein 2 (MeCP2) are associated with infant death in males, while females begin to display signs of mental retardation, autism, and epilepsy between 6 and 18 months of age [28], coincident with the time when dendritic outgrowth is most robust. Mutations in the fragile X mental retardation 1 gene (Fmr1) cause similar cognitive and behavioral impairments, and individuals with Fragile X have abnormal dendrites [29]. Isolating how interactions between different cell types bearing the gene mutations could produce defects in dendritic development in vivo is difficult, such that in vitro models can be the best option for screening for effects of specific interaction between identified cell types. Accordingly, when wild-type neurons were co-cultured with astroglial cells bearing mutations in MeCP2, or Fmr1, they showed altered dendritic development. These are effects that would have been difficult to detect and attribute directly to astroglia, using in situ analyses of tissue from the transgenic animals. It is noteworthy that much of what we know about the development of dendrites has, in fact, been learned using in vitro models (for example, see [30, 31, 32, 33]). The power of these models is that they permit direct microscopic observation and enable manipulation of the extent to which neurons can interact dynamically with astrocytes as they form dendrites.
\nThe first microscopic views of the intact hippocampus, impregnated with Golgi stain, illustrated the extent to which dendritic arborization is patterned (Figure 1A). This distinctly polarized arbor, with zonal variation in branching pattern, also forms in organotypic slice cultures, a method that preserves some populations of afferents, astroglia, and microglia [34] as dendritic outgrowth and maturation takes place [35]. In contrast, dissociated cultures of hippocampal neurons isolated from embryonic rat brain remove spatial cues that come from organized inputs and contain predominantly neurons with an excitatory phenotype. These cells generate MAP2 positive dendritic arbors that proceed to form post-synaptic specializations expected of pyramidal cells in vivo [31]. Thus, an advantage of this in vitro model is that the developmental trajectory parallels development in the intact neuropil [23, 30]. And because they grow at low density while flat on a coverslip, benchmarks of morphological maturation can be readily observed and quantified. For example, processes become tapered and generate spines (see Figure 1C and D). Despite the physical isolation of these neurons, the dendritic arbors that form sometimes have a prominent dendrite that is somewhat thicker and distinct from the other dendrites that form off of the cell body, suggesting a rudimentary form of an apical dendrite. By comparing dendritic architecture of hippocampal pyramidal neurons from the intact brain, slice cultures, and dissociated neurons, we can separate basic features of the dendritic arbor that are expressed robustly across this range of extracellular contexts and therefore likely intrinsically determined from those features that require extracellular influences to be expressed.
\nIn vitro approaches to studying neuron development were transformed when Gary Banker reported a new method that allowed dissociated embryonic hippocampal neurons from the rat to be grown on glass using defined serum-free medium [36]. There was one telling technical detail, however: long-term survival of neurons required astroglial cells to be present in the culture, although not in direct physical contact with neurons. In fact, these cultures were typically prepared with the astroglial cells grown as a separate monolayer culture on the bottom of the culture dish, while the neuronal cultures were grown on glass coverslips that were several millimeters away. These observations revealed that astroglia secreted trophic factors upon which the viability of neurons depended. Other data suggested that astroglia enabled more than just survival. Sympathetic ganglion cells, for example, formed axons readily in vitro, but dendrites could only be produced in the presence of glia [37]. The dendrite-specific factor necessary for this polarized outgrowth was later identified as BMP-7 [38].
\nFurther evidence of the importance of developmental cross-talk between astroglia and dendritic morphogenesis emerged. Astroglia native to the cortex promoted dendrite formation of cortical neurons more effectively than astroglia from other regions of the brain [39, 40, 41, 42]. These studies supported the hypothesis that astroglia could influence dendritic growth in a brain-region specific manner. Taken together, these findings suggest that the developmental interactions between astroglia and the forming dendritic arbor might be multiple and significant.
\nIt was in this context that we sought to observe dendritogenesis in vitro, while controlling the extent to which developing neurons were exposed to astroglial cells. As a first step, cohorts of neurons were grown for several days under two conditions: in medium that had been conditioned by brief exposure to astroglia (24 h or less) versus in co-culture with a feeder layer of astroglia continuously present but with neurons isolated from physical contact. Neurons grown in conditioned medium formed dendritic arbors but did not form synaptic contacts. Conversely, sibling neurons grown with astroglia continuously present (yet not in direct contact) formed dendrites that displayed presynaptic contacts (Figure 2) [43]. Given previous reports that astroglia produced factors essential for synapse formation in retinal ganglion cells (reviewed in [44]) and in hippocampal neurons [17], the failure of synapses to form in glial-deprived cultures was not surprising.
\nDendritic arbors of neurons that are glial-deprived are more extensive but have few presynaptic contacts (B), compared to those co-cultured with astroglia (A). MAP2-stained dendrites are green, Synapsin1 puncta, representing presynaptic contacts, are red. Modified from Withers et al. [43].
What was unexpected, however, was that the dendritic arbors that formed in the glial-deprived neuron cultures were more extensive than those of neurons grown in an astroglial co-culture, with significantly more primary and higher-order branches [43]. These findings revealed that astroglia exert two effects on dendritic development that seem paradoxical. On the one hand, astroglia were permissive to synapse formation, and on the other hand, their presence limited dendritic outgrowth. A similar inhibitory effect by astroglia has been reported to occur in brain stem neurons in vitro [45] and the enabling effects of astroglia on synapses formation have been characterized in detail (see references above).
\nThrombospondin (TSP) is the synaptogenic factor that is produced by astroglia and promotes the formation of presynaptic contacts onto dendrites both in vitro and in vivo [14]. Thus, in the glial-deprived paradigm, a straightforward prediction was that if TSP was added, the neurons growing under glial deprivation would form presynaptic contacts. They did. A second prediction could also be made: if TSP mediated the astroglial restriction of dendrite outgrowth as well, then those same neurons would be expected to have arbors that would be reduced in size compared with glial-deprived neurons not exposed to TSP. Instead, glial-deprived neurons + TSP still had dendritic arbors that were significantly larger than those growing in the presence of astroglia, and after 48 h of exposure, they were even greater than those growing under glial deprivation without TSP. A simple interpretation of these data is that the astroglia effects on dendritic growth are separate from the effects produced by TSP. The selective effects of TSP seem to suggest a mechanistic dissociation between the inhibition of dendritic growth and the formation of synapses.
\nCo-plating neurons and astroglia on the same coverslip offers opportunities for local interaction between the two cell types that could involve signals both soluble and contact-dependent. In our work, we have observed that neurons in full contact with astroglia had dendritic arbors with reduced size compared with neurons that did not contact astroglia at all. These effects could be mediated by the same mechanism as described earlier, but given that the neuron has grown while adhering to an astroglial island, it seems very likely that the signal(s) originated from the astroglial cell on which it resided. The interesting case comes when physical contact is limited, when a neuron straddles an astroglial cell, such that part of the growing arbor touches and part does not (Figure 3). When in partial contact, the dendritic arbor forms asymmetrically, with the most extensive arborization not in direct contact. One interpretation of this biased growth is that it is the product of an interplay between the action of soluble factors produced by astroglia and a separate inhibition of growth when dendrites are in direct contact with the surface of astroglial cells.
\nAsymmetry of dendritic arbors in partial contact with astroglia (A and B). The dendritic arbors are revealed by MAP2 immunostaining (green). Polymerized actin, stained with fluorescently conjugated phalloidin (blue), highlights astroglia, as well as growth cones at the tips of dendrites.
In vivo, the onset of astrogliogenesis occurs before robust dendritic outgrowth begins and immediately precedes peak synaptogenesis in the hippocampus [46, 47, 48, 49, 50, 51]. For humans and nonhuman primates, the dendritic arbors of forebrain neurons take years to reach their full extent [52]. Dendritic development in rats is similarly protracted, with the elaboration of branches and the addition of synaptic contacts upon them occurring over weeks [53, 54]. This timing makes astroglia good candidates for secreting signals and providing physical cues to guide dendrite growth. Clues to the role astroglia might play in vivo could come from analyzing their spatial relationships with dendrites in mature tissue (see Figures 4 and 5) and the temporal sequence by which these relationships arise during development.
\nCytoarchitecture of the CA1 field of the hippocampal formation from rat brain illustrates laminar variation in dendritic branching and astrocyte morphology. (A) Immunostaining for the dendritic marker MAP2. (B) The dendritic arbor of a typical CA1 (modified from [55]). (C) Immunostaining for the astrocytic marker GFAP from the same region as (A). (D) The colorized overlay, with dendrites in red, astroglia in green, and nuclei in blue. The white box surrounds the field shown in panels and (C). The field within which dendrites develop is tessellated with astroglia: the size of individual astrocytic territories is appropriate to exert local influences on a sub-laminar scale, and the astrocytes themselves appear to show cytoarchitectural variations across laminae.
Illustration of how differential contact between astroglia and neurons can contribute to patterns of dendritic arborization. (A) Dendritic arbors of neurons grown in vitro are inhibited by contact with astroglia. (B) Dendritic arbors of CA1 hippocampal neurons show varied branching across laminae, coincident with changes in the distribution, and size, of astroglia. Astroglia, red; dendrites, blue; axons, green.
The effects of physical contact between a dendritic branch and astroglia in vitro provide an example of how functional domains within the dendritic field might be organized, at least in part, based on cross-talk between a specific dendritic branch and a neighboring glial cell. In support of this hypothesis, within intact neuropil, individual astroglia are arranged in nonoverlapping territories that occupy a fraction of the dendritic arbor of an individual principal neuron [56]. Stains that identify dendrites and astroglia in tissue show their interwoven relationship (see Figure 4A, C, and D). Further, the spatial domain of a single astrocyte contacts synapses of multiple neurons [57], with fine processes extending dynamically to make physical contact at individual synapses [58]. There is an extensive literature documenting astroglial-synapse interactions that is well beyond the scope of this chapter, see [59]. These data fit well with the growing recognition that astroglia may contribute to the construction and function of cortical circuits and maps, physically defining and coordinating synaptic territories [60, 61, 62]. Further, dendrite-astroglia interactions during development could help to scale the growth of a synaptic network to match the available nutritional network [63], similar to the mechanisms involved in building the retina [64]. Control over dendrite arbor shape could be an important part of these mechanisms.
\nThe arbors of pyramidal neurons in hippocampal subfield CA1 offer a useful model because this population of cells has elaborate arbors, yet the arrangement of arbor branches repeats with striking regularity (see Figure 4B). The story of how this pattern of arborization arises in development is summarized nicely by Pokorny and Yamamoto [35]. In that report, dendrite branching and elongation, as measured in Golgi-impregnated pyramidal cells, was not synchronous but rather followed a distinct sequence. For example, the apical dendrite extended nearly to its mature length by postnatal day (P)10, but the lateral branches along the apical shaft had only extended a minor fraction of their mature length. There was also a temporal separation when these lateral branches formed. The number of lateral branches that arose from the apical shaft within the proximal stratum radiatum peaked at P15, whereas more distally, the number continued to be added out to P48. These zones within stratum radiatum correspond to afferent inputs from associative and commissural fibers (proximal stratum radiatum) and Schaffer collaterals (distal stratum radiatum). Branching within stratum lacunosum-moleculare, originating from the most distal portions of the apical dendrite, did not peak until after P48 and appeared to be more pronounced in the preterminal branches. The availability of afferents, which enter during embryonic development (for a review, see [65]), could be an important source of cues for dendritic development.
\nDuring the time frame when CA1 pyramidal cells are growing dendrites, astroglial cells in this region go through a number of transitions in number, and structure, that could be meaningful for establishing arbor pattern. Though relatively sparse before P10, astrocytes are present at the time when the apical dendrite is forming, and during the first 2 weeks of postnatal development, astroglia extend long filopodia-like processes [66]. An intriguing possibility is that during early stages of dendritic branch formation, the long filopodial extensions on glia serve a function related to branch formation or guidance, analogous to the guidance processes extended by radial glial cells. By the time astroglia begin to extend elaborate spongiform processes more characteristic of mature astroglia, the architecture of the arbor has been established, although branch growth continues beyond P30, when astrocytes have established nonoverlapping territories characteristic of mature neuropil [66].
\nStriking changes in the shape or spatial orientation of astroglia also accompany the most active periods of dendritic branch formation and growth. Astroglia are initially spherical but take on a polarized shape with development [66, 67]. In the stratum radiatum, this shape change is oriented perpendicularly to the cell body layer, stratum pyramidale. In the stratum lacunosum-moleculare, the astroglia are elongated parallel to the cell body layer [67]. Coincidentally, this is the zone of the apical dendritic arbor that shows the most prominent lateral spread.
\nIn vitro, local encounters between growing dendrites and astroglial cells can exert significant biases in the spatial patterning of the arbor. We have observed long filopodial-like processes extending from astroglia that resemble those reported in developing tissue in vivo (see the earlier section). These extensions could provide a mechanism for spatial capture of dendrites [43]. Time-lapse recordings of living cells have shown that, although slow growing, dendritic branches are dynamic structures that extend and retract growth cones and various forms of filopodia [68, 69, 70] (Withers and Wallace, unpublished observations). Cycles of extension and retraction create the opportunity for multiple physical or molecular interactions between these two cell types, analogous to neuron-astroglia interactions that occur during neuron migration [71, 72]. Collectively, such interactions could determine the trajectory of dendritic branch growth in three-dimensional space.
\nComparison of dendritic arbors of neurons and arrangement of astrocytic processes in neuropil suggests that the structures of these two cell types co-vary in a nonrandom manner (see Figure 4). Such a view, however, only begins to represent more nuanced phenotypic heterogeneity of astroglia based on patterns of gene expression that are of emerging importance in current research, for review, see [73]. Likewise, these kinds of analyses only begin to disclose the developmental shifts in phenotype of astrocytes across lamina that may accompany distinct stages of dendritic branch formation. Such shifts appear to occur. As early as P8, GFAP-positive astroglia are densely arranged in the stratum lacunosum-moleculare, while remaining comparatively sparse in the stratum radiatum [67]. Additionally, two different transporters for glutamate show a different time course of expression and distinctive localization in different populations of astroglia in the developing hippocampus [48]. While such complexities are far from resolved, there is enough data available, we argue, to make the case that (1) patterning of dendritic branches is subject to the influence of astroglia and that (2) this relatively neglected developmental effect is distinct from the actively studied influences on synapse formation. The purpose of this chapter was to build on the hypothesis proposed by Procko and Shaham [8] by adding supporting evidence based on direct analysis of dendritic arbor formation in principle neurons of the central nervous system. Both the documented impact of astrocytes on dendritic arbor formation in vitro, and the fact that astrocytes are present but distributed differentially, during the extended period of dendritic outgrowth in vivo, support the argument that astrocytes could be a key part of the network of extrinsic influences that locally refines dendritic arbor geometry during development.
\nThis work was supported by funding from NIH 1R15HD061831 and NSF DBI-1039958 and a generous gift to Whitman College from the family of Dr. Robert F. Welty. We thank the many undergraduate students who have contributed to the research findings described here and NoahLani Litwinsella for the artwork in Figure 5.
\nAortic root dilation (AoD) is frequently an incidentally discovered, asymptomatic finding in that is seen on various imaging modalities [1]. The anatomy of the aortic root includes the annulus, sinuses of Valsalva, sinotubular junction and ascending aorta [1], with the size being a function of a patient’s biologic variables such as height, age, BSA, and gender [1, 2]. However, while natural variations in the size of the aortic root are well known, the identification of progression from normal to pathologic AoD is a key clinical diagnosis that carries significant cardiovascular risk including aortic dissection, rupture, valvular regurgitation and cardiac tamponade [1, 3, 4, 5]. The etiology of pathological AoD is varied, ranging from congenital, infectious, autoimmune, and idiopathic conditions; and influences the medical and surgical management [1, 5]. Due to the variety of clinical conditions that can result in AoD, and the risks associated with worsening AoD, a thorough understanding of the pathophysiology of AoD, noninvasive imaging modalities and pharmacologic therapies is critical. The aim of this chapter is to review the most common conditions associated with AoD, appropriate imaging modalities, and treatment strategies to manage AoD.
\nMultiple etiologies of AoD exist such as Marfan syndrome, bicuspid aortic valve, Loeys-Dietz and Ehler-Danlos syndromes, idiopathic conditions, hypertension, infections, and inflammatory disorders. In this chapter, we will discuss the various etiologies categorized into two standardized groups—genetically-mediated and nongenetically mediated AoD.
\nGenetically-mediated aortic root dilation or enlargement is the leading cause of thoracic aortic aneurysms. Marfan syndrome (MFS), the prototype condition for AoD, and bicuspid aortic valve has led to a greater understanding of AoD pathophysiology, pharmacologic treatment, timing of surgical intervention and optimal surveillance strategies with noninvasive imaging [6].
\nMFS is one of the most common hereditary disorders of connective tissues and is characterized by manifestations in cardiovascular, skeletal, and ocular systems [7]. MFS is the most common genetic cause of thoracic aortic aneurysms (TAAs). Its inheritance is almost exclusively autosomal dominant and mostly involves a mutation of the fibrillin-1 (FBN1) gene encoding the connective tissue structural protein fibrillin-1 [8]. The widely accepted incidence of Marfan syndrome is ~1 in 5000 individuals [9].
\nAlthough the inheritance pattern is predominantly autosomal dominant, rare cases of autosomal recessive FBN1 gene mutations has been described [10]. While patients with Marfan phenotypes usually have an affected family member, 25% of the cases are sporadic due to de novo mutations [9]. In addition, in <10% of Marfan cases, no mutation of FBN1 was determined [11]. Since it was first identified as the main cause of Marfan syndrome, FBN1 mutations, depending on how it is mutated, were linked to a variety of syndromes and phenotypes [12]. Animal studies investigating the pathophysiology of the disease demonstrated over-expression of TGF-β in the mitral valve preceding prolapse, the aorta associated with dilatation, skeletal muscle associated with myopathy, and the dura leading to ectasia [12]. Later, mutations in TGF-beta receptor 2 (TGFBR2) and TGFBR1 genes were identified in some patients with Marfan phenotypes and subsequently implicated in the disease process in FBN1 mutation negative individuals [13, 14, 15]. These genes were also linked to another condition later, namely Loeys-Dietz syndrome (LDS) [14].
\nThe diagnosis of Marfan syndrome is established by using a combination of clinical manifestations, family history, and the presence of FBN1 mutation. In order to facilitate accurate recognition of the syndrome and improve patient management and counseling, a set of defined clinical criteria, called the Ghent nosology was developed [16] and later revised [17] (Table 1). Apart from the genetic testing for FBN1 mutation, Ghent nosology uses a systemic score calculation using clinical manifestations of Marfan and an aortic root dilatation Z-score (see noninvasive imaging below).
\nPatients with family history of Marfan disease | \n
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Patients without family history of Marfan disease | \n
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Revised Ghent nosology.
One of the major causes of mortality and clinical hallmark of Marfan syndrome is aortic root dilation and related complications such as dissection, rupture and/or aortic valvular regurgitation. Aortic root dilation is typically first identified on echocardiography in 60–80% of Marfan patients [18]. Therefore, surveillance echocardiography has been routinely used to serially monitor aortic dimensions. If the aortic root diameter is above 4.5 cm in adults, aortic dilation rates are above 0.5 cm/year, and/or significant aortic insufficiency is already present, more frequent monitoring is recommended [6] (see Diagnosis and Surveillance of Aortic Root Dilation below for more detailed guidelines).
\nBicuspid aortic valve is one of the most frequent congenital heart anomalies in adults, affecting 0.9–2% of the population [19]. Most cases of bicuspid aortic valve are familial and studies show that heritability of the disease is ~90% making it an autosomal dominant pattern with incomplete penetrance [20]. Bicuspid aortic valve can occur alone or with other congenital cardiovascular disorders such as coarctation of the aorta, supravalvular or subvalvular aortic stenosis, and ventricular septal defect [21].
\nThe diagnosis is often established by transthoracic echocardiogram (TTE), which has high sensitivity (~92%) and specificity (~96%) [22]. TTE is also useful for surveillance of potential complications of bicuspid aorta such as aortic stenosis, aortic dilation, aortic regurgitation, and infective endocarditis [23]. Given the risk of inheritance, first degree relatives are also recommended to be screened with TTE [21].
\nPrevalence of aortic dilation in patients with bicuspid aortic valve disease ranges from 20 to 84% depending on the criteria used in different studies [24]. The risk of aortic dilation increases with age and the risk of dissection increases as the aortic diameter increases [25, 26]. When the aortic root diameter is above 4.5 cm, there is a family history of aortic dissection, or aortic diameter change is rapid it is recommended to perform echocardiogram annually [21]. More frequent surveillance is recommended for patients with aortic root diameters approaching surgical thresholds (see Surgical Interventions section below).
\nLoeys-Dietz syndrome (LDS) is a rare congenital syndrome characterized by hypertelorism (widely spaced eyes), a split uvula or cleft palate, tortuous arteries and aortic aneurysms. LDS shares many features with Marfan syndrome [14]. Most of the LDS cases are sporadic or show an autosomal dominant pattern of inheritance [14].
\nThe incidence and prevalence of the disease is still not well established.
\nLoeys-Dietz syndrome was initially classified into two subtypes based on the severity of the cutaneous and craniofacial features but later was divided into six subtypes stratified by genotypes [27]. These subtypes are labeled 1–6 and associated with mutations in TGFBR1, TGFBR2, SMAD3, TGFB2, TGFB3, SMAD2, respectively [27]. Type 1 and type 2 are the most commonly seen subtypes with frequencies of 20 and 55% among all subtypes, respectively [28].
\nAortic root dilation is a hallmark feature of this disease entity and is frequently seen in patients (~80%) [29]. Another vascular manifestation is aneurysms throughout the arterial tree. This is a concerning clinical manifestations of the disease and can cause aggressive arteriopathy; therefore, early operative intervention at ascending aortic diameters of ≥42 mm is recommended [30].
\nEhlers-Danlos syndromes (EDS) are a heterogeneous and relatively rare group of connective tissue disorders characterized by skin hyperextensibility, joint hypermobility, and tissue fragility [31]. Ehler-Danlos syndrome can present with a variety of clinical manifestations and can be caused by different kinds of genetic mutations. Overall prevalence of EDS is ~1 in 5000 and EDS hypermobile (hEDS) is the most common type [31].
\nVascular complications can be seen with different types of EDS; however, it is most commonly seen in type IV (vascular or arterial ecchymotic type; vESD), characterized by an autosomal dominant mutation in COL3A1 (collagen, type III, α-1 gene) encoding type III procollagen [32]. Up to 80% with vESD patients suffer from vascular complications by the age 40 years [32]. Therefore EDS patients, especially vEDS, patients should be routinely evaluated for aortic root disease. These patients are recommended to undergo elective operation at smaller diameters (4.0–5.0 cm) to avoid acute dissection or rupture. Patients with a growth rate of more than 0.5 cm/year in an aorta that is <5.5 cm in diameter are recommended to be considered for operation [33].
\nAortic root dilation is an established phenomenon that has shown strong correlations to key pathobiological factors such as age, body surface area (BSA), height and gender. The correlation of aortic root size with age and BSA were initially described in the development of screening nomograms using M-mode echocardiograms [34]. Follow up studies with 2D echocardiography further validated these correlations, allowing for the development of nomograms for normal patient populations or adjusted for patients with underlying congenital disorders (i.e., Marfan syndrome) [2, 35]. These studies evaluating AoD by echocardiograms are further supported by reviews of autopsy data that show clear correlations to key pathobiological factors such as increased age and height with AoD [36].
\nDespite the validation of age as being correlated strongly with AoD, the mechanism of age on the development of AoD still remains an area of active research. One of the predominant hypotheses is based on the idea of cyclic stress, and how the aorta degrades through gradual mechanical decline of elastin proteins [37]. Elastic arteries, namely the aorta, are estimated to dilate by 10% with each beat [38]. It is hypothesized that the shear stress over a normal lifetime results in the degradation of elastic lamella, resulting in arterial dilation and stiffening [38]. This is corroborated by histologic data demonstrating damage to medial elastin of the proximal aorta [38]. Furthermore, there is evidence to suggest that in the absence of risk factors such as hypertension or atherosclerosis, the aortic wall undergoes age-associated reprograming that is proinflammatory promotes progression of arterial disease [39]. Wang et al. demonstrated in pathologic samples of aortas that age correlated with increased smooth muscle cell invasion, and increased production of downstream angiotensin II mediators [39].
\nIn addition to age and BSA, gender is another key factor which can increase the risk and progression of AoD [40]. In the Framingham study of 1849 men and 2152 women, not currently diagnosed with cardiac disease or having a cardiac history, aortic root was 2.4 mm smaller in women than men with m-mode echocardiography [40]. A systematic review in 2014 of 10,741 patients with hypertension revealed men had a significantly higher incidence of AoD relative to women [41].
\nIn conclusion, a series of biological variables are correlated with AoD, and it is important to take these into account as they are potential confounders or contributors in the evaluation of patients with pathologic AoD. Even exercise capacity has been correlated with AoD, with a recent meta-analysis showing that athletes defined by participation in National Collegiate Athletic Association (NCAA) or international equivalent had an aortic root diameter that was larger than nonathletic controls [42], and a statistically significant increase by measurement of sinuses of Valsalva and aortic root annulus [42]. It is important to understand the significance of biological variables such as age, height, BSA, or gender to fully evaluate pathologic AoD without the influence of known confounders.
\nHypertension is a well-known risk factor for aortic dissection, and in some studies, it is estimated to factor into roughly half of the overall risk for aortic dissection [43]. A recent prospective cohort study of 30,447 patients, 86% of patients who developed aortic dissection had hypertension [4]. However the relationship between hypertension and AoD is not as clearly established. In a Framingham study of 3195 patients, there was no relationship between the development of AoD with hypertension [44]. A subsequent follow up study of Framingham participants evaluating aortic root diameter was positively correlated with mean arterial pressure, but negatively associated with pulse pressure, indicating that the mechanism behind AoD is more complicated [45]. Moreover, investigations have shown that in patients with other comorbidities for AoD, such as, Turner syndrome, hypertension is significantly associated with increased prevalence of AoD [45]. This has led to interesting insights into the cyclic stress hypothesis of the development of AoD [43]. If AoD develops due to chronic shear stress, then it would be expected that AoD is correlated with higher pulse pressure (PP), which would presumably lead to greater stress and aortic dilation [43]. However, studies have reported an inverse relationship between AoD and PP [43]. Additionally a systematic review in 2014 showed that in a population of 10,791 hypertensive patients, 9.1% had AoD with a significant gender skew toward men [41]. However there was no significant correlation of mean arterial pressure or pulse pressure values and AoD [41]. While hypertensive patients have a higher incidence of AoD, the mechanism remains to be further investigated. Moreover, these unclear correlations between MAP, PP, and AoD suggest that the aorta is not static, but a dynamic structure whose response to stress, such as hypertension, is still being elucidated [43].
\nSince the first mass production of penicillin in 1945, the modern era of antibiotics has resulted in a decrease in the prevalence of mycotic aneurysms due to bacterial infections in developed countries [46, 47]. However they can still be found in developing countries, and are rare but well described causes of mycotic aneurysms [46]. Most common pathogens include Salmonella, Staphylococcus and Streptococcus pneumonia, and while rare have been in the pathogenesis of mycotic aneurysms of the aortic root [46, 48, 49]. Other common bacteria include Mycobacterium tuberculosis and Treponema pallidum, which will be discussed below, and more rare causes include Listeria, Bacteroides, Clostridium septicum, and Campylobacter jejuni [46]. With the majority of bacterial aortitis, aneurysm development is generally saccular, and Salmonella has been reported in case studies to predominantly affect the abdominal aorta than the thoracic [46, 48]. Infections with Staphylococcal species generally are related to underlying aortic valve infections, but have been reported to progress into aneurysms of the aortic root [46, 49].
\n\nTreponema pallidum, a sexually transmitted spirochete which is the causative organism of syphilis, is a well characterized cause of aortitis [46, 50, 51]. Cardiovascular involvement is limited to late stage, or tertiary syphilis, and generally occurs 5 to upwards of 40 years after primary infection [50, 51]. Aortitis, and aneurysm development is due to invasion of the vasa vasorum, resulting in obliterative endarteritis that leads to degradation of the aortic media [50, 51]. The chronic inflammation results in fibrosis of the intima, a phenomenon known as “tree-barking” that ultimately progresses to aneurysm development. In an autopsy study in 1960 of 51 aortic aneurysms secondary to syphilitic aortitis, 7.8% were found at the sinuses of Valsalva and 29.4% involved the ascending aorta, representing a majority of the sample [52]. This predominance to the ascending thoracic aorta have been further corroborated in later studies, however the detailed echocardiographic analysis of syphilitic aortitis, specifically in relation to AoD is limited due to the rarity of the disease presentation [46, 50].
\nTuberculosis is a relatively common infection especially in developing countries [53]. Mycobacterium tuberculosis, the causative pathogen, is a known cause of mycotic aortic aneurysms [46, 50]. Pathogenesis of tuberculous mycotic aneurysm is believed to be due to lymphatic spread or hematogenous seeding, and mortality rates are reported as high as 60% in patients who develop this complication [50]. While more commonly affecting the distal aortic arch and descending aorta, there are case reports detailing aortic root aneurysms due to tuberculosis [50, 54].
\nThere have been case reports proposing an association between aortic aneurysms and HIV [50]. In a variety of these cases the causes are generally multifactorial, as the majority of cases have reported coinfections (Q fever and leishmaniasis) or comorbid autoimmune conditions (giant cell arteritis) [55, 56]. It is still an area of investigation as to whether there is a true association, and there is sparse data showing a relationship with AoD.
\nAnkylosing spondylitis, a seronegative spondyloarthropathy, is a chronic, progressive rheumatologic disorder, and was one of the first found to be associated with aortitis [50, 57]. The proposed mechanism of AoD in ankylosing spondylitis is fibrous growth development along the intima, which leads to subsequent weakening [57]. Prior TEE studies further evaluated the prevalence of AoD in ankylosing spondylitis, and 82% of patients with ankylosing spondylitis had aortic root abnormalities [58]. Specifically, 61% of patients had aortic root thickening and 25% of patients had AoD [58]. AoD in these populations is a relatively common phenomenon and is associated with significant cardiac morbidity [45, 57].
\nRelapsing polychondritis is another autoimmune disorder, which is a multisystem inflammatory disorder that primarily affects the cartilaginous structures of the body [59]. Cardiovascular involvement is common, estimated to be the second most frequent cause of death and can result in aneurysm development in 5% of cases of both thoracic and abdominal aorta [50, 59]. AoD has been known to occur, albeit rare, with cases of requiring surgical revision after the development of aortic regurgitation [60, 61].
\nTakayasu arteritis is a chronic granulomatous large vessel vasculitis, predominantly found in pediatric populations [50, 62]. A rare disorder, the pathogenesis is characterized by granulomatous panarteritis that can affect the entirety of the aorta and major branches, however predominantly affects the common carotid and subclavian artery [62]. While rare, there are reports of AoD from Takayasu arteritis resulting in aortic regurgitation [63, 64].
\nGiant cell arteritis is a large vessel vasculitis that is characterized by chronic granulomatous inflammation [50]. While commonly affecting carotid, temporal and vertebral arteries, it has been known to affect the ascending aorta, at times resulting in dissection or aortic valve insufficiency [50]. The development of AoD from GCA may be influenced by other comorbid conditions such as HIV; however, this association is currently only supported with case reports [55].
\nAdditionally left ventricular hypertrophy is reported to be positively correlated with AoD. Early retrospective reviews of echocardiographic studies have shown a positive relationship between LVH and AoD, and this has been further supported in subsequent systematic reviews [41, 65]. Patients with AoD with concomitant left ventricular hypertrophy are shown to have an increased risk of adjusted cardiovascular events [66]. However as with previous studies, the exact mechanism between LVH and AoD is still being determined.
\nAortic root dilation is typically a silent disease, with most cases being diagnosed incidentally on imaging. AoD can become symptomatic as the aneurysm enlarges. Aortic root aneurysms grow at an average of 1–4 mm/year [5], with a faster rate of growth noted in patients with bicuspid aortic valves, Marfan syndrome, ESRD, male gender, and smokers [5, 67]. When the aneurysm enlarges to the point of compressing surrounding structures the patient may begin to observe symptoms—the most common of which is chest pain, seen in up to 75% of patients [5, 68]. Other nonspecific symptoms can include back pain, abdominal pain and fatigue (though only present in 5% of patients).
\nAdditionally, patients may present with symptoms secondary to complications of a dilated aortic root such as aortic insufficiency and congestive heart failure. Thus, patients can develop dyspnea as the presenting symptom of aortic root dilation up to 40% of the time [68]. Other presenting symptoms may be related to the complications noted in Table 2 [69, 70, 71, 72, 73, 74].
\nComplication of aortic root aneurysm | \nPresenting symptom | \n
---|---|
Aortic insufficiency, aortic regurgitation | \nDyspnea, diastolic murmur, congestive heart failure symptoms | \n
Aortic dissection | \nSharp chest pain, may radiate to the back | \n
Thromboembolism | \nSymptoms of stroke | \n
Compression of tracheal or bronchus | \nHemoptysis, cough, recurrent pneumonitis | \n
Compression of left recurrent laryngeal nerve | \nHoarseness | \n
Compression of superior vena cava | \nSigns of superior vena cava syndrome | \n
Compression of esophagus | \nDysphagia | \n
Complications and presenting symptoms of aortic root dilation.
Acute aortic emergencies that occur secondary to aortic root dilation include dissection, rupture, and aortic insufficiency. As the aortic root diameter increases, the risk for aortic dissection and rupture rises [75]. Aortic dissections are the most common acute aortic emergencies [76], and can be classified depending on the segment of the aorta affected: type A dissections involve the ascending aorta (seen in aortic root dilation), while type B dissections are those that occur distal to the left subclavian artery.
\nAortic dissection most commonly presents with acute onset chest pain that may radiate to the back. The character of the pain has traditionally been described as ripping or tearing in nature, however over half of patients may instead complain of sharp pain [77]. In addition, geriatric populations are less likely to have an acute onset of pain [78]. Physical exam findings that may be present include unequal blood pressures in the upper extremities, a new diastolic murmur indicative of acute aortic regurgitation, or muffled heart sounds secondary to tamponade (with proximal extension of the dissection). Imaging may be notable for widening of the mediastinum on CXR [77]. In order to aid in the diagnosis of a dissection, an aortic dissection detection risk score (ADD-RS) has been developed. The score is comprised of three categories: the presence of high risk conditions such as Marfan syndrome, the presence of typical symptoms (such as abrupt onset chest pain), and the presence of physical exam findings such as unequal blood pressure readings in the upper extremities. Each group is given a score of 1 if a feature is present, and the total score helps pave the next steps of workup—a score of 0 can be followed by diagnostic workup of other pathologies, while scores of 2–3 should be followed by expedited workup and immediate surgical consultation for possible aortic dissection [79].
\nAortic rupture is also an acute and life-threatening complication of aortic root dilation. It can present similarly to aortic dissection with regards to chest pain, however rupture can lead to severe and abrupt hypotension. Moreover, contingent with the site of rupture the patient may have symptoms such as hemoptysis [80] (if there is rupture into the lung), hematemesis [81] (if there is rupture into the esophagus), or cardiogenic shock [82] (if there is rupture into the pericardial cavity with resultant tamponade physiology).
\nAortic root dilation may also lead to aortic insufficiency. Roughly 30% of aortic insufficiency is now recognized as being caused by aortic root dilation, surpassing the incidence of any valvular cause [83]. The pathophysiology is related to stretching of the aortic valve annulus secondary to aortic root dilation, which results in incomplete closure of the aortic leaflets during diastole. Unfortunately, at the onset of aortic regurgitation, patients may be asymptomatic; therefore, congestive heart failure can develop when the regurgitant valve goes unnoticed.
\nWhile aortic root aneurysms are known to grow at an average of 1–4 mm/year [5], it is difficult to ascertain how fast an individual’s aortic root aneurysm will grow, therefore necessitating surveillance imaging. The frequency of surveillance imaging recommended is dependent on the etiology of the aortic root dilatation as well as its size, with genetically mediated aortic disease having a lower threshold for more frequent (biannual) imaging [84]. At the very least however patients are recommended to have annual imaging for aortic root dilation to closely monitor the aortic diameter. The impact that frequent imaging (CT, MR angiography or echocardiography) has on public health is likely significant, with cumulative costs. In addition, any patient with a bicuspid aortic valve should be screened for a thoracic aortic aneurysm, as well as screening all first-degree family members of a patient with genetic conditions such as Marfan syndrome [85].
\nThe aortic root is the most proximal segment of the aorta. It extends from the annulus of the aortic valve to the sinotubular junction (STJ). It is composed of the left, right, and non coronary sinuses of Valsalva. The diameter of the aorta decreases as it moves distally. The aortic root is assessed using multimodality imaging techniques. These include transthoracic echocardiogram (TTE), cardiac magnetic resonance imaging (cMRI), and cardiac computed tomography angiography (cCTA).
\nTTE is widely used for the detection and monitoring of aortic root pathology. Early studies established age- and sex-specific nomograms for aortic root measurements [86]. These studies used the motion mode (M-mode) of TTE, in which the amplitude of the ultrasound pulses amplitudes is converted to corresponding level on gray-scale imaging [86]. Using the M-mode, the American Society of Echocardiography (ASE) has recommended using the leading-edge to leading-edge approach for measuring the aortic root [87]. Later studies used 2D TTE and obtained reference measurements of the aortic root. This is now preferred over M-mode images, which may be off-axis and are subject to aortic motion that may produce erroneous measurements.
\nOn echocardiogram, the aortic root diameter is typically measured in the parasternal long-axis view from the right coronary sinus to the opposite sinus of Valsalva. When unable to obtain the long axis view, the parasternal short axis view may provide more accurate measurements. However, universal landmarks to measure the root in this view have not been established. Some suggest measuring the diameter from the right coronary sinus to the opposite commissure. These measurements are typically performed at end diastole, as this represents the resting aortic diameter [88]. In adults, these measurements correlate with age and body size. In addition, the aorta is about 2 mm larger in men compared to women due to differences in body size [89]. Normal values stratified by body surface area and age have been published by the ASE [87].
\nImportantly, TTE is limited by its two-dimensional images and thus does not give a complete depiction of the aortic root. It is also limited by patient factors that limit the visualization windows and thus aortic root measurement. Since the aorta is not a straight tube, it can be imaged obliquely leading to over-estimation of its true diameter. Newer modalities, such cMRI and cCTA, can provide three-dimensional images.
\nDespite ECG-gated CT being the most accurate modality for evaluating the thoracic aorta, it is limited by the radiation and contrast exposure. This is particularly important in younger patients with connective tissue disorders that require serial follow up imaging. Cardiac MRI provides an alternative approach for imaging the thoracic aorta including the aortic root and is considered the preferred modality in select groups. It can be performed with ECG gating to provide motion-free evaluation of the aorta. In addition, young patients, in whom this is more commonly used, can hold their breath for longer periods, allowing acquisition of images with high spatial resolution.
\nCardiac MRI evaluation of the aorta does not require contrast use. MRI sequences used include balanced steady-state free precession (SSFP) sequences, fast imaging employing steady-state acquisition (FIESTA), true fast imaging with steady-state precession (FISP), and balanced fast-field echo (FFE) sequences. These sequences provide a high signal-to-noise ratio and adequate contrast between vessel wall and blood pool [90]. When used with ECG gating and contrast enhanced MRA, images tend to have less artifact, higher resolution, and overall short imaging time. Another approach is to use ECG gating 2D balanced SSFP sequence that is oriented perpendicular to the aortic root in two planes to assess the aortic valve and root throughout the cardiac cycle. In addition, prospective ECG gating and respiratory navigation with three-dimensional balanced SSFP sequences can provide 3D aortic imaging without contrast administration [91, 92].
\nIt is important to note that different methods of aortic measurement have been described and guidelines are less well defined. Aortic root measurements can be challenging given different approaches. Burman et al. found in the Framingham Heart Study that cusp-commissure dimensions better corresponded with reference echocardiographic aortic root measurements [89, 93]. This best correlated with study measurements after averaging the three end-diastolic cusp-commissure measurements [93]. In addition, there is a lack of consensus with regard to measurements used (inner lumen only versus lumen and wall) and whether measurements should be adjusted to body surface area, sex, and age.
\nAlthough TTE is widely used for the imaging and surveillance of aortic root, cardiac computed tomography angiography (cCTA) is currently the most commonly used technique for the study of the thoracic aorta. Main advantages of cCTA are fast scanning times, low artifact sensibility, and wide availability including emergency rooms operating 24 h [94].
\nThe new generation CT scanners acquire high-resolution 3D datasets of the thoracic aorta, showing sensitivities up to 100% and specificities of 98–99% [95]. ECG synchronization is vital for detailed assessment of the aortic root anatomy since it allows suppression of pulsation artifacts [96]. ECG gating also allows viewing images in a particular phase of the cardiac cycle. Unfortunately, the ECG-gated technique can increase the acquisition time and required breath-hold time. In order to minimize the increased acquisition times, employment of a 64 or wider ECG-gated row detector system is suggested [95, 97].
\nModern CT scanners can be used to employ several different cardiac synchronization methods such as prospective ECG triggering where images are only acquired during a specified portion of the cardiac cycle, starting at a predetermined delay from the R wave; retrospective ECG gating where the desired cardiac phase is selected retrospectively from the raw data [95, 97]. The details of each technique will not be discussed in this chapter; however, it is important to determine the advantages and disadvantages of different techniques. The main limitations of CT are related to the radiation exposure and the use of iodinated contrast media and different techniques come at a higher cost of each limitation.
\nFor the surveillance of aortic root, any technique can be used and be useful; therefore, the technique with the least amount of radiation exposure should be selected such as prospective sequential triggering without padding, retrospective gating with tube-current modulation optimized for diastolic-phase datasets only, or a prospectively triggered high-pitch helical acquisition [95, 97]. Retrospective ECG gating acquires redundant helical CT data which allows the reconstruction of images at different cardiac phases and providing detailed images which can be useful in complicated cases and pre-/post-operative imaging since pseudoaneurysm or small leaks which are some of the most common complications of aortic root surgery can only be detected during a specific phase of the cardiac cycle. Iodinated contrast-media is another risk related to CT imaging given the risk of contrast induced nephropathy and allergic reactions of various severity. Surveillance CT data for the dimensions of aortic root can be acquired without contrast injection; however, a complete endoluminal evaluation can only be achieved by the injection of contrast-medium [97].
\nIt is standard of care to monitor the size of aortic aneurysms that are below surgical threshold, <5.5 cm for nongenetic aneurysms and <5.0 cm for genetically-mediated aneurysms [98]. In general, physicians should be conscientious about patient cumulative radiation exposure as there is evidence that it can increase cancer incidence and cancer mortality [99]. One study estimated that ionizing radiation exposure results in 0.7% of total expected baseline cancer incidence and 1% of total cancer mortality. These rates increase with greater cumulative exposure [99]. Therefore, physicians should opt to perform serial CT imaging with longer intervals in the most appropriate patients. A study investigating patients with moderate-risk thoracic aortic aneurysms (defined as size <5.0 cm) showed that patients with aneurysms below 4.3 cm had overall lower risk of significant aneurysm growth or size reaching surgical threshold. Thus, the authors suggested that these subset of patients undergo surveillance CT scans less frequently.
\nManagement focuses on slowing the rate of growth and the complications of aortic root dilation. The line of management that is chosen for a patient depends on symptoms and size of the aneurysm. For patients who are asymptomatic and have root dilation <55 mm, medical management is advised. In patients with Marfan syndrome or a bicuspid aortic valve, the cut off of ≤50 mm is used for medical management [1, 100].
\nThe use of beta blockers has shown a survival benefit in patients with aortic root dilation secondary to Marfan syndrome [101]. While data on survival benefits for patients with bicuspid aortic valves is sparse, the common practice is to also prescribe beta blockers given that both conditions share a similar pathology and therefore both are likely to benefit from beta blockade. The mechanism by which beta blockers slow the progression of aortic root dilation is through their negative inotropic and chronotropic effects, reducing the peak left ventricular ejection rate and therefore decreasing shear stress and the rate of aortic dilation [102].
\nThe goal blood pressure for patients with thoracic aortic aneurysms is <130/80 mmHg. In patients who cannot tolerate beta blockers, calcium channel blockers (CCB) are an alternative group of medications available. While less studied as compared to beta blockers, CCB have also been found to reduce the rate of aortic root dilation [103]. Other agents that can be used for additional blood pressure control include ACE-inhibitors and ARBs.
\nIn order to reduce the risk for complications such as aortic dissection, patients should be counseled on smoking cessation, and cessation of drugs that increase aortic wall stress such as cocaine or other stimulants. In addition patients should have dyslipidemia well controlled, which can be achieved through the use of atorvastatin 40–80 mg daily in individuals with aortic root aneurysms [104, 105].
\nPatients should be counseled on avoiding high intensity and collision sports, such as boxing and cycling. Instead patients should take part in low dynamic sports, such as, golf [5, 106]. Pregnancy should be avoided in patients with Marfan syndrome with an aortic diameter >40 mm, if a patient does chose to become pregnant however there must be close follow up with surveillance imaging of the aortic diameter [5, 101].
\nEmergent surgical interventions are indicated for management of an aortic dissection or rupture, or a symptomatic aneurysm. In addition, surgical repair can be performed electively in high risk patients to prevent propagation of an aneurysm (Table 3). Indications for elective surgical intervention include the absolute size of the aneurysm—if the diameter is over 55 mm, or over 50 mm in patients with Marfan syndrome or bicuspid valves. Other indications for elective surgery include if the rate of growth of an aneurysm surpasses 10 mm/year, and if there is concurrent aortic insufficiency [1, 100]. In addition, patients who undergo aortic insufficiency repair who have concurrent aortic root dilation should be considered for aortic replacement at the time of their surgery—that is since 25% of patients with aortic root diameters >40 mm will eventually also require intervention for their aortic aneurysm [107].
\nEmergent surgical repair | \nElective surgical repair | \n
---|---|
\n
| \n\n
| \n
Indications for emergent and elective surgical repair of aortic root dilation.
As opposed to supravalvular aortic aneurysms, aortic root aneurysms involve the coronary ostia as well as the aortic valve, which have implications on the type of surgical procedure available for patients. There are two approaches for a surgical intervention: radical and conservative. In a radial surgical intervention the patient’s aortic valve and root are replaced (commonly referred to as the Bentall procedure), whereas in conservative interventions only the aortic root is replaced [108].
\nThe Bentall procedure involves replacing the aortic valve with a prosthetic valve, and thus has the caveat of requiring indefinite anticoagulation [5]. If patients have a high bleeding risk it may therefore be worthwhile investigating replacement of the aortic root while preserving the valve. In addition, it is important to note that a large number of patients with aortic root dilation are young (secondary to its association with Marfan syndrome), and therefore lifelong anticoagulation in cases such as these confers a cumulative bleeding risk. Preserving the aortic valve while surgically treating the aortic root dilatation is made possible by the development of two surgical procedures: the first is removing the aortic root while keeping the valve intact. The second method is through re-implantation of the aortic valve [5]. Both the Bentall procedure as well as aortic valve-preserving procedures have been shown to have comparable short and long-term outcomes with regards to the risk of death and valve associated complications. The main difference however is that patients undergoing valve sparing operations were significantly more likely to develop moderate to severe aortic regurgitation later [108].
\nIn patients with both severe aortic stenosis and ascending aortic aneurysm, undergoing surgical aortic valve replacement (sAVR) and concomitant surgical intervention for aortic aneurysms above 4.5 cm is recommended by the American College of Cardiology (ACC) foundation guidelines [84]. However, in high-risk surgical patients, undergoing a transcatheter aortic valve replacement (TAVR) has become an alternative approach that obviates the need for parallel surgical aortic aneurysm intervention. This raises the concern for the safety of TAVR catheter-based delivery system in patients with aortic aneurysms since intraoperative rupture or dissection risk potentially increases. However, a clinical study showed that TAVR does not increase intraoperative aortic dissection/rupture risk or mortality with a median follow-up of 14 months [109]. Therefore, there are no recommendations against performing TAVR in patients with ascending aortic aneurysms.
\nNone.
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. 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After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. 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