Demographic characteristic of the patients and preoperative symptoms
- Recent developments in the growth of CNTs
- Methods to modify the surfaces of CNTs and decorate their surfaces for specific applications
- Applications of CNTs in biocomposites such as in orthopedic bone cement
- Application of CNTs as chemical sensors
- CNTs for fuelcells
- Health related issues when using CNTs
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It is well known connection between the stroke and diseases of carotid artery (stenosis, aneurysm, kinking). In the XIX century postmortem studies showed association of ischemic brain lesions and plaque formation in carotid bifurcation [1]. Later in 1937 Egaz Moniz performed first angiography while neurologists started to consider connection between carotid and brain lesions, and very soon idea for surgical treatment was born [2]. In 1951, in Buenos Aires, Carrea performed external to internal carotid artery bypass, and published it in 1955 [3]. In the period from 1955-1975 different important cardiovascular surgical groups published their reports about surgical treatment of carotid stenosis in symptomatic patient using different reconstructive procedures. Eastcot, Pickering and Rob in 1954 reported resection of carotid bifurcation and internal to common carotid artery bypass, while DeBakey, then Row and Cooley performed carotid endarterectomy (CEA) – plaque removal instead of bypass [4, 5, 6, 7]. Afterwards idea of plaque removal instead of bypass was accepted widely, and its’ efficacy in stroke prevention was later proved in multiple trials [8, 9, 10, 11, 12, 13].
Still, diverse pathologies of carotid artery were treated even before this obsession with carotid stenosis. French surgeon LeFevre used external carotid artery for flow restoration in case of traumatic lesion of internal carotid artery [14]. In the golden fifties, when carotid surgery was born, other authors reported their experience in treatment of carotid aneurysms [15, 16]. Although Dimitza used resection and reanastomosis, Beall had to use graft interposition. In this position authors were using autologous and synthetic graft with similar results; however in region susceptible to infection, autologous graft was preferred. DeBakey also reported his results in usage of graft replacement in case of carotid trauma [17]. In the beginning of treatment of carotid stenosis there were also reports of different techniques similar to those described in trauma and aneurysmatic disease. Dehnman et al treated carotid occlusion with homograft while Doyle et al used saphenous vein for treatment of carotid stenosis [18, 19]
On the other side, endarterectomy as surgical method for the treatment of stenotic arterial lesions was performed on superficial femoral artery, by Dos Santos, and later with extensive usage of Heparin it gain more success and showed its role in aorto-iliac position [20, 21]. Further experience showed its’ excellent effect in focal stenotic lesions in vessels with large-caliber and high-flow rate. In everyday clinical practice this technique has proved efficient in patients with localized disease limited to the distal aorta or proximal iliac arteries and distal common femoral artery obstructing deep femoral artery orifice (profundoplasty) [22, 23, 24]. On the contrary in extensive atherosclerotic pattern that are more frequent in clinical practice, endarterectomy is technically demanding with poor long term results [25]. Later trough history, short lesions were preferably treated by endovascular means, leaving bypass reconstruction for longer ones, while isolated endarterectomy is becoming almost forgotten except in carotid bifurcation. It is rarely recognized in the literature that in some, not frequent, situations endarterectomy in stenotic carotid artery is not possible or it might be jeopardized. What are modes of reconstruction of carotid artery when CEA fails or is not possible? If bypass or graft replacement is alternative in peripheral occlusive disease, should we apply it in carotid position as well in situations when extensive disease is encountered or technical challenge happens?
The aim of this chapter is to show results and experience of a single high volume center in usage of synthetic graft in the treatment of extensive carotid atherosclerotic disease and to analyze published results related to this topic.
Clinic for Vascular and Endovascular Surgery of the Serbian Clinical Center is located in Belgrade, Serbia, and it was part of the Second surgical clinic, the cradle of cardiovascular medicine in the former Yugoslavia. First vascular procedures were performed in its’ facilities in the sixties (1966) by outstanding pioneers of this, in that time, new branch of surgery – V. Stojanovic and B. Vujadinovic. Figure 1 (A and B). Further development of this institution was supported by the fact that it becomes educational and referral center. Intensive cooperation with leading world centers of excellence, sending its practitioners for education and organizing demonstrational operations in own facilities contributed to popularization and development of cardiovascular surgery in the former Yugoslavia, Balkans and Eastern Europe with consequent progress in treatment of cardiovascular patients in this institution. Later S.Lotina, (Figure 1 - C) successor of Stojanovic and Vujadinovic, has significant role in development of vascular surgery in this institution, since he struggled for segmentation of cardiovascular surgery in the late eighties and middle nineties and eventually achieved expansion of independent vascular department with surgeons and angiologists dedicated to this field. Later, Lazar Davidovic, (Figure 1 - D) one of his pupils, becomes new leader of this department accomplished to improve it to the level of the clinic. After finishing his education with fellowship at Pitié-Salpêtrière hospital in Paris, under the service of Prof Eduard Kieffer, where he improved his experience in aortic and carotid surgery, adopting eversion technique, L. Davidovic brought new modern perspectives in the diagnosis and treatment of vascular patients not only in this institution but rather in the whole country of Serbia. Since then the number of carotid and aortic procedures is annually increasing in this institution reaching almost 600 carotid and almost 500 aortic in the year 2011, with sensible and gradually introduction of endovascular procedures (carotid, peripheral stenting and endovascular repair of aortic pathology) according to published results, guidelines recommendation and available financial support of national health care system.
Leaders of development of vascular surgery in Serbian Clinical Centre in last 60 years. A. Vojislav Stojanovic (1955-1971) B. Borislav Vujadinovic (1971-1985) C. Slobodan Lotina (1985-2002) D. Lazar Davidovic (2002- still leading Clinic for Vascular and Endovascular Surgery)
In the period from January 2003 to October 2006, at the Clinic for Vascular and Endovascular Surgery of the Serbian Clinical Centre, 1250 procedures due to carotid artery stenosis in 1127 patients were performed. Carotid stenosis was repaired by eversion or conventional endarterectomy (CEA) and synthetic graft (Dacron®) interposition in 987 (78, 96 %), 205 (16, 4 %) and 58 (4, 64 %) patients respectively. We retrospectively analyzed prospectively gathered data related to the subgroup of patients operated with graft replacement.
Indications for conventional EA with usage of protective intraluminal shunt were contralateral occlusion, recent stroke or transitory ischemic attack and intraoperative stump pressure below 40mmHg. These patients were excluded from this analysis. Other patients were operated with eversion technique. Eversion EA was performed in the same manner as described elsewhere in the literature [26].
Indications for graft replacement (GR) were: extensive atherosclerotic disease proximal and/or distal to carotid bifurcation revealed intraoperatively during dissection or preoperatively by means of ultrasound, digital subtraction angiography (Figure 3.) or multidetector computed tomography; long segment of thrombotic surface after EA; bad quality of arterial wall after EA; inadequate end of the endarterectomy cleavage; any other technical problem that could endanger the success of procedure. Decision for GR was made by operating surgeon.
GR was performed after complete resection of carotid bifurcation and its removal. Dacron graft of 6 or 8 mm in diameter was used depending on the ICA and CCA diameter. Initially anastomosis between the graft and ICA was made, in the continuous fashion, “parachute” technique, with Prolene 6-0 suture. Upon finishing the anastomosis clamp was removed proximaly on the synthetic graft in order to verify anastomotic compatibility. Afterwards proximal anastomosis between CCA and synthetic graft was sutured with Prolene 5-0 in the same fashion. Flushing and air removal is of outmost importance before declamping since there is in-line flow directly to endocranial vascular bed without any patent branch. Reattachment of ECA was performed selectively according to its quality, position and already spent time for GR (Figure 2 and 3.).
Schematic presentation of carotid graft replacement. A. Resection of carotid bifurcationB. Suturing distal anastomosis C. Suturing proximal anastomosis
In this period of time (2003-2006) cervical plexus block was introduced for carotid surgery in our institution, and consequently we changed the indications for conventional endarterectomy and shunt usage performing it only in case of neurological deterioration of the patient during carotid cross clamping. However patients treated with conventional EA with extensive atherosclerotic disease were not analyzed in this paper and GR was performed without usage of the intraluminal shunt.
Among 1045 procedures performed in 956 patients there were 987 (94, 45%) treated with eversion EA and 58 (5, 55%) with GR. After excluding patients treated with conventional and eversion EA, we retrospectively analyzed preoperative, intraoperative and postoperative data of the patients treated with GR in order to investigate results of this alternative procedure and to try to define optimal indications for its’ usage. After analyzing initial results deeper investigation was performed by dividing group of patients treated with GR in two groups according to the indication and decision to perform GR:
Group A, when decision to perform GR was made according to the ultrasonography exam and intraoperative findings before any attempted EA;
Group B when GR was made after failed EA as a bailout procedure.
In the preoperative data we analyzed age, sex, co-morbid conditions and preoperative ultrasound descriptions. All patients were preoperatively examined by ultrasonography means, describing quality and length of the plaque. All exams were made by experienced ultrasonographer. The quality of plaque was described as lipid, fibrous or calcified with or without present ulceration. The length of the plaque was defined as the longitudinal extent of the plaque narrowing arterial lumen for 30% and more. Plaques longer than 4cm were named as long.
After removing atherosclerotic plaque from internal carotid artery (ICA) and common carotid artery (CCA) its’ quality (morphology) and length were assessed too. From intraoperative data we used the intraoperative length of atherosclerotic disease, reasons to perform GR (before any attempt to perform eversion or after attempted eversion), cross clamping time and restoration of external carotid artery flow.
Postoperative data were related to the neurological outcome and mortality rate as well as early surgical (hemorrhage, cranial nerve lesions, and wound infection) and cardiac complications. All patients were followed for one month and yearly thereafter with clinical and ultrasound examination.
Among treated patients significant number was symptomatic - 30 (51, 72 %) patients with previous transitory ischemic attack (12 – 40%), ocular symptoms (2 – 6, 66%) or stroke (16 – 53, 33%). Demographic characteristics of the patients and symptoms distribution were presented in the Table 1. There was no significant difference in terms of co-morbid conditions between the groups.
Demographic characteristic of the patients and preoperative symptoms
There was no significant difference between ultrasonography and intraoperative findings in the group A. There was significant difference between ultrasonography and intraoperative findings of the plaque length on the CCA and ICA among patients of group B. There was significant number of patients with plaque length of 4cm and more in the CCA, described in the ultrasonography exam and found intraoperatively. Tables 2 and 3\n\t\t\t
Comparison of ultrasonography and intraoperative findings in the patients of the group A
Comparison of ultrasonography and intraoperative findings in the patients of the group B
Intraoperative data were presented in the table 4. Among 58 patients, 22 (37.93%) were operated in conditions of general anesthesia and 26 (62.07%) under cervical plexus block. Mean cross clamping time was measured and presented in Figure 2. There was significantly longer cross clamping time when GR was made after attempted EA. ECA flow restoration was made in 9 (15.6%) patients with intraoperative decision of the operating surgeon according to the quality of ECA, its’ position related to the implanted graft and elapsed time of the procedure. Reimplantation of ECA did not influence on neurological complication rate.
Early postoperative recovery was uneventful in 36 patients (95%). Early death was reported in 2 patients (5%), due to fatal stroke in the early postoperative time. More one patient had transitory ischemic attack (2,5%) and one had minor stroke (2,5%). Total rate of neurological complications is 7.5%. Comparison of the neurological complications between the groups found higher rates when EA was unsuccessful and GR performed as a bail out procedure. Permanent cranial nerve injuries were reported in 1 patient (2.5%). There was neither early myocardial infarction nor death based on any other cause in this series.
Patients were followed by means of ultrasonography one month after the procedure and yearly thereafter. Mean follow up time was 32 months. Two patients were lost from follow up while 4 patients (10.52%) died during this period of time. Restenosis of less than 75% was reported in 2 patients (5.26%), restenosis of 75-99% was found in 1 patient (2.78%) successfully treated with carotid stenting (Figure 5). In one patient total occlusion of reconstructed artery was revealed with no neurological symptoms.
Mean cross clamping time
Published results since 1979
Restenosis at the proximal anastomosis (A) resolved with carotid stenting (B)
There is no doubt that, over all, endarterectomy is the optimal technique for surgical repair of carotid stenosis. This is the only location where EA is the preferable method nowadays. Choice of EA (conventional or eversion) might cause some discussion between vascular surgeons however the last meta-analysis gave slight advantage to eversion, which was also shown by randomized trial in our institution [27, 28]. Previous Meta analysis showed no difference between the two techniques [27]. The former includes a standard longitudinal carotid arteriotomy with or without patch angioplasty, whereas the second encompasses an oblique transection and eversion of the internal carotid artery and its’ reimplantation into the common carotid artery [29, 30, 31]. Regarding the carotid artery closure after conventional EA, carotid patch angioplasty is preferable to primary closure [32].
Conventional EA requires usage of graft material that is extending procedure and expose patient to the risk of infection [33]. Eversion EA on the other side does not provide sufficient insight in to the complete endarterectomized surface in the zone at the end of the removed atherosclerotic plaque. Also preparing carotid bifurcation for eversion EA requires its complete deliberation from surrounding tissue which might increase the risk of distal embolizations. Elongated internal carotid artery makes patch suturing more complex while shunt placement in these situations is raising the difficulties. Redundant ICA might simplify eversion EA on the other side. Both of these techniques are related to some advantages and disadvantages including surgeons’ familiarity as a specific one. Both of the techniques requires volume of patients in order to achieve good results what might influence the diverse adoption between the teams. According to one multinational registry there is difference in the usage rate of these techniques – in eight European countries EA was performed without patch (34%), with patch (40%) or with eversion (26%). Finally, guidelines of the most important and leading societies are leaving the choice between the two techniques to the operating surgeon [32, 34]. Does it mean that any procedure that removes atherosclerotic plaque from carotid bifurcation and restores flow in a short and long term would be effective in stroke prevention? The similar theory said M.E. DeBakey sixty years ago before his first carotid procedure. DeBakey reasoned that, since endarterectomy and graft replacement in other arteries could be performed, the carotid artery should not be an exception [35].
Carotid stenosis is most frequently localized at the carotid bifurcation leaving proximal and distal segments free from disease providing suitable conditions for endarterectomy. Extension of the atherosclerotic process towards proximally or distally might make endarterectomy cumbersome and risky, while multiple severe atherosclerotic changes at different levels of supra-aortic branches require anatomical or extra-anatomical bypass procedure. Group of patients analyzed in this chapter belongs somewhere between these two patterns of carotid disease – not enough extensive for anatomical bypass through sternotomy while substantially extensive and challenging for eversion EA.
From technical point of view atherosclerotic process that extends proximally and/or distally aggravates endarterectomy jeopardizing the procedure. Initial problem is carotid clamping. It is necessary to extensively dissect internal and common carotid artery in order to provide safe clamping. Clamping at inadequate location of diseased artery might cause plaque rupture with consequent prone to thrombosis causing perioperative embolizations. Also, clamping at inadequate location could cause incomplete EA causing thrombosis especially at the internal carotid artery location. Preventing incomplete EA in this situation requires additional dissection which is more challenging during clamped and transected carotid artery, it prolongs cross clamping time and might stress inexperienced surgeon provoking other mistakes. Reaching healthy zone is important likewise for shunt users in order to prevent placing a shunt through atherosclerotique plaque inducing distal embolizations. Once reaching the conform clamping zone we are faced with technicaly demanding extensive EA. In case of eversion technique problems are visualization of the end of the plaque zone, adequate flushing of the left surface and removal of small residual intimal particles that are prone to mobilization causing distal embolizations [36]. Extensive dissection of internal carotid artery and its deliberation from surrounding tissue facilitate its eversion. On the contrary, common carotid artery is even more difficult to evert through the whole circumference since the posterior wall is fixed with the external carotid artery. Due to that flexibility of common carotid artery depends on deliberation of external carotid artery from surrounding tissue too. In case of extensive athersoclerosis of common carotid artery and average to minimal process on internal carotid artery it is advisible to transect common carotid artery proximal from its’ bifurcation instead of transecting internal carotid artery. This techniqe provides easier EA of common carotid artery in a longer segment [7]. Another technical possibility to deal with extensive atherosclerotic disease in common carotid artery could be semi closed endarterectomy by using Vollmars rings. Finally, for those who preffer conventional technique the very process of EA is quite easier with adequate visualisation of the end of the plaque zone, however, finally the Achille heel of this method is long patch anastomosis that is technicaly demanding and more prone to neointimal hyperplasia or false aneurysm. Anastomotic bleeding on the long patch is another technical difficutly especialy when using intraluminal shunt. Upon removing the shunt, brain perfusion is reduced until complete haemostasis is provided making declamping safe. Loosing time on resolving anastomotic bleeding could cause ishemic brain injury. Overcoming all these technical difficulties does not guarantee sucess since long endarterectomy is leaving long thrombogenic surface prone to in situ thrombosis or distal embolizations jeopardizing the results of the procedure regardless to excellent surgical technique.
All these difficulties were encountered in peripheral vascular surgery inducing usage of different conduits in the reconstructive bypass procedures; similar was done in carotid surgery although less frequently. Bypass in this location could have a good long term potential since it is connecting two healthy arteries with high blood flow and loaded recipient vascular bed, like cerebral, which is inducing low resistance. Still low number of publications is describing this technique in the last 30 years with usage of different conduits. Consequently in the two most respected guidelines for treatment of carotid stenosis this option is not mentioned. However a short review of the published data related to this technique is given below with some technical remarks from the authors of this chapter.
In 1979 M.E.Debakey published his experience in usage of synthetic graft for repair of carotid artery injury [37]. In the same year Cormier and all started to use this type of reconstruction reporting their experience eight years later [38]. Among 62 treated patients 54 (87%) were treated due to extensive atherosclerotic disease, with 5% stroke rate and 97% patency in the 23 months long term follow up. Later, different types of reconstruction were reported using various conduits. Camiade and all used PTFE graft suture with side to end proximally and end to side anastomosis distaly [39]. This technique minimizes dissection of carotid bifurcation and preserves patency of external carotid artery. Authors performed this procedure in 110 patients, indicated it in case of extensive atherosclerotic disease in 45 (41%), while using it also for reconstruction in case od restenosis (16.4%) or kinking (26.4%). There were some other authors reporting usage PTFE graft with similar patency of 95-97% in the long term [40, 41]. The only author that used Dacron graft was Valdeniz with results comparable to those published with PTFE [42]. Autologous saphenous vein was also reported by various authors, some of them complaining on high restenosis rate. French authors are reporting good early and long term results [43, 44, 45]. In 212 patients treated due to extensive atherosclerotic disease (76%), restenosis (5.6%), kinking (8.49%) and aneurysm (4.24%) they reported 5% stroke rate and 96% patency after average 104 months of follow up. On the other side according to the Leicester group saphenous vein is prone to early restenosis in this position even though they performed different anastomotic techniques [46]. According to the diameter of the vein graft and common carotid artery they located anastomosis at the lateral wall of common carotid artery, at the origin of internal carotid artery or at the origin of external carotid artery after its’ exclusion. After average follow up of 60 months patency rate was 83% with significant incidence of restenosis. According to opinion of the authors of this chapter vein graft could be perfect for this procedure, however one might expect misfit of the calibers. Additionally harvesting this graft could be time consuming if so if the graft replacement is performed as a bailout procedure it might prolong cross clamping time and procedure. It is not convenient for carotid procedures performed in cervical plexus block and finally saphenous vein is important conduit for coronary revascularization and should be preserved for that occasion as well. This conduit could be unavailable in patients with varicose syndrome and previous coronary revascularization. Latest publication is from W. Moore reporting 17 years of experience using both synthetic and saphenous vein grafts with satisfying results [47]. 31 PTFE and 10 saphenous grafts were followed for 50 months with patency of 90% and 80%, respectively. Carotid graft replacement is already proved procedure in some other pathology like carotid artery aneurysm and restenosis [48, 49].
Summarized published data show 613 carotid procedures where bifurcation was reconstructed with GR. In all these publications the most frequent indication for graft usage was extensive atherosclerotic disease with involvement of common or distal internal carotid artery – 328 procedures (53.5%). Other indications were carotid recurrent stenosis, technical failure of attempted EA, stenosis after radiation therapy, carotid aneurysm and carotid stenosis associated with kinking. Among 613 carotid stenosis treated with GR, 290 (47,3%) procedures were performed with PTFE graft, 272 (44,37%) with saphenous graft and 51 (8,31%) with Dacron. Extensive and detailed information regarding published data are shown in the Table 4.
When it comes to carotid stenosis, EA is the method of choice in majority of patients. Small subgroup of patients had extensive carotid atherosclerotic disease that involves common or internal carotid artery in a segment longer than 4cm. In these situations modification of surgical procedure is necessary since EA might be jeopardized. Optimal scenario would be to assess extension of atherosclerotic process preoperatively through ultrasonography or MSCT angiography or intraoperatively during dissection of carotid arteries. In case of extensive atherosclerotic process, decision to perform carotid graft replacement without any attempt of EA could simplify procedure, shorten cross clamping time and avoid technical and thromboembolic complications. Conduit choice is the matter of operating surgeon. Upon clamping and resecting diseased segment, suturing distal anastomosis first is recommendable in order to provide easier manipulation and better visualization of anastomotic line. Next step is suturing the proximal anastomosis then flushing and finally carotid declamping. Reimplantation of external carotid artery is not mandatory and the decision should be made as the preference of the surgeon. Efforts to perform EA even in case of extensive disease could be effective especially in experienced hands, however in case of any doubts in wall quality or end of the plaque zone, graft replacement should be performed before flow restoration in order to prevent fatal complications that this procedure carries.
There is not enough evidence to provide any accurate criteria for usage of carotid graft replacement instead of endarterectomy. This chapter showed results, experience and technical details of a single high volume center and presented not so reach published material. Decision to perform graft replacement should be made individually according to anatomy and morphology of carotid disease. Wide surgical experience affords expertise and improves individual decision making.
Authors would like to thank to Katarina Kaplarski for providing illustrations of the procedure.
Presented study is a part of a scientific research project (Grant OI175008) supported by the Ministry of Education and Science of the Republic of Serbia.
Aortic 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
\n
| \n
\n
| \n
\n
| \n
Patients without family history of Marfan disease | \n
\n
| \n
\n
| \n
\n
| \n
\n
| \n
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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