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Medical Conditions Predisposing toAortic Dissection andPreventive Strategies
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aneurysms, and dissection of all the arteries [2]. Patients may present also mild craniofacial-, skin-, and skeletal features [2]. Aneurysm-osteoarthritis syndrome represents at least 2% of all the syndromic familial thoracic acute aortic dissec­tions [2].
Other Syndromic Conditions
Aortic root dilatation has been described in patients with other forms of Ehlers­Danlos syndrome, but the progression to AAD is rare. Furthermore aortic root enlargement (without progression to dissection) may be present in congenital con­tractural arachnodactyly or Beals syndrome (mutation in FBN2). Similarly to Noonan syndrome and Alagille syndrome, patients with autosomal dominant poly­cystic kidney disease have vascular complications including AAD [3].
Non Syndromic Familial Thoracic Aneurysm andDissection Conditions [22]
Non syndromic familial thoracic aneurysm and dissection conditions can be catego­rized in those without and with known gene mutation. One on ve of those without known genetic mutation shows a familial aggregation, with a rst degree relative affected. These patients have an autosomal dominant transmission, with a great clinical variability and a decreased penetrance.
On the other hand when a mutation is recognised the followings are the most important genes identied: MYH11: encoding a myosin heavy chain produced in smooth muscle cell (SMC), is associated also with patent ductus arteriosus; ACTA2: encoding the SMC-specic alpha actin, is associated also with coronary artery disease, stroke and Moyamoya disease; MYLK: encoding myosin light chain kinase. Patients with this mutation usually experience AAD without aortic enlargement; TGFB2: encoding TGF-beta Type 2, has some features overlapping MFS; PRKG1: encoding PKGI, a type I cGMP-dependent protein kinase that con­trols SMC relaxation. Patients present aortic aneurysm and acute ADs at relatively young ages [1, 2].
Bicuspid Aortic Valve
Bicuspid aortic valve (BAV) is the most common congenital cardiac defect (preva­lence at birth of 1–2%; the male:female ratio ranges from 2:1 to 4:1) [1–3]. It has been associated with Notch1 gene mutations, with a high rate of familial cluster­ing, resulting in an autosomal dominant inheritance with reduced penetrance [2,
3]. BAV in the majority of cases (70%) is the result of a fusion between left coro-
nary cusp (LCC)—with right coronary cusp (RCC) [2]. Patients with BAV may have a higher risk of develop an aortic dilatations [2]. In particular, LCC-RCC
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fusion is associated with dilatation in both ascending and aortic root [2]. Notably the prevalence of BAV in patients with AAD is only slightly higher than in the general population [2]. Among 3393 patients with AAD enrolled in the IRAD registry, 113 (3.3%) had BAV of which 82.3% type A AAD and 17.7% type B AAD [23].
E. Bossone et al.
Non Genetic Conditions
Inammatory Vasculitis
Takayasu Arteritis
Takayasu arteritis is an idiopathic vasculitis, characterised by a T-cell-mediated panarteritis, involving the aorta and its branches [1–3]. With an overall rate of 2.6 per million of inhabitants, the most common onset of the disease is in the third decade, with a more prominence in the female sex [1–3]. Firstly described in Japan, it has been demonstrated to affect all ethnic groups, even if with an Asian overrep­resentation, with two specic disease distribution (Japanese and India), which differ for vessels involved. Indeed, thoracic aorta and great vessels are prevalently involved in Japanese distribution, whereas abdominal aorta and renal arteries are typical in Indian one [3]. Clinically it may be distinguished an acute phase (characterised by systemic symptoms) and a chronic phase (with vascular symptoms, such as upper extremity claudication, dizziness, vision loss, stroke, carotid artery pain) [3]. Malignant hypertension suggests involvement of the renal arteries [3]. Different cohort studies have reported different localisation of the aneurysm formation (in about 30% of the population) [3]. Also stenosis of the aorta are very common (in about 53% of patients) [3]. In this regard it is important to obtain an imaging assess­ment of the entire aorta (TTE+CT or MRI). Positron Emission Tomography (PET)/ CT or MRI is useful to visualise active disease [3].
Giant Cell Arteritis
Giant cell arteritis, also known as temporal arteritis, affects the aorta and its second­ary and tertiary branches in about 20–25% of the patients (Fig. 6) [1–3, 24]. Typically, giant cell arteritis affects patients over 50years, with a trend in older population (around 80years) [3]. When the aorta is involved, dilatations of the aor­tic root and of the ascending aorta are the typical features, with a risk of aneurysms rupture or AD [25]. Epidemiological studies suggest a genetical predisposition, with a higher incidence for patients with northern Europe ancestry (e.g. higher in Scandinavian than in Southern Europe) [3]. However, when compared to Takayasu arteritis, aortic involvement is less common [3].
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Behçet Arteritis
One third of the patients affected with Behçet disease (characterised by the classic triad of oral ulcerations, recurrent genital ulceration, uveitis or retinal vasculitis or skin lesions) have a vascular involvement [3]. Any vessels can be affected, and aneurysms formation may occur in multiple and different sites over follow-up [3]. Even if not common, aortic aneurysm rupture can be a fatal event [3].
Other
Atherosclerosis
Atherosclerosis along with systemic hypertension and advance age is considered to be a major determinant of the AAD pathophysiologic process [1–3]. Lipid accumu­lation in the aortic intima-media layer may lead to aortic plaque formation and in turn weaken the underlying media [1–3]. Thus it remains “conditio sine qua no” to adopt preventive measures targeting cardiovascular risk factors [1–3].
Pregnancy
Due to substantial hemodynamic changes and related increase in wall stress, AAD may rarely occur during pregnancy mostly in the last three months and in the peri­partum period [3]. In this regard, among 6,566,826 pregnancies in 4,933,697
Fig. 6 18F-FDG positron emission tomography (PET) scan of a woman with giant cell arteritis. The PET scan reveals aortitis affecting the whole aorta. Reprinted, with permission, from Bossone E, etal. Aortitis. Vascul Pharmacol. 2016;80:1–10 [24].
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women, only 36 cases of AAD or rupture have been identied [26]. Thus it is advised all pregnant women with known aortic root or ascending aortic dilatation should undergo monthly (or bimonthly) clinical -imaging (two dimensional echo­cardiography doppler exam) surveillance [3]. If clinically indicated, MRI (without contrast agents) has to be preferred to CT in order to avoid exposing both the mother and fetus to ionizing radiation [3].
Polycystic Kidney Disease
Autosomal dominant polycystic kidney disease may present AAD as a complica­tion, although AAD is less common than cerebral aneurysms in these patients [3]. However, to date there is no enough evidence to recommend a focused screening in this population [3].
Chronic Corticosteroid or Immunosuppression Agent Administrations
Chronic corticosteroid or immunosuppression agents represent risk factors for infective aortitis (in particular, tuberculosis and fungal infections). In addition, oral steroid usage per se have been associated with abdominal aortic aneurysm expan­sion and aortic dissection [27].
Fluoroquinolones Exposure
Fluoroquinolones (one of the most commonly prescribed class of antibiotics) treat­ment seems to increase the risk of aortic aneurysm and dissection. For this reason, clinicians should consider alternative class of antibiotics in patients with connective tissue disorder or pre-existing aortic aneurysm [28].
Infections Involving theAortic Wall
Several microorganisms have been associated with aortic aneurysms namely Staphylococcus aureus, Salmonella species, Escherichia coli, Streptococcus spe­cies, Neisseria species, and gram negative bacilli [1]. Tertiary syphilis (caused by Treponema pallidum) may involve the cardiovascular systems including ascending aorta aneurysms, coronary arterial stenosis and aortic valvulitis with mitral regurgi­tation in ~40%, ~30% and ~29% of cases respectively. However it should be point out that over the last decades the prevalence of tertiary syphilis is dramatically decreasing due to early stage antibiotic treatment [1]. Fungal (e.g. Candida or Aspergillus) are more frequent in the setting of impaired immunity (such as patients
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affected with human immunodeciency virus, or under immunosuppressive therapy) [2, 24, 29, 30].
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Iatrogenic
Iatrogenic AAD may occur (although rarely) during cardiac catheterization, coro­nary artery bypass graft surgery (CABG), or other invasive vascular procedures [4,
31]. The Registry on Aortic Iatrogenic Dissection (RAID) reported only 74 cases
(0.07%) of ascending AAD (66.9±10.8years, 67.6% male) among 108,083 con­secutive cardiac catheterizations (62% diagnostic and 38% therapeutic procedures) [31]. Interestingly they had favourable in hospital (only 2 deaths due to cardiogenic shock) and long term outcome (no deaths and/or major dissection-related complica­tions) with conservative approach (36 underwent only medical treatment, 35 angio­plasty with stenting, and 3 cardiac surgery) [31].
Preventive Strategies
Despite diagnostic and therapeutic exponential progress, the aortic diseases burden remains still high [32]. Thus, there is an increasing need to promote at individual and population levels healthy lifestyles including no exposure to tobacco in any form, low saturated fat diet, regular vigorous physical activity (30–60 min most days) optimal LDL-C and blood pressure levels, HbA1c <7%. Population screening programs should also be design and implement in relation to systemic hypertension and abdominal aneurysm [2, 7, 33]. In addition the usefulness of screening patients at risk of MFS (positive family history and/or the presence of characteristic clinical physical features) is well recognized [2, 3]. On the other hand the value of screening rst-degree relatives of BAV patients remains debatable (no data support the cost­effectiveness of a screening programme) [2].
Population Screening Programs
Systemic Hypertension
Systemic hypertension is frequently an asymptomatic condition (silent killer) war­rants population screening programmes or opportunistic blood pressure measure­ments in all adults (18 years or older). In fact a substantial number (>50%) of screened subjects are unaware to have hypertension. An optimal ofce blood pres­sure is dened as systolic <120mmHg and diastolic <80mmHg [11, 33].
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Abdominal Aortic Aneurysm
Current evidence supports cost effectiveness abdominal ultrasound (A-US) popula­tion screening for abdominal aortic aneurysm (AAA) in all men >65years of age [2]. It may be considered in women >65years of age with history of current/past smoking and in rst-degree siblings of a patient with AAA [2]. In the absence of structured screening programs it is suggested among above high risk cohorts to perform during TTE an A-US “opportunistic glimpse” for AAAs [2].
AAD: Long Term Follow Up
AAD is a lifelong disease affecting the entire aorta (holistic approach). Thus, patients with AAD need close clinical and imaging follow-up regardless of the ini­tial therapeutic strategy [2, 3]. MRI (in addition to TTE/A-AUS) should be consid­ered the rst imaging technique choice (CT second choice) being radiation free [2,
3]. Medical treatment “cornerstone” includes an optimal blood pressure and heart
rate control (blood pressure <120/80mmHg, heart rate <60bpm (rst line: beta­blockers) as well as HDL-C <1.4mmol/L (<55 mg/dL), or a reduction of at least 50% if the baseline (rst line: statins) [11, 34]. Furthermore the patient should avoid isometric exercise while may perform mild to moderate aerobic exercise (walking, slow jogging, and recreational cycling) (Table2) [7, 33, 35–38].
Table 2 Acute aortic dissection: long-term follow-up
Ten-year survival rate from 30% to 60% Late complications
Progressive aortic insufciency. Progressive diameter increase, aneurysm formation, and rupture. Recurrent dissection or progression of dissection. Leakages/haemorrhage at surgical anastomoses/stent-grafted sites. Malperfusion.
Patients at particularly high risk
Those with Marfan syndrome—very high risk of recurrent dissection or aneurysm formation
with rupture.
Those with a patent false lumen—increased incidence of late complications and death.
Medical treatment
A.Optimal blood pressure (<120/80mmHg) and heart rate (<60 b.p.m.) control. First line: beta-blockers. Second line: ACE-inhibitors or ARBs. Third line: calcium channel blockers (long-acting dihydropyridine). B.Lipid-lowering therapy: target <1.4mmol/L (<55mg/dL), or a reduction of at least 50% if
the baseline. First line: statins. Second line: statins + ezetimibe. Third line: statins + ezetimibe + PCSK9 inhibitors.
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Table 2 (continued)
Imaging surveillance
TTE+A-US + CT or MRI of chest and abdomen before discharge and at 1, 3, 6, and
12months and annually thereafter
Patient education and lifestyle goals
Adherence to medical treatment. Genetic counselling. Smoking cessation and risk factor modication for atherosclerotic disease. Avoid cocaine or other stimulating drugs such as methamphetamine, strenuous physical
activities (isometric exercise, pushing, or straining that would require a Valsalva manoeuvre), and contact sports (e.g. competitive football, ice hockey, or soccer, etc.).
Mild aerobic exercise and daily activities are not restricted. Common sense approach to sexual activity, avoiding straining or maximal exertion.
ACE angiotensin-converting enzyme, ARBs angiotensin II receptor blockers, b.p.m. beats per min- ute, CT computed tomography, LDL low-density lipoprotein, MRI magnetic resonance imaging, PCSK9 proprotein convertase subtilisin/kexin type 9, TTE transthoracic echocardiography, A-US Abdominal ultrasound Modied from Bossone E, LaBounty TM, Eagle KA.Acute aortic syndromes: diagnosis and man­agement, an update. Eur Heart J. 2018;39(9):739–749d [7].
a
Similar surveillance strategy for intramural haematoma and penetrating aortic ulcer is recom-
mended [2]
Acknowledgments We are grateful to Dr. Brigida Ranieri and to Chiara Sepe for data manage­ment and technical support.
a
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What Do theGuidelines Say
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fortheTreatment ofAcute Aortic Syndromes?
JordanP.Bloom, NavyathaMohan, andThoralfM.Sundt
Guidelines inGeneral
Before delving deeply into the guidelines that exist regarding acute aortic syn­dromes, a few general concepts about guidelines are in order. First, it is important to clarify our terminology. Clinical practice guidelines are commonly dened as “sys­tematically developed statements to assist practitioner and patient decisions about appropriate healthcare for specic clinical circumstances” [1]. Typically, the stan­dards of evidence and the formality of the process for constructing guidelines is more rigorous than that for “consensus documents” or “expert opinion” pieces. Still, there can be considerable confusion generated around these terms, motivated in no small measure by the high citation rates such publications achieve, beneting both editors and authors. Hybrid terms such as “consensus guidelines” have even been proffered [2].
The drive to produce guidelines is understandable. Clinical practice guidelines exist as tools to provide evidence-based decision support for busy clinicians in the face of an ever-accelerating volume literature on almost any subject. In the current era, with a proliferation of cardiovascular techniques, technologies and pharmacol­ogies, it is impossible for an individual to keep truly up-to-date on all aspects of cardiovascular care. The deluge of information, good and bad, and the focus on evidence-based care has generated such an appetite for guidelines that we now nd ourselves with the second-order problem of being inundated with guidelines them­selves. A current PubMed search of the word guidelines results in close to 15,000 published manuscripts.
J. P. Bloom · N. Mohan · T. M. Sundt (*) Division of Cardiac Surgery, Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA e-mail: TSUNDT@mgh.harvard.edu
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_8
105© Springer Nature Switzerland AG 2021
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