Acute aortic syndrome | Medicina Clínica (English Edition)

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Contrast-enhanced axial images of a patient with type A IMH involving the ascending and descending aorta (A) and a patient with a classic aortic dissection in the aortic arch (B). (A) Shows the semi-circumferential aortic wall thickening (*) typical of IHM and displacement of the calcified intima (arrow). (B) Shows the true lumen is the central lumen and the false lumen is the lateral lumen. Ao: aorta; PA: pulmonary artery." ] ] ] "textoCompleto" => "IntroductionThe nosography of acute aortic syndrome (AAS) was described in 2001.<a class="elsevierStyleCrossRef" href="#bib0005">1</a> It refers to a heterogeneous group of patients with a similar clinical presentation, most notably 'aortic pain'. It encompasses four types of acute aortic lesions: classical aortic dissection (CD), intramural haematoma (IMH), penetrating aortic ulcer (PAU) and incomplete dissection (ID).<a class="elsevierStyleCrossRef" href="#bib0010">2</a> This review aims to outline the pathogenesis of AAS and update the epidemiology, diagnostic strategy and current management of these patients.<a class="elsevierStyleCrossRef" href="#bib0015">3</a>Components of acute aortic syndrome. Definition, pathophysiology and classificationsThe morpho-anatomical characteristics of the constituent elements of AAS can be seen in <a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>.<elsevierMultimedia ident="fig0005"></elsevierMultimedia>From a surgical and prognostic point of view, patients with AAS are classified into two categories depending on whether the lesion affects (type A) or not (type B) the ascending aorta.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> There is a third category (non-A, non-B type) in which the lesion is located exclusively in the aortic arch, or the aortic arch is reached after retrograde propagation of a tear located in the descending aorta and does not involve the ascending aorta (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). There are other dissection classifications (DeBakey, Penn, DISSECT, etc.), but the TEM classification<a class="elsevierStyleCrossRef" href="#bib0020">4</a> deserves special consideration for its simplicity and usefulness in the clinical assessment of these patients. It considers three essential data: the type of dissection “type”, the location of the port of entry “entry” and the presence or absence of malperfusion “malperfusion”. This last aspect will be key in the treatment and prognosis of these patients.<elsevierMultimedia ident="fig0010"></elsevierMultimedia>By definition, CD is characterised by a separation of the aortic media and an intimal-medial tear. The most common hypothesis holds that the tear, also called the “entry”, is the dissection genesis of the tunica media. The inflow of pressurised blood then dissects the media lengthwise and a double lumen aorta is formed.<a class="elsevierStyleCrossRef" href="#bib0025">5</a> Thus, in CD we have three differential elements: the intimal-medial flap, two aortic channels (true lumen and false lumen) and a port of entry (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).<a class="elsevierStyleCrossRef" href="#bib0025">5</a>The most common histopathological lesion in CD is degeneration of the media consisting of fragmentation of the elastic fibres and accumulation of mucoid material in the extracellular matrix.<a class="elsevierStyleCrossRefs" href="#bib0025">5–7</a> The aortic wall becomes less compact and a kind of parietal “aluminosis” occurs, decreasing its resistance to haemodynamic stress. Degeneration of the tunica media is considered to be the final common pathway in different causes of AAS (hypertension, Marfan syndrome, etc.). In connective tissue diseases and aortic aneurysms this degeneration is more important than in hypertensive patients.<a class="elsevierStyleCrossRefs" href="#bib0015">3,5</a>We do not know why a patient ultimately dissects. Hypothetically, a genetic predisposition would favour degeneration of the media which, with or without the influence of cardiovascular risk factors (especially hypertension), would lead to aortic dilatation. Subsequently, a precipitating factor (hypertension, physical or emotional stress, etc.) would lead to an intimal-medial tear.<a class="elsevierStyleCrossRef" href="#bib0040">8</a>According to its original definition, IMH is a dissection without an intimal-medial tear (no port of entry). It is therefore a dissection in which the two lumens are not communicating (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). It is an intraparietal haemorrhage contained within the aortic wall and has been attributed to a rhexis of the vasa vasorum that arborise from the adventitia into the media.<a class="elsevierStyleCrossRefs" href="#bib0025">5,9</a> It is likely that many cases of CD and IMH, especially type A, have the same pathogenesis.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> Thus, IMH would actually represent CD with acute thrombosis of the false lumen (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).<a class="elsevierStyleCrossRef" href="#bib0050">10</a> There is one distinctive feature of IMH: the absence of pressurised flow within the false lumen. This explains the characteristic morphology of this entity on imaging techniques (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>) and its dynamic behaviour, as it can either spontaneously reabsorb or progress to a CD.<a class="elsevierStyleCrossRefs" href="#bib0025">5,9</a><elsevierMultimedia ident="fig0015"></elsevierMultimedia>Most ulcerated aortic atherosclerotic plaques involve the intima and do not extend into the tunica media. PAU is an atherosclerotic plaque that, after initial erosion and ulceration, ruptures the internal elastic lamina and penetrates the tunica media.<a class="elsevierStyleCrossRef" href="#bib0055">11</a> They are focal lesions that occur within extensive atherosclerosis and are mainly located in the descending aorta (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). They are often accompanied by limited intramural haemorrhage that may spread along the descending aorta, but usually the existing parietal fibrosis and calcification prevent the haemorrhage from progressing lengthwise. PAU may progress to aortic dilatation (saccular aneurysm), progressive destruction of the media (pseudoaneurysm and rupture) or more rarely to dissection. In the latter case, the port of entry is the excavated area or 'crater' of the PAU. The clinical course of these patients is variable, but most are asymptomatic at the time of diagnosis and only a few develop an AAS.<a class="elsevierStyleCrossRefs" href="#bib0015">3,12,13</a>ID was described by Murray and Edwards in 1973<a class="elsevierStyleCrossRef" href="#bib0070">14</a> and refers to those cases of AAS in which there is laceration of the intima and underlying media (intimomedial tear) without significant intramural haematoma<a class="elsevierStyleCrossRef" href="#bib0015">3</a> (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). The base of the lacerated area usually contains a certain proportion of media and adventitia. There is no false lumen as such, and it is accompanied by some degree of subadventitial haematoma causing eccentric protrusion of the aortic wall. It occurs most commonly in the ascending aorta, and it is often accompanied by aortic regurgitation. It can be easily missed without a high index of suspicion.<a class="elsevierStyleCrossRef" href="#bib0075">15</a> In contrast to ID, CD may be referred to as complete aortic dissection.<a class="elsevierStyleCrossRef" href="#bib0015">3</a>A unique feature of these aortic lesions is that they can occur synchronously, i.e., simultaneously in different aortic segments or, even more often, one after the other in the same aortic segment. Thus, IMH may be the prelude to CD, many cases of PAU are accompanied by some degree of IMH, and, exceptionally, PAU may progress to dissection and an ID to a CD. Any of these lesions can lead to aortic rupture.<a class="elsevierStyleCrossRef" href="#bib0015">3</a>Current epidemiology of acute aortic syndromeHospital-based studies, retrospective case series and case-control studies underestimate both the incidence and lethality of AAS by not including out-of-hospital deaths.Recently, large population-based cohort studies have estimated the average annual incidence of CD to be between 6 and 7.2 cases per 100,000 population per year.<a class="elsevierStyleCrossRefs" href="#bib0080">16,17</a> The incidence of IMH and PAU is lower than that of CD.<a class="elsevierStyleCrossRef" href="#bib0090">18</a> ID accounts for approximately 5% of all patients with type A AAS. Type A lesions are more common in patients with CD and ID, while type B lesions are more commonly diagnosed in patients with IMH and PAU.<a class="elsevierStyleCrossRef" href="#bib0090">18</a>The incidence of AAS is twice as common in men as in women and increases with age.<a class="elsevierStyleCrossRefs" href="#bib0085">17,18</a> The average age of these patients varies according to the type of aortic lesion; it is lower in CD cases (68 years) and higher in PAU cases (77 years).<a class="elsevierStyleCrossRef" href="#bib0090">18</a> Women with CD have a different clinical presentation, arrive later at the hospital, in worse clinical condition than men, and have higher mortality.<a class="elsevierStyleCrossRefs" href="#bib0080">16,17,19</a> 30–50% of patients with type A CD die at home or before reaching the hospital.<a class="elsevierStyleCrossRefs" href="#bib0080">16,17,20</a>Analysis of the US national database shows an increase in hospitalisations for CD while hospital mortality (26%) is virtually the same.<a class="elsevierStyleCrossRef" href="#bib0105">21</a>Aortic centres, aorta code and aortic pathology teamsThe clear relationship between patient volume and surgical outcomes makes it necessary and justifiable to centralise the management of acute aortic disease in ‘aortic centres’ (centres with high surgical volume and surgeons with expertise in aortic surgery).<a class="elsevierStyleCrossRefs" href="#bib0110">22–24</a>In this regard, care networks have been set up under the "aorta code" umbrella for the care of patients with AAS.<a class="elsevierStyleCrossRef" href="#bib0120">24</a> They consist of a multidisciplinary team with experience in aortic disease, are available every day at all hours and are activated from the Emergency Departments of the hospitals belonging to the network. The “aorta code” seeks to accomplish three things: 1) to increase the level of alertness and awareness of AAS among ED physicians for early detection of patients with AAS; 2) to accelerate the transfer of the patient to the aortic centre of reference; and 3) to provide optimal treatment by activating a highly specialised team.At the aortic centre, the aortic team is responsible for quickly determining the best therapeutic strategy for each patient (open surgery, endovascular treatment, hybrid procedures combining open and endovascular surgery, conservative treatment) and for close follow-up.Centralising the management of AAS patients in “few centres and few hands” offers the best opportunity to improve outcomes.<a class="elsevierStyleCrossRef" href="#bib0125">25</a>Diagnosis of acute aortic syndrome in the emergency department. Three-step diagnostic algorithmIn the emergency department, an accurate diagnosis in the shortest possible time is essential. If in acute coronary syndromes the aphorism “time is muscle” has been proposed as a rule of action, here, in AAS, time is even more important, and we could say that “time is life”. There are three reasons why detection of the AAS patient in the ED is a diagnostic challenge: the low prevalence of the disease, a variable clinical presentation and the absence of specific biomarkers. Therefore, the risk of error and delay in diagnosis is high and the consequences are significant. To get round this situation, continuous training programmes in emergency departments and the use of a simple diagnostic algorithm are key.The latest European Society of Cardiology guidelines on the diagnosis and treatment of aortic disease recommend a confusing and complex diagnostic algorithm.<a class="elsevierStyleCrossRef" href="#bib0130">26</a> Currently, most emergency departments do not follow a specific algorithm for the diagnosis of AAS. Our group proposes the application of a three-step diagnostic algorithm<a class="elsevierStyleCrossRef" href="#bib0015">3</a> (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).First step. Calculate the a priori probability of having an AAS by considering the three risk categories proposed by the American Society of Cardiology (predisposing conditions, pain characteristics and physical examination findings).<a class="elsevierStyleCrossRef" href="#bib0135">27</a> In 2011, an aortic dissection risk score was introduced to facilitate detection.<a class="elsevierStyleCrossRef" href="#bib0140">28</a> Each category is assigned a point if a risk marker of that category is present. A score of 0 implies a low risk of AAS; if the score is 1, the risk is intermediate; and if it is ≥ 2, the risk of having an AAS is high. The pretest probability calculation is a Class I recommendation.<a class="elsevierStyleCrossRefs" href="#bib0130">26,27</a>Among the risk factors, the most common is a history of long-term severe hypertension<a class="elsevierStyleCrossRef" href="#bib0145">29</a> and, surprisingly, it does not appear in the predisposing conditions of high risk of dissection.<a class="elsevierStyleCrossRef" href="#bib0140">28</a> Adding this factor increases the sensitivity of the risk score.It is essential to quickly recognise the so-called “aortic pain”.<a class="elsevierStyleCrossRef" href="#bib0150">30</a> This is a very intense, sharp (stabbing), tearing, throbbing, pulsating and migratory chest pain. If it radiates to the neck, it indicates that the ascending aorta is affected, whereas if it is located in the back or abdomen, the diseased segment is usually the descending aorta.<a class="elsevierStyleCrossRef" href="#bib0025">5</a> Including “aortic pain” as a discriminator in the clinical presentation of chest pain in the Manchester triage system or similar classification systems results in early detection of patients with AAS.<a class="elsevierStyleCrossRef" href="#bib0020">4</a> On the other hand, as might be expected, if we are lax with pain characteristics, the specificity of the risk scale decreases. Likewise, a systematic physical examination and the ability to detect high-risk findings will increase the sensitivity of the scale.<a class="elsevierStyleCrossRef" href="#bib0150">30</a>In short, to correctly assess the a priori probability of having an AAS it is necessary to consider risk factors, pain characteristics and physical examination findings. However, it has been shown that the application of this risk score alone in the emergency department is not sufficient. It has a low specificity and an unacceptable number of false positives.<a class="elsevierStyleCrossRefs" href="#bib0155">31,32</a>Second step. After clinical suspicion and physical examination, in-hospital assessment of all patients with chest pain includes an electrocardiogram and a blood test with troponin and D-dimer.<a class="elsevierStyleCrossRef" href="#bib0165">33</a> Elevated blood D-dimer levels have a high sensitivity in the diagnosis of AAS, correlate with the extent of aortic injury and are higher in CD than in IMH.<a class="elsevierStyleCrossRef" href="#bib0170">34</a> The higher the D-dimer levels, the higher the probability that the patient has AAS, especially if it is ≥ 1600 ng/ml.<a class="elsevierStyleCrossRef" href="#bib0175">35</a> No less important is its high negative predictive value. That is, normal D-dimer levels virtually rule out the diagnosis of AAS.<a class="elsevierStyleCrossRef" href="#bib0170">34</a> The accuracy of the dissection risk score has been shown to improve when combined with D-dimer levels.<a class="elsevierStyleCrossRef" href="#bib0180">36</a> It should be noted that an elevated D-dimer level does not distinguish between AAS and pulmonary embolism, but it does prompt, in both cases, an urgent chest CT scan that can confirm or exclude both entities.<a class="elsevierStyleCrossRefs" href="#bib0140">28,31,37</a>Acute coronary syndrome is the most important differential diagnosis in patients with AAS.<a class="elsevierStyleCrossRef" href="#bib0190">38</a> In patients with aortic pain, the combination of a normal ECG, normal troponins and elevated D-dimer levels are a red flag for AAS and makes it unlikely that the patient has an acute coronary syndrome (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).<a class="elsevierStyleCrossRef" href="#bib0015">3</a> It should be kept in mind, however, that elevated troponin levels do not totally exclude an AAS and a chest CT should not be omitted if D-dimer levels are elevated and the clinical suspicion of AAS is high.Chest radiography is classically performed in all patients with chest pain and is useful in many cases. It is important to remember that it is often normal in patients with AAS and therefore does not exclude the presence of AAS.<a class="elsevierStyleCrossRef" href="#bib0010">2</a>Third step. Imaging is necessary to reach a definitive diagnosis of AAS.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> CT, which is widely available in emergency departments, is the diagnostic technique of choice<a class="elsevierStyleCrossRefs" href="#bib0195">39,40</a> (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). Any patient with a risk score ≥ 1 and elevated D-dimer levels should have a CT scan of the aorta (from the neck to the iliofemoral vessels), especially if troponin levels are normal and there is no change in the electrocardiogram. CT should be performed without contrast, to avoid false negatives in patients with IMH and with contrast,<a class="elsevierStyleCrossRefs" href="#bib0195">39,40</a> and synchronised with the ECG, to avoid false positives due to aortic root motion and ascending aorta.<a class="elsevierStyleCrossRef" href="#bib0205">41</a>A transthoracic echocardiogram (TTE) in the ED may be useful, as it provides information on some relevant aspects: pericardial effusion, ventricular function, aortic regurgitation, etc.<a class="elsevierStyleCrossRef" href="#bib0210">42</a> It is important to bear in mind that a normal TTE does not exclude the diagnosis of AAS. Although transoesophageal echocardiography has excellent diagnostic accuracy in AAS and its complications,<a class="elsevierStyleCrossRefs" href="#bib0215">43,44</a> we advocate avoiding its routine use in AAS, especially if the patient is unstable. On the other hand, it is very useful in the operating room, especially if we decide to preserve the aortic valve.<a class="elsevierStyleCrossRefs" href="#bib0015">3,27</a> At present, the role of MRI in patients with suspected AAS in the ED is anecdotal.Differential diagnosis of acute aortic syndrome by computed tomographyFamiliarity with the different constituents of the AAS and similar entities is important for the proper interpretation of a CT scan.<a class="elsevierStyleCrossRefs" href="#bib0015">3,40,41</a>CD with acute thrombosis versus IMH. In both cases, the two lumens, false and true, are not communicating. When the port of entry of the CD is small and the exit (decompression port) is absent or closed, acute and rapid false lumen thrombosis can occur.<a class="elsevierStyleCrossRef" href="#bib0010">2</a> In these cases, the CT images obtained resemble those of patients with IHM. The distinction between the two entities is not always possible, but by combining axial and sagittal planes we can observe an alteration of the intima contour corresponding to the intimomedial tear of the CD. By definition, there is no such tear in IMH.<a class="elsevierStyleCrossRefs" href="#bib0015">3,41</a>Aortitis versus IMH. The typical CT image of IMH is a semi-circumferential thickening of the aortic wall with no contrast within the aortic wall and a smooth luminal surface (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>). In aortitis, the aortic wall thickening is circumferential. Positron emission tomography will be helpful in distinguishing the inflammatory process from IMH.<a class="elsevierStyleCrossRef" href="#bib0225">45</a><elsevierMultimedia ident="fig0020"></elsevierMultimedia>Mural thrombus versus IMH. Dilated aorta can be accompanied by mural thrombosis which in some cases simulates IMH. In contrast to mural thrombosis, hyperdense aortic wall thickening can be seen on non-contrast images (hyperdense crescent sign). In addition, IMH shifts the calcification of the intima inwards into the aortic lumen whereas, in mural thrombus, the calcifications are usually located along the outer edge of the aortic wall.<a class="elsevierStyleCrossRef" href="#bib0205">41</a>PAU versus ulcer-like imaging. PAU and ulcer-like images are not the same entity. The latter are the result of an intimomedial tear and are accompanied by a dissecting intraparietal haematoma. On CT they appear as punch-like areas with extensive communication with the aortic lumen and are not accompanied by alteration of the aortic wall contour.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> They are not accompanied by calcified atherosclerotic lesions and are in fact the port of entry to CD with acute false lumen thrombosis.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> The detection of these lesions is associated with a higher number of aortic events at follow-up (aneurysms, pseudoaneurysms, focal dissections and aortic rupture).<a class="elsevierStyleCrossRef" href="#bib0230">46</a>The typical CT imaging for PAU corresponds to a wide-necked, punch-shaped aortic parietal lesion, which, unlike ulcer-like images, causes remodelling of the parietal contour. It settles around calcified atherosclerotic plaques and is usually accompanied by some degree of IMH.<a class="elsevierStyleCrossRef" href="#bib0055">11</a> Most ulcers are located in the descending aorta and arch.In summary, the distinction between the different entities is made on the basis of lesion morphology, interface with the aortic lumen, presence of hyperattenuation on non-contrast images, coexistence with atherosclerotic lesions and location of calcification.Current treatment of acute aortic syndromeEvery patient with AAS should be treated in a Cardiovascular Acute Care Unit with three immediate goals: control of blood pressure (≤ 120−100 mmHg), heart rate (≤60 bpm) and pain. For this, we use a combination of intravenous beta-blockers, hypotensive agents and sedatives.Type A CD. It is a surgical emergency.<a class="elsevierStyleCrossRefs" href="#bib0130">26,27,47</a> The type of intervention depends on the aortic segments involved, the condition of the aortic valve and the clinical condition of the patient. The goals of surgery are to prevent aortic rupture, correct valve regurgitation and resolve any malperfusion. A replacement of the ascending aorta and hemiarch with resuspension of the aortic valve is performed in most patients.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> When the aortic root is severely compromised or in connective tissue diseases (Marfan syndrome), the usual treatment is replacement of the root and ascending aorta with a composite valve tube; the coronary arteries are reimplanted in the tube.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> This technique, a modified version of the classic Bentall-De Bono procedure, is the standard treatment in type A CD with aortic root involvement.<a class="elsevierStyleCrossRef" href="#bib0240">48</a> If the dissection respects the sinuses of Valsalva, the interposition of a supracoronary tube may be sufficient. Aortic valve preservation techniques are a valid alternative in haemodynamically stable patients with favourable anatomy and in the hands of experienced surgeons.In order to avoid future reinterventions, some authors recommend total aortic arch replacement in the following situations: significant arch dilatation, extensive arch tears and dissection of the supra-aortic trunks.<a class="elsevierStyleCrossRef" href="#bib0245">49</a> The ‘elephant trunk’ technique using hybrid prostheses allows total repair of the arch and the proximal segment of the descending aorta while closing the port of re-entry.<a class="elsevierStyleCrossRef" href="#bib0250">50</a>An individualised therapeutic approach should be taken based on the surgeon's experience, extent of the lesion, haemodynamic status and clinical profile of the patient.<a class="elsevierStyleCrossRef" href="#bib0255">51</a>Type B CD. Medical treatment remains the treatment of choice for uncomplicated type B CD.<a class="elsevierStyleCrossRefs" href="#bib0130">26,27</a> The indicated treatment in complicated type B CD is thoracic endovascular aneurysm repair (TEVAR).<a class="elsevierStyleCrossRefs" href="#bib0130">26,27</a> The main complications of type B CD are listed in <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>. TEVAR may be considered to prevent future aortic complications in some patients with uncomplicated type B CD.<a class="elsevierStyleCrossRefs" href="#bib0130">26,27,52</a> Regarding Marfan syndrome, whether TEVAR is more appropriate than open surgery is still under discussion.<a class="elsevierStyleCrossRef" href="#bib0265">53</a> The latter is a good alternative when endovascular treatment fails or is contraindicated.<a class="elsevierStyleCrossRefs" href="#bib0130">26,47,54</a><elsevierMultimedia ident="tbl0005"></elsevierMultimedia>Non-A, non-B type CD. Treatment must be individualised. The port of entry is usually in the arch in half of the cases and in the descending aorta in the other half.<a class="elsevierStyleCrossRef" href="#bib0275">55</a> Endovascular techniques, open surgery (elephant trunk) or hybrid aortic repair offer good results.<a class="elsevierStyleCrossRefs" href="#bib0110">22,56</a>Incomplete dissection. If the lesion involves the ascending aorta it is treated as a type A CD: emergent surgery.<a class="elsevierStyleCrossRef" href="#bib0015">3</a>Type A IMH. The optimal treatment of these patients is not well established. European and American clinical practice guidelines recommend emergency surgery,<a class="elsevierStyleCrossRefs" href="#bib0130">26,27</a> while Asian guidelines only recommend surgery if the clinical course is poor.<a class="elsevierStyleCrossRef" href="#bib0285">57</a> It is true that mortality in patients with type A IMH is lower than in those with type A CD and that complications such as aortic regurgitation, tamponade and malperfusion syndromes are less common in patients with type A CD.<a class="elsevierStyleCrossRef" href="#bib0290">58</a> Our group advocates initial medical treatment in patients without poor outcome indicators (aortic diameter < 50 mm and absence of intimomedial tears) and haemodynamically stable, especially if they are elderly and have comorbidities. The rest require urgent surgery (<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>).<a class="elsevierStyleCrossRef" href="#bib0015">3</a><elsevierMultimedia ident="tbl0010"></elsevierMultimedia>Type B IMH. Initial treatment is medical.<a class="elsevierStyleCrossRefs" href="#bib0130">26,27</a> Close follow-up with CT scan and D-dimer levels is important.<a class="elsevierStyleCrossRefs" href="#bib0015">3,59</a> If complications occur, the treatment of choice is TEVAR.<a class="elsevierStyleCrossRef" href="#bib0295">59</a> The presence of intimomedial tears is associated with a higher rate of aortic complications.<a class="elsevierStyleCrossRef" href="#bib0015">3</a>Penetrating aortic ulcer. Treatment is similar to that of type B IMH. In symptomatic patients or those with large or complicated ulcers, treatment with TEVAR should be considered.<a class="elsevierStyleCrossRefs" href="#bib0045">9,47</a>Prevention of acute aortic syndromeMeasures to prevent the onset of AAS can be summarised in four points: a thorough family medical history, preventive surgery, control of high blood pressure and pharmacological treatment.A family history of aortic dissection and aortic aneurysm are risk factors for AAS.<a class="elsevierStyleCrossRef" href="#bib0130">26</a> Periodic monitoring with imaging techniques and genetic testing is advisable in individuals with a family history of AAS or aortic aneurysm. In patients with aortic aneurysm, clinical practice guidelines recommend aortic repair depending on the diameter of the aneurysm (>50−55 mm), the rate of progression of aortic dilatation, the presence of other risk factors and the clinical profile of the patient.<a class="elsevierStyleCrossRefs" href="#bib0130">26,27</a>Aortic wall ‘stabilising’ treatments such as beta-blockers and angiotensin II receptor antagonists should be used early in order to prevent aneurysm progression. However, the use of these drugs in patients without connective tissue disorders has not been shown to decrease the likelihood of developing an AAS.Hypertension is an independent predictor of type A CD.<a class="elsevierStyleCrossRef" href="#bib0145">29</a> Therefore, careful control of blood pressure is essential.Population-based cohort studies have shown that the use of fluoroquinolones is associated with an increased risk of CD and aortic aneurysm.<a class="elsevierStyleCrossRef" href="#bib0300">60</a> In addition, patients with aortic aneurysm have more complications if treated with this type of antibiotics.<a class="elsevierStyleCrossRef" href="#bib0300">60</a> Therefore, fluoroquinolones should not be used in these patients whenever a therapeutic alternative is available.Final considerationsProgress has been made in the diagnosis and treatment of patients with AAS over the past two decades, but many challenges remain. To mention a few, it is essential to find specific AAS biomarkers for early diagnosis, to promote the creation of aortic centres and aorta codes, to expand the intravascular therapeutic offer for patients with type A AAS and high surgical risk, and to conduct multicentre clinical trials to test the efficacy of preventive interventions.FundingNone.Conflict of interestThe authors declare that they have no conflicts of interest." "textoCompletoSecciones" => array:1 [ "secciones" => array:16 [ 0 => array:3 [ "identificador" => "xres2080285" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1774688" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres2080286" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1774687" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Components of acute aortic syndrome. Definition, pathophysiology and classifications" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Current epidemiology of acute aortic syndrome" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Aortic centres, aorta code and aortic pathology teams" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Diagnosis of acute aortic syndrome in the emergency department. Three-step diagnostic algorithm" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Differential diagnosis of acute aortic syndrome by computed tomography" ] 10 => array:2 [ "identificador" => "sec0035" "titulo" => "Current treatment of acute aortic syndrome" ] 11 => array:2 [ "identificador" => "sec0040" "titulo" => "Prevention of acute aortic syndrome" ] 12 => array:2 [ "identificador" => "sec0045" "titulo" => "Final considerations" ] 13 => array:2 [ "identificador" => "sec0050" "titulo" => "Funding" ] 14 => array:2 [ "identificador" => "sec0055" "titulo" => "Conflict of interest" ] 15 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2023-04-25" "fechaAceptado" => "2023-07-24" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1774688" "palabras" => array:5 [ 0 => "Acute aortic syndrome" 1 => "Aortic dissection" 2 => "Intramural aortic hematoma" 3 => "Aortic code" 4 => "Penetrating aortic ulcer" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1774687" "palabras" => array:5 [ 0 => "Síndrome aórtico agudo" 1 => "Disección aórtica" 2 => "Hematoma intramural aórtico" 3 => "Código aorta" 4 => "Úlcera penetrante aórtica" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "Acute aortic syndrome embraces a group of heterogenous pathological entities involving the aortic wall with a common clinical profile. The current epidemiology, clinical presentation, diagnosis and treatment strategy are discussed in this review. Besides, the importance of multidisciplinary aortic teams, aortic centres and the implementation of an aortic code are emphasized." ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "El síndrome aórtico agudo agrupa distintas entidades que afectan a la pared aórtica y que tienen una presentación clínica común. En esta revisión se exponen aspectos relevantes sobre su epidemiología, presentación clínica, diagnóstico y estrategias de tratamiento. Además, se analiza la importancia de los equipos multidisciplinares y los centros de aorta en la atención y el pronóstico de los pacientes con síndrome aórtico agudo." ] ] "multimedia" => array:6 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2560 "Ancho" => 3175 "Tamanyo" => 591744 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Components of acute aortic syndrome. D: dissection; CD: classical dissection; FL: false lumen." ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1574 "Ancho" => 1508 "Tamanyo" => 180948 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Classification of acute aortic syndrome." ] ] 2 => array:8 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1464 "Ancho" => 2508 "Tamanyo" => 257974 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0015" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Three-step diagnostic algorithm for acute aortic syndrome. TTE: transthoracic echocardiogram; CT: computed tomography." ] ] 3 => array:8 [ "identificador" => "fig0020" "etiqueta" => "Fig. 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 510 "Ancho" => 1207 "Tamanyo" => 67141 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0020" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Computed tomography. Contrast-enhanced axial images of a patient with type A IMH involving the ascending and descending aorta (A) and a patient with a classic aortic dissection in the aortic arch (B). (A) Shows the semi-circumferential aortic wall thickening (*) typical of IHM and displacement of the calcified intima (arrow). (B) Shows the true lumen is the central lumen and the false lumen is the lateral lumen. Ao: aorta; PA: pulmonary artery." ] ] 4 => array:7 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0025" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Complications of type B classical dissection \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Malperfusion syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Haemodynamic instability (hypotension-shock) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Progressive aortic dilatation \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Signs of aortic rupture/periaortic haematoma \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab3444429.png" ] ] ] ] ] 5 => array:7 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0030" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Indicators of poor outcome in type A IMH \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Aortic diameter ≥ 50 mm \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Progressive aortic dilatation \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- IMH thickness ≥ 11 mm \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Detection of ulcer-like lesions \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Moderate-severe pericardial effusion/ tamponade \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Pleural effusion ≥ moderate \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Periaortic haematoma/radiological signs of impending rupture \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Haemodynamic instability (hypotension-shock) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Refractory pain \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">- Malperfusion syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab3444430.png" ] ] ] ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:60 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Acute aortic syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "I. 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Acute aortic syndrome

Síndrome aórtico agudo

Isidre Vilacostaa,

Corresponding author

i.vilacosta@gmail.com

Corresponding author.

, Carlos Ferreraa, Alberto San Románb

a Instituto Cardiovascular, Hospital Clínico San Carlos, Madrid, Spain

b Instituto de Ciencias del Corazón, Hospital Clínico Universitario de Valladolid, Valladolid, Spain

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          "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Computed tomography&#46; Contrast-enhanced axial images of a patient with type A IMH involving the ascending and descending aorta &#40;A&#41; and a patient with a classic aortic dissection in the aortic arch &#40;B&#41;&#46; &#40;A&#41; Shows the semi-circumferential aortic wall thickening &#40;&#42;&#41; typical of IHM and displacement of the calcified intima &#40;arrow&#41;&#46; &#40;B&#41; Shows the true lumen is the central lumen and the false lumen is the lateral lumen&#46; Ao&#58; aorta&#59; PA&#58; pulmonary artery&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">The nosography of acute aortic syndrome &#40;AAS&#41; was described in 2001&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> It refers to a heterogeneous group of patients with a similar clinical presentation&#44; most notably &#39;aortic pain&#39;&#46; It encompasses four types of acute aortic lesions&#58; classical aortic dissection &#40;CD&#41;&#44; intramural haematoma &#40;IMH&#41;&#44; penetrating aortic ulcer &#40;PAU&#41; and incomplete dissection &#40;ID&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> This review aims to outline the pathogenesis of AAS and update the epidemiology&#44; diagnostic strategy and current management of these patients&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Components of acute aortic syndrome&#46; Definition&#44; pathophysiology and classifications</span><p id="par0010" class="elsevierStylePara elsevierViewall">The morpho-anatomical characteristics of the constituent elements of AAS can be seen in <a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">From a surgical and prognostic point of view&#44; patients with AAS are classified into two categories depending on whether the lesion affects &#40;type A&#41; or not &#40;type B&#41; the ascending aorta&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> There is a third category &#40;non-A&#44; non-B type&#41; in which the lesion is located exclusively in the aortic arch&#44; or the aortic arch is reached after retrograde propagation of a tear located in the descending aorta and does not involve the ascending aorta &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; There are other dissection classifications &#40;DeBakey&#44; Penn&#44; DISSECT&#44; etc&#46;&#41;&#44; but the TEM classification<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> deserves special consideration for its simplicity and usefulness in the clinical assessment of these patients&#46; It considers three essential data&#58; the type of dissection &#8220;type&#8221;&#44; the location of the port of entry &#8220;entry&#8221; and the presence or absence of malperfusion &#8220;malperfusion&#8221;&#46; This last aspect will be key in the treatment and prognosis of these patients&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">By definition&#44; CD is characterised by a separation of the aortic media and an intimal-medial tear&#46; The most common hypothesis holds that the tear&#44; also called the &#8220;entry&#8221;&#44; is the dissection genesis of the tunica media&#46; The inflow of pressurised blood then dissects the media lengthwise and a double lumen aorta is formed&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Thus&#44; in CD we have three differential elements&#58; the intimal-medial flap&#44; two aortic channels &#40;true lumen and false lumen&#41; and a port of entry &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The most common histopathological lesion in CD is degeneration of the media consisting of fragmentation of the elastic fibres and accumulation of mucoid material in the extracellular matrix&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#8211;7</span></a> The aortic wall becomes less compact and a kind of parietal &#8220;aluminosis&#8221; occurs&#44; decreasing its resistance to haemodynamic stress&#46; Degeneration of the tunica media is considered to be the final common pathway in different causes of AAS &#40;hypertension&#44; Marfan syndrome&#44; etc&#46;&#41;&#46; In connective tissue diseases and aortic aneurysms this degeneration is more important than in hypertensive patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;5</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">We do not know why a patient ultimately dissects&#46; Hypothetically&#44; a genetic predisposition would favour degeneration of the media which&#44; with or without the influence of cardiovascular risk factors &#40;especially hypertension&#41;&#44; would lead to aortic dilatation&#46; Subsequently&#44; a precipitating factor &#40;hypertension&#44; physical or emotional stress&#44; etc&#46;&#41; would lead to an intimal-medial tear&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">According to its original definition&#44; IMH is a dissection without an intimal-medial tear &#40;no port of entry&#41;&#46; It is therefore a dissection in which the two lumens are not communicating &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; It is an intraparietal haemorrhage contained within the aortic wall and has been attributed to a rhexis of the <span class="elsevierStyleItalic">vasa vasorum</span> that arborise from the adventitia into the media&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;9</span></a> It is likely that many cases of CD and IMH&#44; especially type A&#44; have the same pathogenesis&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Thus&#44; IMH would actually represent CD with acute thrombosis of the false lumen &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> There is one distinctive feature of IMH&#58; the absence of pressurised flow within the false lumen&#46; This explains the characteristic morphology of this entity on imaging techniques &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41; and its dynamic behaviour&#44; as it can either spontaneously reabsorb or progress to a CD&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;9</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">Most ulcerated aortic atherosclerotic plaques involve the intima and do not extend into the tunica media&#46; PAU is an atherosclerotic plaque that&#44; after initial erosion and ulceration&#44; ruptures the internal elastic lamina and penetrates the tunica media&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> They are focal lesions that occur within extensive atherosclerosis and are mainly located in the descending aorta &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; They are often accompanied by limited intramural haemorrhage that may spread along the descending aorta&#44; but usually the existing parietal fibrosis and calcification prevent the haemorrhage from progressing lengthwise&#46; PAU may progress to aortic dilatation &#40;saccular aneurysm&#41;&#44; progressive destruction of the media &#40;pseudoaneurysm and rupture&#41; or more rarely to dissection&#46; In the latter case&#44; the port of entry is the excavated area or &#39;crater&#39; of the PAU&#46; The clinical course of these patients is variable&#44; but most are asymptomatic at the time of diagnosis and only a few develop an AAS&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;12&#44;13</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">ID was described by Murray and Edwards in 1973<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> and refers to those cases of AAS in which there is laceration of the intima and underlying media &#40;intimomedial tear&#41; without significant intramural haematoma<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; The base of the lacerated area usually contains a certain proportion of media and adventitia&#46; There is no false lumen as such&#44; and it is accompanied by some degree of subadventitial haematoma causing eccentric protrusion of the aortic wall&#46; It occurs most commonly in the ascending aorta&#44; and it is often accompanied by aortic regurgitation&#46; It can be easily missed without a high index of suspicion&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> In contrast to ID&#44; CD may be referred to as complete aortic dissection&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">A unique feature of these aortic lesions is that they can occur synchronously&#44; i&#46;e&#46;&#44; simultaneously in different aortic segments or&#44; even more often&#44; one after the other in the same aortic segment&#46; Thus&#44; IMH may be the prelude to CD&#44; many cases of PAU are accompanied by some degree of IMH&#44; and&#44; exceptionally&#44; PAU may progress to dissection and an ID to a CD&#46; Any of these lesions can lead to aortic rupture&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Current epidemiology of acute aortic syndrome</span><p id="par0055" class="elsevierStylePara elsevierViewall">Hospital-based studies&#44; retrospective case series and case-control studies underestimate both the incidence and lethality of AAS by not including out-of-hospital deaths&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">Recently&#44; large population-based cohort studies have estimated the average annual incidence of CD to be between 6 and 7&#46;2 cases per 100&#44;000 population per year&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16&#44;17</span></a> The incidence of IMH and PAU is lower than that of CD&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> ID accounts for approximately 5&#37; of all patients with type A AAS&#46; Type A lesions are more common in patients with CD and ID&#44; while type B lesions are more commonly diagnosed in patients with IMH and PAU&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The incidence of AAS is twice as common in men as in women and increases with age&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">17&#44;18</span></a> The average age of these patients varies according to the type of aortic lesion&#59; it is lower in CD cases &#40;68 years&#41; and higher in PAU cases &#40;77 years&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> Women with CD have a different clinical presentation&#44; arrive later at the hospital&#44; in worse clinical condition than men&#44; and have higher mortality&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16&#44;17&#44;19</span></a> 30&#8211;50&#37; of patients with type A CD die at home or before reaching the hospital&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16&#44;17&#44;20</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Analysis of the US national database shows an increase in hospitalisations for CD while hospital mortality &#40;26&#37;&#41; is virtually the same&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Aortic centres&#44; aorta code and aortic pathology teams</span><p id="par0075" class="elsevierStylePara elsevierViewall">The clear relationship between patient volume and surgical outcomes makes it necessary and justifiable to centralise the management of acute aortic disease in &#8216;aortic centres&#8217; &#40;centres with high surgical volume and surgeons with expertise in aortic surgery&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">22&#8211;24</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">In this regard&#44; care networks have been set up under the &#34;aorta code&#34; umbrella for the care of patients with AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> They consist of a multidisciplinary team with experience in aortic disease&#44; are available every day at all hours and are activated from the Emergency Departments of the hospitals belonging to the network&#46; The &#8220;aorta code&#8221; seeks to accomplish three things&#58; 1&#41; to increase the level of alertness and awareness of AAS among ED physicians for early detection of patients with AAS&#59; 2&#41; to accelerate the transfer of the patient to the aortic centre of reference&#59; and 3&#41; to provide optimal treatment by activating a highly specialised team&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">At the aortic centre&#44; the aortic team is responsible for quickly determining the best therapeutic strategy for each patient &#40;open surgery&#44; endovascular treatment&#44; hybrid procedures combining open and endovascular surgery&#44; conservative treatment&#41; and for close follow-up&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Centralising the management of AAS patients in &#8220;few centres and few hands&#8221; offers the best opportunity to improve outcomes&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Diagnosis of acute aortic syndrome in the emergency department&#46; Three-step diagnostic algorithm</span><p id="par0095" class="elsevierStylePara elsevierViewall">In the emergency department&#44; an accurate diagnosis in the shortest possible time is essential&#46; If in acute coronary syndromes the aphorism &#8220;time is muscle&#8221; has been proposed as a rule of action&#44; here&#44; in AAS&#44; time is even more important&#44; and we could say that &#8220;time is life&#8221;&#46; There are three reasons why detection of the AAS patient in the ED is a diagnostic challenge&#58; the low prevalence of the disease&#44; a variable clinical presentation and the absence of specific biomarkers&#46; Therefore&#44; the risk of error and delay in diagnosis is high and the consequences are significant&#46; To get round this situation&#44; continuous training programmes in emergency departments and the use of a simple diagnostic algorithm are key&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">The latest European Society of Cardiology guidelines on the diagnosis and treatment of aortic disease recommend a confusing and complex diagnostic algorithm&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Currently&#44; most emergency departments do not follow a specific algorithm for the diagnosis of AAS&#46; Our group proposes the application of a three-step diagnostic algorithm<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">First step</span>&#46; Calculate the a priori probability of having an AAS by considering the three risk categories proposed by the American Society of Cardiology &#40;predisposing conditions&#44; pain characteristics and physical examination findings&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> In 2011&#44; an aortic dissection risk score was introduced to facilitate detection&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> Each category is assigned a point if a risk marker of that category is present&#46; A score of 0 implies a low risk of AAS&#59; if the score is 1&#44; the risk is intermediate&#59; and if it is &#8805; 2&#44; the risk of having an AAS is high&#46; The pretest probability calculation is a Class I recommendation&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27</span></a></p><p id="par0110" class="elsevierStylePara elsevierViewall">Among the risk factors&#44; the most common is a history of long-term severe hypertension<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> and&#44; surprisingly&#44; it does not appear in the predisposing conditions of high risk of dissection&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> Adding this factor increases the sensitivity of the risk score&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">It is essential to quickly recognise the so-called &#8220;aortic pain&#8221;&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a> This is a very intense&#44; sharp &#40;stabbing&#41;&#44; tearing&#44; throbbing&#44; pulsating and migratory chest pain&#46; If it radiates to the neck&#44; it indicates that the ascending aorta is affected&#44; whereas if it is located in the back or abdomen&#44; the diseased segment is usually the descending aorta&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Including &#8220;aortic pain&#8221; as a discriminator in the clinical presentation of chest pain in the Manchester triage system or similar classification systems results in early detection of patients with AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> On the other hand&#44; as might be expected&#44; if we are lax with pain characteristics&#44; the specificity of the risk scale decreases&#46; Likewise&#44; a systematic physical examination and the ability to detect high-risk findings will increase the sensitivity of the scale&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">In short&#44; to correctly assess the a priori probability of having an AAS it is necessary to consider risk factors&#44; pain characteristics and physical examination findings&#46; However&#44; it has been shown that the application of this risk score alone in the emergency department is not sufficient&#46; It has a low specificity and an unacceptable number of false positives&#46;<a class="elsevierStyleCrossRefs" href="#bib0155"><span class="elsevierStyleSup">31&#44;32</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Second step&#46;</span> After clinical suspicion and physical examination&#44; in-hospital assessment of all patients with chest pain includes an electrocardiogram and a blood test with troponin and D-dimer&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a> Elevated blood D-dimer levels have a high sensitivity in the diagnosis of AAS&#44; correlate with the extent of aortic injury and are higher in CD than in IMH&#46;<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a> The higher the D-dimer levels&#44; the higher the probability that the patient has AAS&#44; especially if it is &#8805; 1600&#8239;ng&#47;ml&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> No less important is its high negative predictive value&#46; That is&#44; normal D-dimer levels virtually rule out the diagnosis of AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a> The accuracy of the dissection risk score has been shown to improve when combined with D-dimer levels&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a> It should be noted that an elevated D-dimer level does not distinguish between AAS and pulmonary embolism&#44; but it does prompt&#44; in both cases&#44; an urgent chest CT scan that can confirm or exclude both entities&#46;<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">28&#44;31&#44;37</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">Acute coronary syndrome is the most important differential diagnosis in patients with AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a> In patients with aortic pain&#44; the combination of a normal ECG&#44; normal troponins and elevated D-dimer levels are a red flag for AAS and makes it unlikely that the patient has an acute coronary syndrome &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> It should be kept in mind&#44; however&#44; that elevated troponin levels do not totally exclude an AAS and a chest CT should not be omitted if D-dimer levels are elevated and the clinical suspicion of AAS is high&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Chest radiography is classically performed in all patients with chest pain and is useful in many cases&#46; It is important to remember that it is often normal in patients with AAS and therefore does not exclude the presence of AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Third step&#46;</span> Imaging is necessary to reach a definitive diagnosis of AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> CT&#44; which is widely available in emergency departments&#44; is the diagnostic technique of choice<a class="elsevierStyleCrossRefs" href="#bib0195"><span class="elsevierStyleSup">39&#44;40</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46; Any patient with a risk score &#8805; 1 and elevated D-dimer levels should have a CT scan of the aorta &#40;from the neck to the iliofemoral vessels&#41;&#44; especially if troponin levels are normal and there is no change in the electrocardiogram&#46; CT should be performed without contrast&#44; to avoid false negatives in patients with IMH and with contrast&#44;<a class="elsevierStyleCrossRefs" href="#bib0195"><span class="elsevierStyleSup">39&#44;40</span></a> and synchronised with the ECG&#44; to avoid false positives due to aortic root motion and ascending aorta&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p><p id="par0145" class="elsevierStylePara elsevierViewall">A transthoracic echocardiogram &#40;TTE&#41; in the ED may be useful&#44; as it provides information on some relevant aspects&#58; pericardial effusion&#44; ventricular function&#44; aortic regurgitation&#44; etc&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">42</span></a> It is important to bear in mind that a normal TTE does not exclude the diagnosis of AAS&#46; Although transoesophageal echocardiography has excellent diagnostic accuracy in AAS and its complications&#44;<a class="elsevierStyleCrossRefs" href="#bib0215"><span class="elsevierStyleSup">43&#44;44</span></a> we advocate avoiding its routine use in AAS&#44; especially if the patient is unstable&#46; On the other hand&#44; it is very useful in the operating room&#44; especially if we decide to preserve the aortic valve&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;27</span></a> At present&#44; the role of MRI in patients with suspected AAS in the ED is anecdotal&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Differential diagnosis of acute aortic syndrome by computed tomography</span><p id="par0150" class="elsevierStylePara elsevierViewall">Familiarity with the different constituents of the AAS and similar entities is important for the proper interpretation of a CT scan&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;40&#44;41</span></a></p><p id="par0155" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">CD with acute thrombosis versus IMH</span>&#46; In both cases&#44; the two lumens&#44; false and true&#44; are not communicating&#46; When the port of entry of the CD is small and the exit &#40;decompression port&#41; is absent or closed&#44; acute and rapid false lumen thrombosis can occur&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In these cases&#44; the CT images obtained resemble those of patients with IHM&#46; The distinction between the two entities is not always possible&#44; but by combining axial and sagittal planes we can observe an alteration of the intima contour corresponding to the intimomedial tear of the CD&#46; By definition&#44; there is no such tear in IMH&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;41</span></a></p><p id="par0160" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Aortitis versus IMH</span>&#46; The typical CT image of IMH is a semi-circumferential thickening of the aortic wall with no contrast within the aortic wall and a smooth luminal surface &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Fig&#46; 4</a>&#41;&#46; In aortitis&#44; the aortic wall thickening is circumferential&#46; Positron emission tomography will be helpful in distinguishing the inflammatory process from IMH&#46;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a></p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0165" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Mural thrombus versus IMH</span>&#46; Dilated aorta can be accompanied by mural thrombosis which in some cases simulates IMH&#46; In contrast to mural thrombosis&#44; hyperdense aortic wall thickening can be seen on non-contrast images &#40;hyperdense crescent sign&#41;&#46; In addition&#44; IMH shifts the calcification of the intima inwards into the aortic lumen whereas&#44; in mural thrombus&#44; the calcifications are usually located along the outer edge of the aortic wall&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p><p id="par0170" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">PAU versus ulcer-like imaging&#46;</span> PAU and ulcer-like images are not the same entity&#46; The latter are the result of an intimomedial tear and are accompanied by a dissecting intraparietal haematoma&#46; On CT they appear as punch-like areas with extensive communication with the aortic lumen and are not accompanied by alteration of the aortic wall contour&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> They are not accompanied by calcified atherosclerotic lesions and are in fact the port of entry to CD with acute false lumen thrombosis&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The detection of these lesions is associated with a higher number of aortic events at follow-up &#40;aneurysms&#44; pseudoaneurysms&#44; focal dissections and aortic rupture&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall">The typical CT imaging for PAU corresponds to a wide-necked&#44; punch-shaped aortic parietal lesion&#44; which&#44; unlike ulcer-like images&#44; causes remodelling of the parietal contour&#46; It settles around calcified atherosclerotic plaques and is usually accompanied by some degree of IMH&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> Most ulcers are located in the descending aorta and arch&#46;</p><p id="par0180" class="elsevierStylePara elsevierViewall">In summary&#44; the distinction between the different entities is made on the basis of lesion morphology&#44; interface with the aortic lumen&#44; presence of hyperattenuation on non-contrast images&#44; coexistence with atherosclerotic lesions and location of calcification&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Current treatment of acute aortic syndrome</span><p id="par0185" class="elsevierStylePara elsevierViewall">Every patient with AAS should be treated in a Cardiovascular Acute Care Unit with three immediate goals&#58; control of blood pressure &#40;&#8804; 120&#8722;100&#8239;mmHg&#41;&#44; heart rate &#40;&#8804;60 bpm&#41; and pain&#46; For this&#44; we use a combination of intravenous beta-blockers&#44; hypotensive agents and sedatives&#46;</p><p id="par0190" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Type A CD&#46;</span> It is a surgical emergency&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27&#44;47</span></a> The type of intervention depends on the aortic segments involved&#44; the condition of the aortic valve and the clinical condition of the patient&#46; The goals of surgery are to prevent aortic rupture&#44; correct valve regurgitation and resolve any malperfusion&#46; A replacement of the ascending aorta and hemiarch with resuspension of the aortic valve is performed in most patients&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> When the aortic root is severely compromised or in connective tissue diseases &#40;Marfan syndrome&#41;&#44; the usual treatment is replacement of the root and ascending aorta with a composite valve tube&#59; the coronary arteries are reimplanted in the tube&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> This technique&#44; a modified version of the classic Bentall-De Bono procedure&#44; is the standard treatment in type A CD with aortic root involvement&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> If the dissection respects the sinuses of Valsalva&#44; the interposition of a supracoronary tube may be sufficient&#46; Aortic valve preservation techniques are a valid alternative in haemodynamically stable patients with favourable anatomy and in the hands of experienced surgeons&#46;</p><p id="par0195" class="elsevierStylePara elsevierViewall">In order to avoid future reinterventions&#44; some authors recommend total aortic arch replacement in the following situations&#58; significant arch dilatation&#44; extensive arch tears and dissection of the supra-aortic trunks&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a> The &#8216;elephant trunk&#8217; technique using hybrid prostheses allows total repair of the arch and the proximal segment of the descending aorta while closing the port of re-entry&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a></p><p id="par0200" class="elsevierStylePara elsevierViewall">An individualised therapeutic approach should be taken based on the surgeon&#39;s experience&#44; extent of the lesion&#44; haemodynamic status and clinical profile of the patient&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a></p><p id="par0205" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Type B CD</span>&#46; Medical treatment remains the treatment of choice for uncomplicated type B CD&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27</span></a> The indicated treatment in complicated type B CD is thoracic endovascular aneurysm repair &#40;TEVAR&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27</span></a> The main complications of type B CD are listed in <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#46; TEVAR may be considered to prevent future aortic complications in some patients with uncomplicated type B CD&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27&#44;52</span></a> Regarding Marfan syndrome&#44; whether TEVAR is more appropriate than open surgery is still under discussion&#46;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> The latter is a good alternative when endovascular treatment fails or is contraindicated&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;47&#44;54</span></a></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0210" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Non-A&#44; non-B type CD&#46;</span> Treatment must be individualised&#46; The port of entry is usually in the arch in half of the cases and in the descending aorta in the other half&#46;<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> Endovascular techniques&#44; open surgery &#40;elephant trunk&#41; or hybrid aortic repair offer good results&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">22&#44;56</span></a></p><p id="par0215" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Incomplete dissection&#46;</span> If the lesion involves the ascending aorta it is treated as a type A CD&#58; emergent surgery&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0220" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Type A IMH&#46;</span> The optimal treatment of these patients is not well established&#46; European and American clinical practice guidelines recommend emergency surgery&#44;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27</span></a> while Asian guidelines only recommend surgery if the clinical course is poor&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> It is true that mortality in patients with type A IMH is lower than in those with type A CD and that complications such as aortic regurgitation&#44; tamponade and malperfusion syndromes are less common in patients with type A CD&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a> Our group advocates initial medical treatment in patients without poor outcome indicators &#40;aortic diameter&#8239;&#60;&#8239;50&#8239;mm and absence of intimomedial tears&#41; and haemodynamically stable&#44; especially if they are elderly and have comorbidities&#46; The rest require urgent surgery &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0225" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Type B IMH&#46;</span> Initial treatment is medical&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27</span></a> Close follow-up with CT scan and D-dimer levels is important&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;59</span></a> If complications occur&#44; the treatment of choice is TEVAR&#46;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a> The presence of intimomedial tears is associated with a higher rate of aortic complications&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0230" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Penetrating aortic ulcer&#46;</span> Treatment is similar to that of type B IMH&#46; In symptomatic patients or those with large or complicated ulcers&#44; treatment with TEVAR should be considered&#46;<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9&#44;47</span></a></p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Prevention of acute aortic syndrome</span><p id="par0235" class="elsevierStylePara elsevierViewall">Measures to prevent the onset of AAS can be summarised in four points&#58; a thorough family medical history&#44; preventive surgery&#44; control of high blood pressure and pharmacological treatment&#46;</p><p id="par0240" class="elsevierStylePara elsevierViewall">A family history of aortic dissection and aortic aneurysm are risk factors for AAS&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Periodic monitoring with imaging techniques and genetic testing is advisable in individuals with a family history of AAS or aortic aneurysm&#46; In patients with aortic aneurysm&#44; clinical practice guidelines recommend aortic repair depending on the diameter of the aneurysm &#40;&#62;50&#8722;55&#8239;mm&#41;&#44; the rate of progression of aortic dilatation&#44; the presence of other risk factors and the clinical profile of the patient&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">26&#44;27</span></a></p><p id="par0245" class="elsevierStylePara elsevierViewall">Aortic wall &#8216;stabilising&#8217; treatments such as beta-blockers and angiotensin II receptor antagonists should be used early in order to prevent aneurysm progression&#46; However&#44; the use of these drugs in patients without connective tissue disorders has not been shown to decrease the likelihood of developing an AAS&#46;</p><p id="par0250" class="elsevierStylePara elsevierViewall">Hypertension is an independent predictor of type A CD&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> Therefore&#44; careful control of blood pressure is essential&#46;</p><p id="par0255" class="elsevierStylePara elsevierViewall">Population-based cohort studies have shown that the use of fluoroquinolones is associated with an increased risk of CD and aortic aneurysm&#46;<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a> In addition&#44; patients with aortic aneurysm have more complications if treated with this type of antibiotics&#46;<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a> Therefore&#44; fluoroquinolones should not be used in these patients whenever a therapeutic alternative is available&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Final considerations</span><p id="par0260" class="elsevierStylePara elsevierViewall">Progress has been made in the diagnosis and treatment of patients with AAS over the past two decades&#44; but many challenges remain&#46; To mention a few&#44; it is essential to find specific AAS biomarkers for early diagnosis&#44; to promote the creation of aortic centres and aorta codes&#44; to expand the intravascular therapeutic offer for patients with type A AAS and high surgical risk&#44; and to conduct multicentre clinical trials to test the efficacy of preventive interventions&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Funding</span><p id="par0265" class="elsevierStylePara elsevierViewall">None&#46;</p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Conflict of interest</span><p id="par0270" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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          "titulo" => "Current epidemiology of acute aortic syndrome"
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          "titulo" => "Aortic centres&#44; aorta code and aortic pathology teams"
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          "titulo" => "Diagnosis of acute aortic syndrome in the emergency department&#46; Three-step diagnostic algorithm"
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          "titulo" => "Differential diagnosis of acute aortic syndrome by computed tomography"
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          "titulo" => "Current treatment of acute aortic syndrome"
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          "titulo" => "Prevention of acute aortic syndrome"
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            0 => "Acute aortic syndrome"
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            2 => "Intramural aortic hematoma"
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            2 => "Hematoma intramural a&#243;rtico"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Acute aortic syndrome embraces a group of heterogenous pathological entities involving the aortic wall with a common clinical profile&#46; The current epidemiology&#44; clinical presentation&#44; diagnosis and treatment strategy are discussed in this review&#46; Besides&#44; the importance of multidisciplinary aortic teams&#44; aortic centres and the implementation of an aortic code are emphasized&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">El s&#237;ndrome a&#243;rtico agudo agrupa distintas entidades que afectan a la pared a&#243;rtica y que tienen una presentaci&#243;n cl&#237;nica com&#250;n&#46; En esta revisi&#243;n se exponen aspectos relevantes sobre su epidemiolog&#237;a&#44; presentaci&#243;n cl&#237;nica&#44; diagn&#243;stico y estrategias de tratamiento&#46; Adem&#225;s&#44; se analiza la importancia de los equipos multidisciplinares y los centros de aorta en la atenci&#243;n y el pron&#243;stico de los pacientes con s&#237;ndrome a&#243;rtico agudo&#46;</p></span>"
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                    0 => array:2 [
                      "titulo" => "Acute aortic syndrome"
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                        0 => array:2 [
                          "etal" => false
                          "autores" => array:2 [
                            0 => "I&#46; Vilacosta"
                            1 => "J&#46;A&#46; San Rom&#225;n"
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                    0 => array:2 [
                      "doi" => "10.1136/heart.85.4.365"
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                        "tituloSerie" => "Heart"
                        "fecha" => "2001"
                        "volumen" => "85"
                        "paginaInicial" => "365"
                        "paginaFinal" => "368"
                        "link" => array:1 [
                          0 => array:2 [
                            "url" => "https://www.ncbi.nlm.nih.gov/pubmed/11250953"
                            "web" => "Medline"
                          ]
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              "identificador" => "bib0010"
              "etiqueta" => "2"
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                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Acute aortic syndrome&#58; a new look at an old conundrum"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:6 [
                            0 => "I&#46; Vilacosta"
                            1 => "P&#46; Aragoncillo"
                            2 => "V&#46; Ca&#241;adas"
                            3 => "J&#46;A&#46; San Rom&#225;n"
                            4 => "J&#46; Ferreir&#243;s"
                            5 => "E&#46; Rodr&#237;guez"
                          ]
                        ]
                      ]
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                    0 => array:2 [
                      "doi" => "10.1136/hrt.2008.153650"
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                        "tituloSerie" => "Heart"
                        "fecha" => "2009"
                        "volumen" => "95"
                        "paginaInicial" => "1130"
                        "paginaFinal" => "1139"
                        "link" => array:1 [
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                            "url" => "https://www.ncbi.nlm.nih.gov/pubmed/19131440"
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                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
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                            0 => "I&#46; Vilacosta"
                            1 => "J&#46;A&#46; San Rom&#225;n"
                            2 => "R&#46; di Bartolomeo"
                            3 => "K&#46; Eagle"
                            4 => "A&#46;L&#46; Estrera"
                            5 => "C&#46; Ferrera"
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                        ]
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                    ]
                  ]
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                    0 => array:1 [
                      "Revista" => array:5 [
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                            4 => "M&#46; Kreibich"
                            5 => "M&#46; Siepe"
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                    0 => array:1 [
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                      "Revista" => array:7 [
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                      "titulo" => "Redefining the histopathological profile of acute aortic syndromes&#58; clinical and prognostic implications"
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                          "autores" => array:6 [
                            0 => "O&#46; Leone"
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                            3 => "A&#46; Corsini"
                            4 => "V&#46; Agostini"
                            5 => "B&#46; Corti"
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                    0 => array:2 [
                      "doi" => "10.1016/j.jtcvs.2018.04.086"
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                      "titulo" => "A systematic histopathologic evaluation of type-A aortic dissections implies a uniform multiple-hit causation"
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                            3 => "R&#46; Poelmann"
                            4 => "R&#46;J&#46;M&#46; Klautz"
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                      "titulo" => "Natural history and serial morphology of aortic intramural hematoma&#58; a novel variant of aortic dissection"
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                        "paginaInicial" => "495"
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                      "titulo" => "Intramural hematoma should be referred to as thrombosed-type aortic dissection"
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                            0 => "K&#46; Uchida"
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                            3 => "T&#46; Minami"
                            4 => "T&#46; Cho"
                            5 => "M&#46; Goda"
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                      "doi" => "10.1093/ejcts/ezt040"
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                      "titulo" => "Penetrating atherosclerotic aortic ulcer&#58; documentation by transesophageal echocardiography"
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                      "doi" => "10.1016/s0735-1097(98)00194-6"
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                            3 => "E&#46;R&#46; Tenorio"
                            4 => "G&#46;A&#46; Sandri"
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                      "Revista" => array:5 [
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Article information

ISSN: 23870206
Original language: English

DOI:10.1016/j.medcle.2023.07.017

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