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MRI being recommended [4,5]. IMH should be differentiated from a thrombosed false lumen of aortic dissection, hemiazygos sheath, aortic atherosclerosis, and aortitis [4–6,51]. Current guidelines recommend CT as the first choice imaging
modality for the IMH assessment, followed by echocardiography as the second choice [4,5].
Penetrating aortic ulcer is the third form of acute aortic syndrome, consisting of a penetration of an ulcerated plaque
within the internal elastic lamina, mostly in the mid and distal part of the descending aorta, resulting in a localized IMH
[52]. The imaging features consist of the presence of a crater out-pouching the aortic wall. Guidelines recommend CT and
MRI as first- and second-line diagnostic imaging modalities for the penetrating aortic ulcer assessment, followed by TEE
as the third line [4,5].
Chronic Aortic Conditions
Chronic aortic conditions consist of aortic aneurysm, aortic atherosclerosis, aortic coarctation, and inflammatory aortic
disease.
Thoracic aortic aneurysm is defined as a dilatation, involving all three vascular layers, with a maximum diameter
exceeding 1.5 times the normal values for age, indexed by body surface area [6,53]. It is classified into two morphological types: fusiform and saccular. Its etiology can be degenerative, secondary to connective tissue disorders (Marfan,
Loyes–Diets, or Ehler–Danlos syndromes), other inherited diseases (Turner syndrome), bicuspid aortic valve, syphilis, or
noninfectious aortitis (Takayasu syndrome) [6]. Imaging methods should provide the following data: maximum diameter
of dilatation, as well as diameters of proximal and distal aneurysm margins, longitudinal extent, involvement of aortic
valve and aortic arch vessels, detection of aortic leakage, detection of thrombus, and differentiation from aortic dissection
[4–6]. TTE is recommended by guidelines as the second-line imaging method (after CT), mainly for the assessment of the
aortic root aneurysm and of the associated cardiac involvement, such as aortic valve disease or myocardial abnormalities
[4,5]. The most powerful predictor of aortic rupture is the diameter of the aortic aneurysm: a diameter above 60 mm has
more than 7% risk of rupture [4,5,54]. TEE is recommended as the third-line imaging method for diagnosis, but mandatory
during surgery, in the operative room [4–6,55]. Several pathological conditions require special attention, such as Marfan
syndrome and bicuspid aortic valve. For the assessment of Marfan syndrome, TTE is used as the first-line imaging method
for diagnosis, follow-up (at every 6 months), after surgical correction, and for family screening [4,5,34,56]. Meanwhile, half
of the patients with bicuspid aortic valve have significant aortic dilatation, as seen in Fig. 14.4 [57]. In these cases, TTE is
the first imaging method for diagnosis, follow-up, and after surgical correction, whereas for the initial assessment CT or
MRI is also recommended [4,5].
Aortic atherosclerotic disease includes uncomplicated and ruptured plaque. It is highly associated with embolic events
[58,59]. TEE is the method of choice for diagnosis of aortic atheroma. A protrusion in the aortic lumen more than 4 mm is
associated with high embolic risk [4]. TEE is also recommended for assessment of aortic atheroma during surgery in order
FIGURE 14.4 Aortic root aneurysm evaluated by three-dimensional transesophageal echocardiography, with a maximum diameter of 60 mm (A),
associated with bicuspid aortic valve (B).
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to reduce bypass complications [4]. Recently, it was shown that 3D TEE has a better accuracy for detecting size, morphology, and extent of atheroma, by comparison to two-dimensional TEE [60].
Aortic coarctation. TTE is useful for the diagnosis of aortic coarctation, being also able to detect associated cardiac
congenital defects and to follow patients after correction. However, the best assessment of aortic coarctation should be done
by CT or MRI [4,5].
Inflammatory aortic disease. Although a very rare condition, mycotic aneurysm is a life-threatening pathology. The
recommended imaging tools for detection are echocardiography, CT, and MRI. It is important to mention that aorta should
be always evaluated in the case of infective endocarditis [4]. For noninfective inflammatory aortic disease, such as Takayasu
disease or giant cells arteritis, echocardiography plays a significant role, showing a homogenous circumferential thickening
of the aortic wall with internal smooth layer or even an aortic dilatation that can lead to dissection or rupture [4,61].
Intraoperative and Postsurgical Echocardiographic Assessment
Surgical echo assessment implies the following [1]: use of echocardiography during surgery for better description
of aorta as well as for evaluation of aortic valve and myocardial function and [2] use of echocardiography for the
follow-up of patients who underwent an aortic repair for aortic aneurysm or dissection [4]. TEE findings are powerful predictors of successful intervention and of postoperative outcome [5,62,63]. There are some echocardiographic
findings that are expected to be found after a surgical intervention, such as the aortic interposed graft appears as a thin
tube with an echo density greater than the aortic wall; the anastomosis is seen as a separate line with an abrupt change
at the borders; sometimes, there is an angulation between the native aorta and the graft that can mimic an aortic dissection; there is frequently a small, concentric peri-graft thickening (less than 10 mm); in more than 80% of patients
who underwent type A aortic dissection repair there is a residual intimal flap in the descending aorta, which is an
expected finding if it does not increase overtime [4,5,16]. Furthermore, TEE has a role in the detection of postsurgical
complications, such as anastomotic dehiscence, formation of a pseudoaneurysm, augmentation of aortic regurgitation, hematoma and graft compression, dilatation of the residual false lumen and compression of the true lumen, false
lumen thrombosis, involvement of the aortic branches, anastomotic stenosis, appearance of a recurrent aortic dissection or aneurysm formation, proximal to the aortic graft [4,64]. However, complete postsurgical assessment requires
supplementary imaging by CT or MRI [4,5].
DUPLEX ULTRASOUND AND OTHER ECHOGRAPHIC TECHNIQUES FOR THE
ASSESSMENT OF ABDOMINAL AORTA
Sonographic Anatomy
Abdominal aorta (AA) represents the segment between aortic hiatus of the diaphragm, situated at the level of the 12th tho-
racic vertebra, and the division into the common iliac arteries, at the level of the fourth lumbar vertebra. In the longitudinal
plane, AA descends anterior to the vertebral column and left to the cava vein, from which it can be distinguished by thicker
and pulsatile walls [65–67]. According to 2015 American Institute of Ultrasound in Medicine recommendations, the measurements should be reported for the proximal part—below the diaphragm, but near the celiac artery; the middle part—near
the level of the renal arteries; and the distal part—above the iliac arteries [68].
Scanning Technique by Duplex Ultrasound and Normal Appearance of Abdominal Aorta
Duplex ultrasound consists of identification of anatomical structures by B-mode, followed by application of color
Doppler for a better visualization of the vessel and flow direction, associated with spectral Doppler for the characterization of flow patterns and velocities. Whenever it is possible, the patient should be advised for an 8–12 h period of fasting, before the procedure, with the purpose to reduce bowel gas and improve the visualization of the aorta. Sonographic
evaluation of AA is performed with the patient lying in a supine recumbent position. A left lateral position for the coronal
scan plane could be useful for the visualization of both common iliac arteries in one image [65]. The standard probe for
this examination is a 3.5–5 MHz curvilinear transducer. It is highly recommended to have the scan configured for an
aortic investigation, but, in the absence of a specific preset it can be used the setting for general abdominal evaluation
with a usual depth at 8–12 cm [67].
Scanning of AA starts in the transverse image plane (probe perpendicular to the long axis of the patient) from
the upper abdomen, marked by the celiac trunk (“the seagull sign”), to the aortic bifurcation [66]. The anatomical
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relationship of pathological modifications of the AA with the origins of renal arteries is a very important landmark,
which can influence the prognostic and the therapeutic decisions in certain clinical conditions. After the transverse
plane imaging, the transducer is turned caudally for the longitudinal or sagittal plane in order to scan the AA throughout its visible length. Some examiners are applying also the coronal view from the left flank [67]. A full scanning of
the aorta should be continued with the interrogation of the iliac arteries in transverse and longitudinal scan planes
[67,68]. For each imaging plane, the technique of duplex ultrasound should be applied. Normally, the flow is of
high-resistance pattern, with a biphasic waveform in the proximal segment of the AA and a triphasic one in the distal
segment [65].
Measurements of the proximal, mid, and distal aorta should be obtained usually from the long-axis view to determine
the antero-posterior diameter at its greatest size, from outer edge to outer edge, in peak systole [67,68]. The diameter of
aorta is considered normal at less than 2.5 cm and decreases slightly from the proximal to the distal segment [65,67]. The
accuracy of duplex ultrasound is impaired by obesity and presence of bowel gas [69].
Echographical Assessment of Abdominal Aorta Diseases
Abdominal Aortic Aneurysm
The main indication for sonographic evaluation of abdominal aorta is the aneurysmal dilatation. Due to the high accessibility and reproducibility of this method, it allows a fast assessment in the case of symptomatic or ruptured AAA, as well as
screening and follow-up of this pathology [70,71]. AAA has the same pathological significance with the thoracic aortic
aneurysm [53] but different relevant dimensions for definition. Thus, an AAA above the celiac artery is diagnosed if the
diameter of aorta is greater than 3.9 cm in males or 3.1 cm in females [68,72]. At the level of the infrarenal segment, an
aneurysm is diagnosed if the diameter of aorta is ≥3 cm [66,68,72]. For women and small adults, the infrarenal aneurysm
is defined by a diameter higher or equal to 1.5 times the diameter of the more proximal infrarenal aorta [73]. Enlargement
of aorta increases the risk of rupture. Because the mortality rate is significantly lower in elective procedures of AAA repair
(3%–5%) than in emergency repair (50%) [74], the most important measure to reduce mortality is to identify enlargements,
which carries a significant risk of rupture (Fig. 14.5). The current opinion is that an AAA larger than 5–5.5 cm should be
electively repaired [75–77].
The latest data regarding the role of ultrasonography in AAA screening are coming from the US Preventive Services
Task Force. They recommend the screening of men aged 65–75 years who have ever smoked and selective screening of
men 65–75 years who have never smoked. Current evidence is insufficient to assess the balance of benefits and harms of
screening for AAA in women aged 65–75 years who have ever smoked and is against routine screening in women who have
never smoked [78].
Ultrasonography should provide the following information regarding an AAA: maximum diameter of aorta, relationship with the renal arteries, extension beyond the iliac bifurcation into the common iliac arteries, and the thrombus
load. The most important pitfalls in the ultrasonographic assessment of AAA are [1] overestimation of the maximum
diameter between transversal and longitudinal planes; this is due to the complex shape of the aneurysm, with the
transversal plane of the patient not being perpendicular to the long axis of the aorta [2]; failing to align the transducer
FIGURE 14.5 Saccular aortic aneurysm in the distal part of the abdominal aorta. In the long-axis view, the maximum antero-posterior diameter, from
outer edge to outer edge, was 6.5 cm, requiring repair intervention.
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in the sagittal plane in patients with tortuous aorta [3]; difficulties in the measurement of the external diameter, in
case of marked thickening of the aortic wall, characteristic for inflammatory AAA [4]; confusion between the localized liquefaction of the inner thrombus and a dissection [65–67]. Fig. 14.6 presents the case of a 67-year-old male
with AAA, starting at the level of the origin of right renal artery. Assessment of this aneurysm at infrarenal level is
detailed in Fig. 14.7. It is difficult to establish the maximum diameter of AAA in longitudinal axis because the aorta
is lined with thrombus and there is a great amount of calcium deposition in the posterior wall (Fig. 14.7A). In order
to have a more accurate delineation of the aortic structures, a contrast-enhanced ultrasound study was performed,
which allowed a better visualization of the walls and of the residual lumen. According to measurements realized
during this study, the maximum diameter of the distal aorta in the sagittal view was 4.34 cm, whereas the residual
lumen was 1.44 cm (Fig. 14.7B). The concentric thrombus had a localized liquefaction that in certain cases can be
confused with a dissection. However, a thick layer of thrombus separating the liquefied region from the flow lumen
is an argument against aortic dissection (Fig. 14.7C). 3D ultrasound imaging has the potential to improve diagnostic
accuracy in such cases [79].
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FIGURE 14.6 Abdominal aortic aneurysm starting at the origin of renal arteries (A). Transverse image of an abdominal aortic aneurysm with visible
thrombus in the left inferior quadrant (white arrow). (B) The cranial end of this aneurysm corresponds to the origin of right renal artery. RRA, right renal
artery; SMA, superior mesenteric artery.
FIGURE 14.7 The abdominal aortic aneurysm, starting at the origin of the renal arteries (Fig. 14.6), is hereby illustrated: (A) Long-axis view shows the
enlargement of the aorta, the presence of thrombus (marked with white arrows), and the important thickening of the posterior wall which makes difficult
the measurement of the external diameter (from outer edge to outer edge); (B) Contrast-enhanced ultrasound realizes a better delineation of the walls and
of the residual lumen, allowing the evaluation of the whole diameter (measuring 4.38 cm); (C) Three-dimensional ultrasound imaging in the transverse
view shows that the aneurysm is lined with a liquefied thrombus on the posterior wall (green arrow); the thick layer separating the liquefied region of
thrombus from the flow lumen is an argument against aortic dissection.
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An AAA with a diameter lower than 5.5 cm has no indication for repair. However, there are no clear recommendations
for the follow-up of these cases. Some authors recommended follow-up at every 12 months for an AAA with a diameter
between 3.0 and 4.4 cm and at every 3 months for an AAA with a diameter between 4.5 and 5.4 cm. An increase in diameter
of more than 5 mm in 6 months or more than 10 mm in 12 months justifies referral of the patient for vascular surgery or
endovascular repair [67].
Abdominal Aortic Dissection
As long as abdominal aortic dissection is usually an extension from the thoracic segment and has limited indications
for repair, it is not considered an emergency condition per se. Even in Stanford type A–DeBackey type I dissection,
involving the aorta along its entire length, the target for repair is only the ascending aorta. Still, ultrasonographical
assessment remains very important for the identification of complications, such as the rapid increase of the aortic
diameter, development of periaortic hematoma, dissection of a previously aneurysmal aorta, and obstruction of collateral branches. All these complications diagnosed during follow-up might require interventions, such as stent graft
placement or surgical cure [80].
We described previously the main ultrasound signs that are characterizing aortic dissection: intimal flap, intimal tear,
and presence of the true and false lumen. Chronic dissection might be confused with AAA because of dilatation of aorta
and thrombosis of false lumen, which might impair visualization of the intimal flap. In such situations, the identification
of intimal calcification in the inner wall of thrombus supports the diagnostic of dissection [65] (Fig. 14.8A). In the absence
of intimal calcification, the flap can become difficult to be observed and contrast-enhanced ultrasound can improve the
accuracy of examination (Fig. 14.8B and C ). Moreover, the false lumen can be recognized by a delayed opacification by
comparison with the true lumen (Fig. 14.8D and E) [81,82].
Abdominal Aortic Stenosis
The most frequent cause of abdominal aortic stenosis is the atherosclerotic disease. Other rare causes are abdominal aortic
coarctation, and some vasculitis of the great vessels, such as Takayasu’s disease. Duplex ultrasound can identify changes
of the luminal diameter, with hemodynamic significance. Aliasing in color Doppler in a certain segment of aorta is raising
the suspicion of a stenosis. This should be confirmed by spectral Doppler, which records high-flow velocities. In the case
of total obstruction, the lack of Doppler signal is the pathognomonic anomaly.
Choice of the Imaging Modality
Duplex ultrasound has nearly 100% sensitivity for the diagnosis of the AAA, with the advantage of being rapid and costefficient and not involving irradiation or nephrotoxicity [65,81]. Contrast abdominal CT or gadolinium-enhanced MRI
are recommended for the suspicion of aortic rupture or when AAA or aortic dissection are considered for repair due to
the important amount of information regarding the relationship of aortic lesions with other anatomical structures. In some
cases, such as important renal disease, contrast-enhanced ultrasound may be an alternative to CT or MRI because it does
not involve the use of nephrotoxic agents. Arteriography can misdiagnose the true diameter of AAA, visualizing only the
flow lumen and not the diameter of the entire vessel.
FIGURE 14.8 Dissection of the distal abdominal aorta: (A) A calcified intimal flap is clearly visualized by B-mode ultrasound (white arrow); (B) Contrast-
enhanced echography allows a better visualization of the intimal flap (green arrow) in segments with a very low B-mode resolution (C). True lumen can be
recognized based on a more precocious and intense opacification (upper arrow) in comparison with the false lumen (lower arrow) (D), while by B-mode the
image is ambiguous (E).
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CONCLUSION
Technological development of imaging methods has led to a significant improvement in understanding both normal aortic
anatomy and aortic disease. Due to the high mortality of acute aortic syndrome and poor prognosis of chronic aortic pathology, rapid and accurate diagnosis is essential. Echocardiography, transthoracic, and transesophageal, as well as duplex
ultrasound, are rapid, precise, and accurate imaging methods for the assessment of aorta. Moreover, echocardiography has
the advantage of applicability in emergency situations and in hemodynamically unstable patients. Thus, TTE remains the
most used imaging method for the assessment of the aortic root. TEE overcomes several limitations of TTE, being essential
for the assessment of ascending and descending thoracic aorta, as well as for the concomitant evaluation of the heart and
pericardium, which can be affected in aortic root disease. TEE represents also an essential imaging tool during surgical or
endovascular treatment. New echocardiographic techniques such as 3D or contrast-enhanced echography will allow better assessment of the aorta. They might be used for the early detection of pathology and for the identification of high-risk
patients who can benefit from early therapeutic measures.
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Chapter 15
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Echocardiography in Acute Aortic
Syndromes
Dorota Sobczyk
John Paul II Hospital, Cracow, Poland
Chapter Outline
Acute Aortic Syndromes: Classification, Clinical Manifestation,
and Management 159
Definition, Pathophysiology, and Classification 159
Epidemiology 159
Clinical Presentation and Prognosis 160
Role of Echocardiography in Diagnosis of Acute
Aortic Syndrome 161
Transthoracic Echocardiography 161
Transesophageal Echocardiography 163
Comprehensive Echocardiographic Management
of Acute Aortic Syndrome 164
Perioperative Echocardiographic Assessment 165
Summary 166
References 166
ACUTE AORTIC SYNDROMES: CLASSIFICATION, CLINICAL MANIFESTATION, AND
MANAGEMENT
Definition, Pathophysiology, and Classification
Acute aortic syndrome (AAS) is a relatively new term that may be defined as a group of emergency, life-threatening condi-
tions including the aorta, with a common pathway and a similar clinical characteristics [1]. AAS is caused by an intimal
tear/an ulcer or a rupture of the intramural vasa vasorum, with subsequent accumulation of the blood within the media and
inflammatory response to blood leading to aortic dilatation and rupture [1–3].
The guidelines recommend the classification of AAS according to both lesion type and location [4]. There are two main
classifications based on the anatomy of the dissection, DeBakey and Stanford. DeBakey system categorizes the dissection
based on location of the primary intimal tear (ascending or descending aorta) and the extent of the dissection (only ascending aorta, only descending aorta or both) [1]. The recent guidelines [4] recommend using the simplified and more practical
Stanford classification that distinguish two types of dissection based only on the involvement of ascending aorta. Type A
refers to the aortic dissection (AD) involving the ascending aorta (that covers class I and II of DeBakey classification) and
type B the remainder (class IIIA and B in DeBakey system). This simple functional approach categorizes patients for an
emergent cardiac surgery (type A) or nonsurgical treatment (thoracic endovascular aortic repair or medical therapy) (type
B). Classification based on the aortic lesion type [4] contains five categories: classic (class 1) or limited (class 3) AD, intramural hematoma (class 2), penetrating atherosclerotic ulcer (class 4), and iatrogenic or traumatic aortic dissection (class 5).
Epidemiology
Aortic intramural hematoma is considered a precursor of aortic dissection and accounts to 10%–25% of all AAS [1].
Penetrating aortic ulcer represents 2%–7% of AAS [1]. However, the most common (and the most serious) AAS is aortic
dissection, caused by an intimal tear, followed by a medial layer disruption and resulting in separation of the aortic wall
layers and formation of a true and a false lumen [1–4]. The incidence of aortic dissection ranges from 2 (The International
Registry of Acute Aortic Dissection) [5–7] to 6 (Oxford Vascular Study) [8] per 100,000 persons per year. The prevalence
of AD in large autopsy series is 0.2–0.8% [1,5].
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00015-8
Copyright © 2018 Elsevier Inc. All rights reserved.
159
160 PART | II Diagnostic Evaluation Methods
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Degeneration and disintegration of the aortic media layer are the most important predisposing factors for nontraumatic
aortic dissection present in diverse conditions [1,2]. There are several genetic connective tissue disorders that are strongly
associated with the occurrence of AAS, usually in younger patients [5]. About 20% of patients with thoracic aneurysm and
aortic dissection have an underlying genetic disorder and altered connective tissues [4,5]. The most frequently mentioned
hereditary connective tissue disorders include Marfan, Loeys–Dietz, Ehlers–Danlos (predominantly type IV), and Turner
syndromes. The other known congenital predisposing conditions are coarctation, annuloaortic ectasia, and bicuspid aortic
valve (associated with AAS in 7%–14% of patients) [6]. Vascular inflammation present in several autoimmune diseases
(e.g., giant cell arteritis, Takayasu arteritis) may also contribute to the degeneration of media layer and subsequently, development of AAS. The most common risk factor associated with AAS is arterial hypertension, usually untreated or poorly
controlled. A total of 65%–75% of patients with AAS have the history of a long-standing hypertension [4]. The other known
risk factors include cigarette smoking, dyslipidemia, pregnancy, use of intravenous drugs (cocaine and amphetamine), iatrogenic aortic intimal tear (e.g., during cardiac surgery, cardiac catheterization, or insertion of intra-aortic balloon pump),
and blunt chest trauma [4]. An autopsy study of road accident fatalities found a ruptured aorta in about 20% of patients [7].
Clinical Presentation and Prognosis
The most frequent and typical initial symptom is severe, sharp chest (80% of patients) or back (40%) pain of an abrupt onset
[1,4,5]. Pain location reflects the site of initial intimal disruption and may change as the dissection extends along the aorta.
Chest pain is usually associated with proximal dissection (type A), whereas back or abdominal pain is more frequently
present in patients with distal AD. The clinical presentation of AAS includes also dyspnea, hypotension, congestive heart
failure, or neurological symptoms. Proximal aortic dissection often mimics acute coronary syndrome (ACS) and shares its
clinical features: pain, ECG changes, and positive cardiac biomarkers [9,10]. True myocardial ischemia may occur in AAS
with the involvement of the coronary arteries. Confusion of AAS with myocardial infarction delays appropriate treatment
and may lead to fatal consequences of antiplatelet and thrombolytic therapy. The differential diagnosis should include also
the other disorders with similar clinical characteristics, e.g., acute pulmonary embolism, pneumothorax, acute pericarditis,
cardiac tamponade, acute cholecystitis, or acute pancreatitis [1–3,7] (Table 15.1).
Partial or complete aortic rupture may cause death in all AAS. The clinical presentation of acute type A dissection is one
of the most important risk factors for in-hospital mortality and outcome [2]. The risk of mortality is increased in patients
with proximal dissection who develop complications, such as severe aortic regurgitation, coronary ostial occlusion (with
subsequent myocardial ischemia), hemorrhagic pericardial effusion and tamponade, and involvement of head and neck vessels arising from aortic arch (with subsequent malperfusion of the brain or stroke) [2,4,11]. It has been recently confirmed
that preoperative malperfusion syndrome is the crucial determinant for in-hospital mortality and surgical outcome [1,5].
The Penn classification enables stratification of patients by operative mortality risk [11,12]. The stratification system [11]
distinguishes four classes of patients, according to presence and extent of ischemia and accompanying cardiovascular collapse. The outcome importance of the Penn presentation class in proximal aortic dissection has been validated in multiple
studies [12]. Mortality from acute proximal aortic dissection (type A) increases rapidly immediately after presentation,
reaching 1%–2% per hour for the first 48 h (50% by 48 h) [1,2,4,13]. Prompt surgical intervention improves prognosis
and lowers the mortality from 55% during the first 14 days to 20% after surgery [13]. Patients with uncomplicated type B
TABLE 15.1 Echocardiographic Differential Diagnosis of Acute Aortic Syndromes
Clinical Diagnosis Echocardiographic Features
Acute coronary syndrome Regional wall motion abnormalities
Acute pulmonary embolism Right ventricular dilatation
Acute pericarditis/tamponade Pericardial effusion
Pneumothorax A-profile
Right ventricular pressure overload: D-sign, McConnell sign, 60/60 sign
Signs of cardiac tamponade: right atrial systolic collapse, right ventricular diastolic collapse, inferior
vena cava plethora, reciprocal changes in ventricular volumes with respiration, respiratory variation
in diastolic filling
Absent pleural sliding
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