Ischemic stroke is responsible for 10% of all deaths and is the second cause of mortality worldwide.
Carotid artery stenosis is the major risk factor for this disease (1).
The degree of luminal stenosis has been used for years as a marker of atherosclerotic stage,
and as an indication for surgical or endovascular intervention (6).
However several studies have underlined the importance of broadening the horizons of stenosis criteria: in this respect clinical trials have shown that a considerable population of patients which are symptomatic for transient ischemic attack or stroke have mild to moderate carotid stenosis,
and consequently the severity of carotid stenosis remains a poor discriminator of stroke risk (7).
The risk of considering only stenosis criteria implies that a great population of patients would be considered to have early-stage carotid plaques,
despite the high risk of morbidity (6,
25).
During last years,
histological studies emphasized the fact that many morphological characteristics such as lipid necrotic core,
thin fibrous cap,
intraplaque hemorrhage and neovasculature can be related to a high embolization risk plaque,
which is described as “vulnerable plaque” (6,
26-29).
However recent studies reported an embolization risk related to lipid content not statistically associated with symptomatic lesions and showed active plaque inflammation as major criteria of vulnerable nature (15,16,19).
In fact,
inflammatory cells within the plaque might cause directly the degradation of all extracellular matrix components,
hypoxic stimuli and formation of vasa vasorum in atherosclerotic lesions.
The intraplaque vasa vasorum are characterized by immature,
thin-walled vessel with high risk of microvessel collapse and progression into more advance plaques.
These lesions are at high risk for intraplaque hemorrhage and plaque rupture (14,15,17,18,20).
High-resolution magnetic resonance imaging (MRI) is the most promising technique to obtain carotid atherosclerotic plaque evaluation.
In fact MR allows direct vessel wall examination thanks to its excellent soft tissue contrast,
sensibility in plaque morphology characterization andinflammation degree evaluation,which can potentially monitor the progression of the disease (6,7).
Cai et al used unenhanced T1W and contrast-enhanced T1W images to measure the intact fibrous cap,
showing a moderate to good correlation between the MR findings and excised histological specimen (6,
7,
13).
Contrast media injection allows to diagnose the inflamed plaques and can highlight vascular supply,
neovasculature growth and increased endothelial permeability within the carotid plaque (6,
7,
20,30).
Alltheseconsiderations areusefulbecauseinflamedplaquefindingswitharecentonsetofsymptomsinevitably raises theattention totheplaque itselfas the causeof theseeventsinacute.
Moreover inflamed plaque characteristics can be potentially diagnosed by only pre- and after contrast media injection T1-weighted,
reducing examination acquisition time in patients with recent symptoms onset.
To date this is the first study in which there is a comparison between symptomatic patientswith high surgical risk characterizedby hyperintense plaque on after contrast T1-weighted images comparedwith those characterized by absence of hyperintense plaque,
trying to differentiate patients with recent tromboembolic event from those with hemodynamic onset of symptoms.
This new approach in investigating atherosclerotic carotid plaque is also a challenging issue for treatment,
because it has the capability of identifying not only symptomatic patients but also patients withhighlyinflamed plaque,
considered as a “pitfall” because of the unsettled surgical-endovascular management (31).Moreover our evaluation allowed us to make different choices on device deployment in the endovascular procedure based on HR-MR examination.
Many hospital structures continue to prefer a surgical treatment to remove the highly inflamed plaque or plaque composed of lipid-rich necrotic core,
irrespective of a degree of luminal stenosis (9,
18),
considering the endovascular procedure as secondary choice in patients with high comorbilities and contraindications to surgical approach.
In fact,
our population cohort was characterized by high surgical risk patients,
with endovascular treatment being the therapeutic option with the highest benefit/risk ratio.
In this perspective,
the choice of the appropriate device to deploy is fundamental.
Nevertheless,
assessment of stent design and filter protection device placement represents a controversial point.
Concerning stent strut,
some authors,
as Schillinger et al.,
reported a non-significant statistical difference between the closed- and open-cell stents.
However,
according to Hart et al.,
an increased coverage of vessel plaque,
with the exclusion of its surface from the blood flow,
remains an established concern for carotid artery stenting.
(31,
32).
This concept is mentioned also by Boisier et al,
who underlined a higher percentage of complication inthe after-procedural period,
compared to the procedural time where a filter protection is placed ( 34,
35).
In this condition closed-cell stents represent the best option to obtain a plaque material scaffolding in the vessel wall in order to reduce complication rates,
which are higher in high risk patients with a device characterized by a larger free cell area (33-35).
Also the cerebral protection device represents a doubtful question.
Though for years the use of a filter protection device represented a fixed point,
several studies produced controversial results.
As reported by Tietke et al.
in their review,
the filter protection device may not eliminate periprocedural embolic events,
but it may potentially enhance the risk of periprocedural complications,
especially during it placement (37).
Nevertheless some authors reported opposite results (36).
In case of stop-flow protection devices,
as Mo.Ma,
it has been demonstrated that they reduce atheromatous debris embolization during stent deployment,
demonstrating it with transcranial Doppler,
especially for debris minor than 100μm,
small enough to pass through the filter but large to occlude arterioles and capillary beds (33,
38).
Moreover,
this protection device avoid guidewire passage through the stenosis while the blood flow isn’t stopped (33).
In the latter fashion the authors can avoid any thrombo-embolism event during the guidewire passage and the unprotected predilatation,
which coincide with 20 % of the microembolic signals during each endovascular phase (33,
39,
40).
The high percentage (57.9 %,
11 over 19 total patients) of embolic debris encountered in our seriesstrengthensthe hypothesisthatinflamed plaqueshave an high embolization risk.
However in patients who should undergo an endovascular procedure with a stop-flow protection device placement,
intracranial vascularization and contralateral carotid anatomy has to be evaluated in order to examine the device tolerance.
Other limits are represented by the high device cost and the high learning curve.
Our study was,
thus,
aimed to identify patients with contraindications to CEA characterized by inflamed plaques with the subsequent devices choice,
as closed-cell or modulated stents and proximal protection devices,
deployed specifically in order to prevent microembolic accidents.
The main limits of this retrospective study is the relatively small number of subjects and the retrospective nature of our study which need to be confirmed by a large randomized studies.
Nowadays the availability of HR-MRI,
as an “in vivo” alternative characterization of plaque morphology and its intrinsic structure,
can lead to the identification of highly inflamed plaques which need to be treated urgently.
The absence in our experience of significant complications rate may evidence not only that CAS can be considered an alternative treatment also for highly unstable plaques,
usually treated by CEA,
but also that this evidence may be a result of an accurate identification of inflamed plaques through morpho-structural evaluation obtained by HR-MRI,
with a subsequent adequate stent and cerebral protection device choice.
We,
thus,
firmly believe that,
in order to perform a correct endovascular treatment of high-risk,
inflamed atherosclerotic plaques,
an accurate imaging evaluation is mandatory.