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The first four lesions were considered as "complicated lesions". Foamy macrophages show brown staining corresponding to the expression of CD68 and weak red staining for CD The fibrous cap overlying the lipid core was highly variable in thickness and cellular constituents. Plaques presented ulcerations with breakdown of the surface of the cap. Their-regularity had a punched-out characteristic or was simply a tear with borders; in rare cases plaques contained virtually no fibrous cap.

The rupture was covered by a thrombus, and in many cases the thrombus was found directly overlying the lipid core of the lesion, entering a large pool of extracellular lipids. As said the borders of the rupture presented a mononuclear infiltration with a high density of macrophages. Figure 9 The histological findings were similar to the ruptured-thrombosed plaques, but there was also extensive disruption of the plaque by an intraplaque hemorrhage.

Intense neovascularization of the lipid core. In panel A, the asterisk indicates a thick neovascularization vessel. Panel B shows the middle arterial layer. In panel C:,a central neoformed vessel outgrowth in "glove finger" is seen into the lipid core. Endothelial pyknotic cells surrounded by scarse pericytes, macrophages, and lymphocytes in the periphery are shown.

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Lipid-rich core is heavily vascularized by great number of thin-walled, neoformed,CDpositive vessels. Vascularization of the shoulder of the plaque. Note thin-walled neoformed vessels of different shapes and sizes. Outer zone shows media and an extensive quantity of thin-walled normal capillaries,longitudinally oriented brown.

Low magnification view of an entire endarterectomy specimen shows actin-positive vessel walls HHF35 and hyperplastic smooth muscle cells asterisc. Media arrowheads shows normal arrangement and at this level is composed of only 5 to 10 layers of smooth muscle cells arrow. Magnification x Intraplaque hemorrhage without plaque rupture IPH Figure None of them had a connection between the hemorrhage and the arterial lumen, in spite of a careful search in serial sections.

Conversely the intimal surfaces were clean and none showed evidence or platelet or fibrin deposition. Hemorrhages varied from microscopic, microfocal or slitlike foci of recent hemorrhage, with no evident changes in the overall makeup of the plaque to massive hemorrhage, elevation and disruption of the intima to massive hemorrhage,elevation and disruption of the intima and occlusive stenosis. Only these massive lesions were considered. Of note, slitlike hemorrhages distant to the main lesion were found in 12 cases, in 5 of them without the presence of a massive intraplaque hemorrhage.

Plaque rupture arrow plus intraplaque hemorrhage and parietal thrombosis. An entire specimen from a carotid endarterectomy frontally cut is shown. Fibrous cap is extremely thin hematoxylin-eosin; original magnification 3.


Sample of carotid endarterectomy. It was characterized by an extensive hemorrhage within the plaque with separation of its varying components and disruption of the intima. Plaque rupture. A intraplaque hemorrhage arrow B-. Breakdown of cap is clearly shown between arrowheads. These plaques contained neither thrombosis nor hemorrhages and consisted of laminated fibrous connective tissue and irregular masses of calcified material. These areas appeared as acellular, roughly circular masses of pale-staining debris.

These plaques consisted of thin fibrous caps covering a lipid-rich core with extensive vascularization. Complicated vs stable calcified, non complicated plaques. Of note, the 5 cases of unstable, soft non complicated plaque presented neoformed vessels surrounding the plaque. Clinical-pathological correlation. The risk factor variables age, gender, hypertension, left ventricular hypertrophy, diabetes, weight, smoking and uric acid could not be correlated with any of the pathological and immunohistochemical findings.

Therefore, carotid endarterectomies provided the material for phenotypic characterization of vascular and cellular components of the plaque. This permitted to known the topography and the distribution of mononuclear infiltrates as well as endothelial cells. Although the cellular composition of advanced atherosclerotic plaques is known to be heterogeneous, [ 31 ] it can be summarized as:. Intimal plaque rupture-inflammatory process.

We demonstrated for the first time[ 30 ] that rupture of carotid plaques is characterized by the presence of a macrophagic infiltration of the caps. The presence of a large number of foamy macrophages in plaque fissuring in human coronary thrombosis had been reported previously [ 29 , 32 - 34 ] and it was suggested that inflammation through enzymatic degradation of the fibrous cap by macrophages might destabilize the plaque, causing weakening at the immediate site of rupture. Complete rupture of the fibrous cap was found to be the cause of thrombosis in 18 cases, intraplaque hemorrhage plus thrombosis in 18 and intraplaque hemorrhage in 5 cases.

Our studies in carotid plaques showed direct apposition of T-lymphocytes to macrophages and a close relation of these cells to endothelial cells. This highly suggests a cell-to-cell interaction, which results in an inflammatory process mediated by cellular adhesion molecules such as CD31 , cytokines, growth factors and other substances as described in coronary arteries[ 29 ] and aorta.

Intraplaque hemorrhage without plaque rupture-plaque vascularization. This subset of carotid lesions was not related to cap erosion, but to plaque vascularization. This seems to be the most plausible mechanism. Theseneoformed vessels showed a weak stain with CD Considering that CD31 PECAM-1 is a molecular adhesion molecule, the lack of expression could be pointing out a functional difference between normal and neoformed vessels.

PECAM- 1 is required for transendothelial migration of leucocytes. The same mechanism postulated for the vessels of the core may operate in neoformed vessels. The presence of histological signs of old hemorrhages and the existence of slitlike hemorrhages at that level strongly suggest that a local origin of bleeding may operate. Lusby et al[ 25 ] demonstrated that the resultant angiogenesis associated with hemorrhages might make those lesions prone to mechanical stress and subsequent hemorrhages.

Accordingly, our observations and those by other authors suggest that intraplaque hemorrhages may occur at any time in the history of carotid plaque. Our results in 76 endarterectomies suggest that the site of plaque rupture is associated with the presence of a large macrophagic infiltration, [ 38 ] as well as T-lymphocytes rare B-lymphocytes and mast cells and lack of smooth muscle cells.

The human carotid body in health and disease

The decision of whether to perform endarterectomy in patients with asymptomatic disease should be made on the basis of data including degree of stenosis and activity of the carotid lesion, as well as issues of medical and surgical morbidity. The relationship between anatomy of carotid plaques and the presence or not of symptoms. For this purpose we carried out an investigation[ 19 ] in order to analyze in a large sample the relation between the anatomy of carotid plaques and the presence of symptoms in endarterectomy specimens.

To avoid an excessive number of plaque subtypes that might blur the relationship with symptoms, [ 31 ] only complicated and non-complicated plaques and ruptured and nonruptured plaques were used for statistical analysis. In plaques, large lipid cores with a fibrous cap and a band of fibrous tissue separating the plaque from the remainder of the media were observed. The cap was frequently vascularized. In most cases, extensive inflammatory infiltrates consisting of macrophages, smaller numbers of T lymphocytes, a few B lymphocytes, and mast cells were observed.

In the remaining cases, the plaque was composed of fibrocellular tissue only. Twelve of 18 unstable, soft, non complicated plaques exhibited neoformed vessels surrounding the plaques. The remaining 6 plaques had huge lipid cores without evident neoformed vessels, suggesting very recent development. Ruptured versus non-ruptured plaques. Only 2 of 51 affected cases demonstrated complicated plaques. Risk factors could not be associated with any pathologic findings. No correlation could be established between plaque type and symptoms Table I.

Areas of carotid plaque rupture were characterized by macrophagic infiltration at the rupture. This finding suggests that inflammation, through enzymatic degradation of the fibrous cap by macrophages, might destabilize the plaque, causing weakening at the site of rupture. Many factors can modulate the development of thrombus.

Long-term preoperative administration of aspirin and use of heparin during surgery may explain the relatively low frequency of thrombosis observed in ruptured plaques. Other possibilities are that fibrin or platelet deposition was missed at previous embolization orduring microscopic examination because of sampling. This subset of lesions was not related to rupture of the cap, but to plaque neovascularization. Lipid cores were highly vascularized with heterogeneous neoformed vessels and with macrophages and T cells in close contact with the endothelial wall.

An increase in the amount of lipid in the core, mechanicalstresses,[ 25 ] and overproduction of oxygen free radicals by macrophages could lead to breakdown of core neoform vessels and IPH production. Complicated and noncomplicated plaques versus symptomatic and asymptomatic disease. Coronary plaque ruptures have been identified in patients who died of noncardiac causes. The frequency of plaque hemorrhage and plaque disruption varied greatly among the various series from both symptomatic and asymptomatic specimens In a review of several studies,[ 25 , 37 , 42 - 46 ] Fisher et al observed that the pooled frequency of plaque hemorrhage and rupture demonstrated a significantly increased frequency in the symptomatic group.

However,pooling data from multiple sources when methods of analysis are different histologicvs macroscopic is hazardous. Some authors stress that IPH indicates only the severity of atherosclerosis;[ 50 , 51 , 54 - 57 ] others suggest IPH has a direct role in pathogenesis of transient ischemic attack or stroke. IPH seems to be more common in plaques causing high-grade stenosis. However, this study included too few patients to be significant. Despite a close relationship between IPH and symptoms,[ 37 , 61 - 63 ] and carotid plaque rupture, thrombosis, and symptoms, [ 25 , 60 , 61 ] it has also been claimed that patients with symptomatic plaques typically have large necrotic cores within the carotid arteries.

Patients with asymptomatic carotid artery stenosis should be screened for other treatable risk factors for stroke with institution of appropriate lifestyle changes and medical therapy Class I; Level of Evidence C. Selection of asymptomatic patients for carotid revascularization should be guided by an assessment of comorbid conditions and life expectancy, as well as other individual factors, and should include a thorough discussion of the risks and benefits of the procedure with an understanding of patient preferences Class I; Level of Evidence C.

The use of aspirin in conjunction with carotid endarterectomy CEA is recommended unless contraindicated because aspirin was used in all of the cited trials of CEA as an antiplatelet drug Class I; Level of Evidence C. The advantage of revascularization over current medical therapy alone is not well established Class IIb; Level of Evidence B. Other points to consider is the necessity of interventionally treating an asymptomatic carotid artery disease are: age 80 years or less, life expectancy higher tan 5 years, hemispheric hypoperfusion, significant intracerebral vascular disease,unstable carotid plaque, rapid progression of the stenoses, presence of silent cerebral infarcts, neck radiotherapy and the necessity of a coronary by pass surgery.

Finally and taking into consideration the mechanisms of atherosclerosis: cells component behavior, IPH, biology and gene expression, it can be seen in the literature a new tendency of treatment in animal models. However, attention should therefore focus on the processes of plaque breakdown andt hrombus formation in humans, whereas the use of animal models should probably be reserved for studying the function of particular genes and for investigating isolated features of plaques,such as the relationshipbetween cap thickness and plaque stability.

They concluded that distinctly expressed genes andmicroRNAscan be linked to plaque instability. On the other hand, Forte et al described the role of polyamines in reducing carotid arteriotomy-induced re stenosis s in vitro and in a rat model suggesting a novel therapeutic approach for this pathophysiological process. The atherosclerotic process in the carotid arteries begins with a thickening of the intima-media complex and, according to factors of disease progression can reach arterial occlusion, throughout intermediate stages of mild, moderate and severe stenosis.

Moreover, depending on several factors, the structure of the plaque can show different evolutionary behaviors, from simple stable plaque, fibrotic, and non stenotic, to that hemorrhagic, ulcerated, with rupture that produces severe stenosis and strokes. Carotid risk factors are identical to those mentioned for coronary disease. The incidence of cerebrovascular events depends primarily on the degree of carotid stenosis but plaque structure is also relevant, as well as the speed of progression of plaque, and consequent carotid disease stenosis and also the presence of systemic thrombogenic factors.

Several studies have described a good correlation between intraplaque hemorrhage IPH with ulceration and cerebrovascular symptoms.

Diseases of the Human Carotid Body

IPH was not only identified in most symptomatic patients but also a close relationship was established between the onset of symptoms and the presence of plaque haemorrhage. Seeger et al[ 81 - 85 ] reported that the composition of plaques from symptomatic patients is significantly different from those asymptomatic. The former contains more total lipid and cholesterol, and less collagen and calcium.

Johnson et al [ 86 ] classified asymptomatic plaques according to ultrasonographic characteristics into calcified, dense and soft. At the end of a 3 year follow-up a large proportion of asymptomatic patients with soft plaques had become symptomatic, while a small proportion of those with calcified plaques have developed symptoms. Hennerici et al [ 87 ] reported that patients with fibrous carotid plaques had a tendency to remain stable while plaque progression was common in those with soft and complex calcified plaques.

Spontaneous regression of minor carotid atheroma occurred in soft plaques corresponding to a reduction in plaque volume while fibrous and calcified plaques did not regress. Despite that currently the presence of symptoms and percentage of luminal narrowing remain the most useful predictors of transitory ischemic cerebral attacks or stroke risk, [ 3 , 75 , 88 , 89 ] there is a body of evidence that plaque morphology is crucial in the development of its natural history. Regarding the relationship of IPH with a higher prevalence of symptoms or hemorrhagic stroke, the results are contradictory.

There are several reasons that make knowledge of plaques structure very important. It is well known that fibrous plaques, are predominantly collagen in content, showing a highly echogenic quality and being generally homogeneous in texture. When lipid content of the plaque increased, the plaque turns more echolucent. However, results were not convincing [ 90 , 91 ]. Other authors mentioned only relevant the percentage of carotid stenosis [ 92 , 93 ]. The accuracy of the carotid ultrasonography procedure in assessing the percentage of luminal diameter narrowing is well established [ 94 , 95 ].

Percentage of stenosis has been the main point of interest for noninvasive carotid testing due to its correlation with stroke risk. Developed technics in ultrasound US permit a more detailed analysis and accurate information about the plaque morphology. This technique is useful to evaluate the natural history and the stroke risk associated to the lesions.

High-resolution B-mode ultrasonography B-mode seems advantageous over arteriography for characterizing atherosclerotic plaque. It was suggested that echolucent plaques have increased lipid and cholesterol levels, making them unstable and prone to rupture and hemorrhage. According to Lehay, [ 99 ] Bluth, [ 84 ] Goes [ ] and the recommendations from the Committee on Standards in Non - invasive Vascular Testing, [ ] carotid plaques were classified as homogeneous or heterogeneous.

But these two groups arose from categorizing the plaques into 4 types according to the scale of l to 4 based on the Geroulakos' classification [ 81 ]. In this classification, Type 1 corresponded to uniformly sonolucent; type 2, predominantly sonolucent; type 3 predominantly echogenic and type 4 uniformly echogenic. In this way types l and 2 corresponded to heterogeneous plaques and types 3 and 4 to homogeneous plaques.

Figures 1 3 and Panels A and B correspond to type 1 plaques-. Panel C Carotid plaque type 2 showing dense echoes white color alternating with most hypoechoic or anechoic areas in black which indicate plaque instability. Panel A: it can be seen between arrows a carotid plaque containing predominantly echogenic areas type 3 that generally correspond to fibrous tissue which gives it stability Panel B. This carotid plaque type 4 is practically composed by echogenic areas between arrows.

The analysis of the complex plaque structure regards defining histological types [ 98 ]:. Inflammation was described as chronic inflammatory infiltrates lymphocytes, histiocytes, macrophages and mast cells within the plaque itself. Hemorrhage was identified by a macroscopic hematoma within the arterial wall with or without extension through the luminal surface.

Hemorrhage is identified by disruption of red blood cells and macrophage engulfment of hemosiderin, to distinguish it from surgical related hemorrhage consisting in preserved erythrocytes. Plaque morphology analyzed by US, identifying those unstable or complicated plaques found a very good correlation unless calcium deposits exist. Ultrasonographically, calcium deposits are characterized by a highly echoreflective area with acoustical shadowing masking the real plaque structure below, resulting in a worse correlation between US and pathology.

Carotid plaques having calcium deposits correspond to a third classification stable, unstable and calcium , as their evolution can be unpredictable. The presence of "acoustic shadows" that mask the true tissue structure is characteristic of this type of plaque on ultrasonography, making morphological interpretation difficult. A type 5 calcified carotid plaque significantly reduces the lumen in the carotid bulb between small arrows The typically acoustic shadowing is clearly seen big arrow.

In this sense, we published the results of an investigation showing ultrasonic vs pathologic correlation of carotid atheromatous plaques. This manuscript involved two ultrasonographers and one pathologist. Thirteen of them had poor quality images and were excluded. The remaining 61 studies, belonging to 59 patients 2 bilateral endarterectomies had been sent from five different laboratories and were analyzed blindly and independently by two different observers.

There were 17 females and 42 males. Age ranged from 52 to 83 years mean 68 years. A very good interobserver correlation was observed and, in turn, with histopathological findings. However, calcium plaques produced less agreement. In our research regarding interobserver agreement, there were 2 non-coincidences vs. Regarding the strictly classification in heterogeneous, homogeneous and calcified plaques, there were 59 coincidences, Coincidences not always were total.

If we consider the fourth group in which operators agreed in plaques being heterogeneous but with difficulties in distinguishing IPH, calcium and lipids as non-coincidences, then the accuracy falls to In others words calcified plaques clearly blurred the diagnosis of plaque structure. This investigation has correlated the ultrasound aspect of carotid atheromatous plaques with pathology demonstrating the highest incidence of intraplaque hemorrhage IPH in those complex, irregular and heterogeneous producing stenosis Figure Two dimensional and color ultrasound image displays a very tight stenosis between arrows caused by an anechoic plaque large arrow B.

The corresponding gross morphology shows an irregular stenotic plaque composed by a brownish tissue arrow. Microscopically this plaque belongs to an intraplaque hemorrhage arrow. Mallory Trichrome. Correlation with histology shows that lipid rich regions are the least echogenic on US and calcified areas are the most. The surface of the plaque with hemorrhage is usually irregular and ulcerated. Surface ulceration is unusual in lipid plaques. By contrast, plaque hemorrhage produces an echolucent area within the plaque, in which its degree may be correlated with the age of hemorrhage.

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  7. The anechoic or highly echolucent qualities of fresh hemorrhage are comparable with those of the lumen, being irregular and randomly distributed through the plaque heterogeneous shape. Ultrasonography fails in detecting plaque ulceration even using color-flow Doppler assisted duplex, as was recently demonstrated by Sitzer et al. Hartmann et al [ ] reported poor results between US and pathology concluding that visual assessment of B-mode images is not reliable.

    Taking all these concepts into consideration, decreased echogenicity would correspond either to lipid deposits or to hemorrhage within a plaque being both of them characteristic of instability. Lipid deposits appear more uniform and are less randomly distributed throughout the plaque. The European Carotid Plaque Study Group [ ] correlated B-mode imaging studies with histology in patients undergoing carotid endarterectomy.

    They concluded that US appearance of carotid plaque is related to histological composition being the echogenicity inversely related to the relative amount of soft tissue. Backscattered radiofrequency derived signals devices have been applied for better characterization of the different components of plaque structure[ - ]. But this technique is more expensive and not always available in most laboratories so we consider that conventional good quality B-mode images allow a reliable differentiation between the three types of plaques. Although carotid ulltrasound is the method of choice to study the structure of carotid plaques MRI also plays a significant role.

    Their statistical analyzes confirmed that the detection of IPH on NMR was associated with an increased risk of cerebrovascular events.

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    In summary, we believe necessary to describe and report the B-mode characteristic of carotid plaques together with the percentage of luminal stenosis. Ultrasonic plaque description correlates with histogy. The adoption of plaque characterization despite of the degree of carotid stenosis would allow recognition of a high-risk subset of patients that may benefit from carotid intervention. Atherosclerosis is the most frequent cause of extracranial carotidartery disease. Among nonatheromatous alterations of the carotid arteries, interest has long been placed on specific anatomical abnormalities called dolichoarteriopathies.

    Carotid dolichoarteriopathies can be classified into three different types [ ] Figure Figures 1 9 and Published studies have reached disparate conclusions with regard to the origin or cause of carotid dolichoarteriopathies, as well as their hemodynamic and prognostic significance. Other investigators similarly believe that a causal connection exists between cerebral flow alteration and severe carotid dolichoarteriopathies, to the point of proposing surgical correction of kinking and coiling to prevent stroke.

    Conversely,other authors consider carotid dolichoarteriopathies as a mere anatomical variety, devoid of clinical consequences. Establishing the clinical impact of dolichoarteriopathies is further complicated by the fact that the mechanisms responsible for their formation are still debated. A: Color flow Doppler imaging discloses an internal carotid artery kinking. B: Color and pulsed-wave Doppler showed turbulences at the site of the kinking.

    However, both maximum systolic velocity and end-diastolic velocity of internal carotid arteries were substantially unaffected by kinking. A double angled internal carotid artery showing a S shaped configuration image corresponding to color Doppler ultrasound.

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    Indeed, Kelly [ ] observed that carotid arteries may be kinked or show loops at some point during intrauterine development, when the descent toward the mediastinum occurs enabling the union of the third aortic arch with the dorsal aorta. Obviously, as these 2 etiological theories are so different from each other, they may also entail different implications both clinically and prognostically. Part of the uncertainty derives from the fact that previous observations had been made in small studies or in selected populations.

    In contrast, lack of consensus exists over the clinical and prognostic significance of these alterations or even about their etiology. With regard to the possibility that dolichoarteriopathies may be the result of a degenerative process, over the years several hypotheses have been put forward trying to explain how they may develop.

    Carotid Artery Disease – Vascular Cures

    Some of these seem quite unlikely, such as the possibility that carotid kinking could be due to kyphosis or lordosis of the spine, which might deviate the carotid axis, [ ] or that inflammation of the tissues around the carotid arteries would cause them to retract. Data gathered in modern times also do not help in establishing firm conclusions. Two rather large reports by Ghilardi et al [ ] and Del Corso et al [ ] described a great prevalence of hypertension and atherosclerosis in patients with carotid dolichoarteriopathies; however, both studies lack a group of normal participants, and deal with a population of patients selected for vascular pathology, and in whom predominance of such cardiovascular risk factors is expected.

    Pancera et al [ ] have reported an association between carotid artery kinking and age and with hypertension as well. This same reasoning applies to the effect of hypertension reported in that study, which was actually based on about a dozen patients. The possibility that carotid dolichoarteriopathies may have an embryological origin had also been suggested in the past.

    Again, however, those reports were not conclusive. Sometimes, this was because of the small numbers of cases studied. In this respect, Weibel and Fields [ ] described at angiography 14 cases of anatomical abnormalities in patients aged between1 and 20 years, while Sarkari et al [ ] reported 8 children aged 9 months to 16 years with symptomatic carotid kinkings and coilings. In a substantially largerstudy, there may have been a selection bias [ ] in that case, angiographies of neck vessels were obtainedin patients aged between 6 months and 82 years.

    Although that finding may seemingly support the view that in fact there is no association with aging and that dolichoarteriopathies have an embryological origin, the significance of such a high frequence in children might have been restricted to the peculiar population studied, as it is quite conceivable that children who were subjected to an invasive procedure such as angiography underwent it because of a high clinical suspicion of carotid abnormalities.

    More than half of the strokes occur because of carotid artery disease. What causes carotid artery disease? Although everyone is affected to some extent, there are several influences determining how severe it is in individual people. Some are fixed, such as being male, having a family history of stroke or angina, or getting older. If you already have peripheral arterial disease PAD or coronary heart disease you are at higher risk of carotid disease and stroke. Furring of the arteries is a normal part of the ageing process; however it does need to be monitored throughout the body, especially around major arteries and the heart where it can cause heart attacks and angina.

    How is the diagnosis made? The diagnosis is usually made with an ultrasound scan of the arteries in the neck duplex , or sometimes after a CT or MR scan. Diagnosis of this condition is important because it increases the risk of you having a stroke in the future. Can medication help? All patients with carotid artery disease can benefit from taking aspirin and a statin and by treating their individual risk factors, such as stopping smoking completely.

    There are multiple benefits from giving up cigarette smoking, including reducing the excessive tendency for blood to clot, increasing the amount of oxygen in the blood and most importantly preserving the cells lining the blood vessels which are very sensitive to the toxins in smoke. The benefit of the aspirin is to reduce the stickiness of small blood cells called platelets which adhere to the irregular surface of the plaque, but can then break off as a small clump.

    Where aspirin is not appropriate, other anti-platelet drugs can be prescribed. The benefit of a statin is partly in reducing the cholesterol, which was the initial reason for them being developed, but they also appear to reduce the tendency for atherosclerotic plaques to crack and so even patients with low cholesterol will benefit from taking them. Will I need an operation?

    In the carotid arteries, the problem is related to the possibility that small pieces of solid material may break off the plaque and pass with the bloodstream into the brain causing a TIA or stroke. It is likely that if you have had a stroke, a TIA or amaurosis fugax that you will be advised to have the operation as soon as possible to prevent a further stroke.

    What happens now? Your surgeon will make sure that you are on the right medications and discuss whether you need surgery or not. More information and advice about vascular health. Whilst we make every effort to ensure that the information contained on this site is accurate, it is not a substitute for medical advice or treatment, and the Circulation Foundation recommends consultation with your doctor or health care professional.

    The Circulation Foundation cannot accept liability for any loss or damage resulting from any inaccuracy in this information or third party information such as information on websites to which we link. The information provided is intended to support patients, not provide personal medical advice. Skip to main content.