MRI and Carotid Duplex assessment of vulnerable carotid atheromatous plaques in acute stroke patients

Document Type : Original Article

Authors

1 Department of Diagnostic Radiology, Faculty of Medicine, Minia University, Minia, Egypt

2 Department of Neurology, Faculty of Medicine, Minia University, Minia, Egypt

Abstract

Background: Stroke is a global health problem that leads to disability. In 2005, stroke was responsible for 5.7 million (16.6%) deaths, and 87% of these deaths occurred in low-income and middle-income countries. Two-thirds of strokes are ischemic in origin and 50% of these are associated with severe internal carotid artery disease. The underlying predominant cause of carotid artery disease is atherothrombosis. Method: 20 patients with acute ischemic stroke were enrolled in this study. They were diagnosed clinically and radiologically by MRI brain, then referred to us to be assessed by carotid Duplex and carotid MRI. Results: All patients had carotid atheromatous plaques that show more than one criteria of the following, lipid rich necrotic core of the atheromatous plaque (90%), surface ulceration of the plaque (90%), thrombus on top (80%), hemorrhage in plaque (75%), only 35% had more than 90% stenosis of the carotid lumen by plaques. MRI assessment for carotid atheromatous plaques at acute ischemic stroke patients, it was evident that the right carotid arteries (CCA, ICA) were more affected 14 (70%), most of the atheromatous plaques had thin fibrous cap with lipid rich core 18 (90%), ulcerated surface18 (90%), calcification15 (75%), thrombus on top 16 (80%) as well as hemorrhage within the plaque 15 (75%) with statistically significant P value (0.01, 0.0001,  0.0001,  0.04, 0.001,0.04) respectively. Most atheromatous plaques 10 (50%) caused about 70-90 % luminal stenosis with statistically non-significant difference P value 0.4. Conclusion: Carotid duplex and MRI had complementary role in assessment of carotid atheromatous plaques in stroke patients.




Keywords

Main Subjects


Introduction

Stroke is clinically defined as the syndrome of rabidly developing symptoms and signs of focal or global loss of cerebral function with no apparent cause other than of vascular origin. It is the third cause of death after coronary artery disease and all types of cancers. [1, 2].

Stroke is a global health problem and is a leading cause of adult disability. Of 35 million deaths attributable to chronic non- communicable diseases that occurred worldwide in 2005, stroke was responsible for 5.7 million (16.6%) deaths, and 87% of thes deaths occurred in low-income and middle-income counties. [3, 4]

Two-thirds of strokes are ischemic in origin and 50% of these are associated with severe internal carotid artery disease, the underlying, predominant cause of carotid artery disease is atherothrombosis. [5, 6]

Vulnerable atheromatous plaques: It is a must to look beyond the lumen and the degree of stenosis and to identify those imaging characters of vulnerable carotid plaques that are best suited for stroke risk prediction including

 lipid rich necrotic core with thin fibrous cap, surface irregularity and ulceration, intra plaque hemorrhage, and to lesser extent calcification. All that would lead to thrombus formation on top, then thrombus embolus formation. Finally, stroke occurs. [7]

Criteria of vulnerable atheromatous plaque:

  • Plaque ulceration: it means intimal defect more than 1 mm in width exposing the necrotic core of atheromatous plaque leading to activation of thrombosis cascade with formation of thrombus on top of ulcerating surface with more narrowing of lumen and increase possibility of detachment of the thrombus and embolization to reach cerebral arteries and completely occluding them. [8]
  • Thinned fibrous cap: it is a layer of fibrous connective tissue that cover the lipid core of the atheromatous plaque, it increases risk of rupture of and increase risk of ischemic stroke [9-11]
  • Large lipid rich necrotic core: it increases risk of rupture of and increase risk of ischemic stroke. [9-11]
  • Presence of intra plaque hemorrhage: -as a result of neovascularity or plaque rupture itself [12]

        Carotid Duplex study: is still the basic examination modality in carotid artery assessment as it is simple, cheap, easy to be applied, non-invasive and rapid. It measures the intima-media thickness as well as the heterogeneity or homogeneity of the atheromatous plaque, in addition to degree of luminal stenosis, blood flow parameters. [13]

        MR imaging: it now provides accurate method of detection of the plaque components and intra plaque hemorrhage. This is very important as the effects of atheromatous plaques nowadays depend on the criteria of the vulnerable atheromatous plaques rather than degree of stenosis. [14-15]

 Aim of the work:

The aim of this study was to assess the criteria of vulnerable atheromatous plaques at ischemic stroke patients using carotid duplex and carotid MRI.

Patients and Method:

Twenty patients, with diagnosis of acute anterior circulation cerebral ischemic event, based on both clinical assessment and cerebral imaging findings (MRI), of both sexes were included in the study, with recent history of stroke (within the last 2 weeks) who were referred to radiology department after being diagnosed- at neurology department, Minia university hospital. Age of patients ranged from 40 up to 70 years old.

Patients with embolic causes of stroke, hemorrhagic cerebral stroke, posterior circulation ischemic stroke and patients with absolute contra indication to MRI assessment were excluded from the study.

Informed consent was taken from all participants in the study or 1st degree relatives. The study was approved by the ethical committee of the Faculty of Medicine.

All patients were diagnosed clinically and radiologically by MRI brain to be acute ischemic stroke, then were subjected to carotid Duplex and carotid MRI:

  1. Carotid Duplex study for the cervical carotid arteries: using color Duplex machine, using high end Ultrasound machine and linear probe of high frequency 7- 9 MH to assess cervical carotid arteries.

B.MRI (Magnetic resonance imaging) for the cervical carotid arteries: using MRI machine, 1.5 Tesla system using cervical coil. Sequences (T1WI, T2WI, PDW and TOF).

 Statistical analysis:

Data entry and analysis was done using SPSS version 21, graphics by Microsoft excel. Data presented as frequency distribution Z test, Chi square test and fisher exact test were used to detect the statistical significance. P value of less than 0.05 considered as a cutoff significance.

 Results

Twenty acute ischemic anterior circulation stroke patients were included in this study 5 (25%) were females and 15 (75%) were males with age ranged from 40 up to 70 year- old. Elderly patients (61-70) year-old representing most of the studied sample in 12 (75%) of cases, as shown in table (1).

Regarding carotid duplex assessment for cervical carotid artery, all 20 patients of the study had carotid atheromatous plauqes. Right carotid arteries (CCA, ICA) were more affected in14 patients (70%), most of the atheromatous plaques were hypoechoic in 12 patients (60%) and had irregular surface in 15 patients (75%) with statistically significant difference (P value 0.01, 0.03, 0.04) respectively. Most atheromatous plaques in9 (45%) of the studied patients caused about 70-90% luminal stenosis, most plaques had calcification in13 (65%) and thrombus on top in12 (60%) of patients with statistically non-significant difference (P value 0.3, 0.2, 0.2) respectively, as shown in table (2).

Regarding carotid MRI assessment for cervical carotid artery, all 20 patients of the study had carotid atheromatous plauqes., right carotid arteries (CCA,ICA) were more commonly affected in14 (70%) patients, most of the atheromatous plaques had thin fibrous cap with lipid rich core in18 (90%) patients,  ulcerated surface in18 (90%), calcification in 15 (75%), thrombus on top in16 (80%) and hemorrhage within the plaque in15 (75%) with statistically significant difference (P value 0.01, 0.0001,  0.0001,  0.04, 0.001,0.04) respectively, as shown in table (3). Atheromatous plaques in 10 (50%) of patients caused about 70-90 % luminal stenosis with statistically non-significant difference (P value 0.4).

Carotid duplex versus carotid MRI: Carotid MRI could detect surface irregularity of atheromatous plaques and thrombus on top of plaque as well as calcification of plaque more than carotid Duplex (90 % versus 75 %), (80% versus60%) and (75 % versus 65%) respectively. MRI and carotid Duplex had nearly similar results regarding detection of luminal stenosis degree, as shown in table (2) & (3).

Only Carotid Duplex could detect free floating thrombus on top of atheromatous plaque. Carotid Duplex is dynamic study, so it could detect movement of thrombus with cardiac cycle. Out of 12(60%) ischemic stroke patients that had thrombus on top of atheromatous plaque [3(15%) of them showed partial free movement with cardiac cycle], as shown in table (2).

Only carotid MRI could detect composition of atheromatous plaques regarding their fibrous cap and lipid core as well as intra plaque hemorrhage, as shown in table (3). 

Vulnerable atheromatus plaque: all 20 acute ischemic stroke patients had one or more characters of the vulnerable carotid atheromatous plaques, detected by carotid MRI. The most common characters noted by carotid MRI were rich lipid necrotic core of plaque in18 (90%) and surface ulceration in 18 (90%) patients, followed by thrombosis on top of plaques, calcification of plaque, hemorrhage within plaque in [16 (80%),15 (75%) and 15 (75%) patients] respectively, as shown in figure (1).  These specific criteria of the atheromatous plaque made patients at high risk for developing ischemic anterior cerebrovascular insults, that is called vulnerable criteria of atheromatous plaque other than degree of luminal stenosis.

 

   

 

 

 

Table (1): Demographic distribution within Acute ischemic stroke patients

Age group(years)

Total number

No=20 (100%)

Female

No=5 (25%)

Male

No=15(75%)

40-50

1(5%)

0(0%)

1(5%)

51-60

7(35%)

2(10%)

5(25%)

61-70

12(60%)

3(15%)

9(45%)

 

 

Table (2): Carotid Duplex assessment of atheromatous plaques within CCA and cervical ICA at ischemic stroke patients (N=20)

Atheromatous plaque characters

Number of patients

Site

Right carotid arteries

14(70%)

Left carotid arteries

6(30%)

P-value

0.01*

Stenosis

Less than 70%

4(20%)

70% - 90%

9(45%)

More than 90%

7(35%)

P-value

0.3

Echogenicity of plaque

 

Hyperechoic

3(15%)

Isoechoic

5(25%)

Hypoechoic

12(60%)

P-value

0.03*

Surface of plaque

 Irregular

15(75%)

Smooth

5(25%)

P-value

0.04*

Thrombus on top

Present

-           Fixed thrombus

-           Free floating thrombus

12(60%)

-           9 (45%)

-           3 (15%)

Absent

8(40%)

P-value

0.2

P-value significant if less than 0.05

 Table (3): Carotid MRI assessment of atheromatous plaques within CCA and cervical ICA at ischemic stroke patients (N=20)

Atheromatous plaque characters

Number of patients

Site

Right carotid arteries

14(70%)

Left carotid arteries

6(30%)

P-value

0.01*

Stenosis

Less than 70%

3(15%)

70% - 90%

10(50%)

More than 90%

7(35%)

P-value

0.4

Composition of plaque

Thin fibrous cap, rich lipid core

18(90%)

Thick fibrous cap, poor lipid core

2(10%)

P-value

0.0001*

Surface ulceration of the plaque

Present

18(90%)

Absent

2(10%)

P-value

0.0001*

Thrombus on top of plaque

Present

16(80%)

Absent

4(20%)

P-value

0.0001*

Calcification

 

Present

15(75%)

Absent

5(25%)

P-value

0.04*

Hemorrhage in plaque

Present

15(75%)

Absent

5(25%)

P-value

0.04*

  P-value significant if less than 0.05

 

 

Figure (1): Criteria of vulnerable carotid atheromatous plaques at  acute ischemic stroke patients by carotid MRI (N=20)

 

 

Discussion

In this study, acute ischemic stroke in 20 patients had higher incidence with increased age, (61-70 years old), that was reported in 12 patients (60%), this was in agreement with the study done by Olivia van et al, 2005[16] and Díaz-Guzmán et al, 2008. [17] who revealed that age-specific prevalence rates of CVD, stroke and transient ischemic attacks increased exponentially with advancing age.

 

Regarding carotid MRI characteristics of athermatus plaque:

          18 (90%) of stroke patients showed rich lipid necrotic core of their carotid atheromatous plaques with significant p value =0.0001. This matched with the findings of Kevin DeMarco et al,2014 [18] study of 97 patients with 50%–99% stenosis referred for carotid MRI, there were significant associations between recent ipsilateral carotid stroke and the presence of a

LRNC (lipid rich necrotic core) as well as the presence of a thin or ruptured FC (fibrous cap), with no correlation between carotid artery stenosis and symptoms.

 

Eighteen (90%) of stroke patients showed surface ulceration of their carotid atheromatous plaques with significant p value =0.0001. This matched with Tobias Saam,2007[19] who reported that one of the vulnerable plaques to had fibrous cap rupture and surface ulceration. Also, in agreement with Alistair C. Lindsay et al, 2012 [20], who clarified that carotid plaques seen in 22 of 41patients (54%) in the symptomatic group with neurological manifestation versus 8 of 40 (20%) in the asymptomatic group (p value 0.05). They were caused by surface rupture (24% vs. 5%; p value 0.03).

 

Fifteen (75%) of stroke patients in our study, showed intra plaque hemorrhage of their carotid atheromatous plaques with significant p value =0.04. This was equivalent to the study done by Alistair C. Lindsay et al, 2012[20]. and in agreement with Kevin DeMarco et al, 2014[18] who noted that during a mean follow-up of 38 months in 154 patients with asymptomatic moderate carotid artery stenosis, 12 carotid cerebrovascular events occurred. Both the presence and size of IPH (intra plaque hemorrhage) correlated with a new ipsilateral carotid stroke or TIA.

 

In this study, 16 (80%) of stroke patients showed thrombus on top of their carotid atheromatous plaques with significant p value =0.0001. This matched with Luigi et al, 2004[21] who showed a thrombotically active carotid plaque associated with high inflammatory infiltrate was observed in (74.0%) of patients with ipsilateral major stroke.

 

In this study, Carotid MRI could detect surface irregularity of atheromatous plaques and thrombus on top of plaque as well as calcification of plaque more than carotid Duplex (90 % versus 75 %), (80% versus60%) and (75 % versus 65%) respectively. MRI and carotid Duplex had nearly similar results regarding detection of luminal stenosis degree, this matched with the findings of Paul J. et al, 2003 [22].

 

Regarding carotid duplex ultrasound (DUS) characteristics of carotid atheromatous plaque in our study:

Atheromatous plaques were classified by DUS into three categories, hypoechoic in 18 (60%), isoechoic in 8 (27%) and hyperechoic in 4 (13%) of the studied patients, but there are different studies with conflict to the accurate assessment of plaque echogenicity. This could be explained by David A. Russell et al, 2007 [23] who reported that change in plaque echoegnicity occurred over months from incidence of CVI (cerebrovascular insult), whether Patricia et al,2012 [24] showed that changes in echogenicity occurred over week. Xiaowei et al, 2016 [25] showed that echogenicity depended on its composition, for example hemorrhage and high fibrous content appeared hyperechoic.

 

Carotid Duplex could detect free floating thrombus on top of atheromatous plaque. Out of 12(60%) ischemic stroke patients that had thrombus on top of atheromatous plaque [3(15%) of them showed partial free movement with cardiac cycle], this was supported by CSABA CSOBAY et al, 2011 [26], who clarified the detection of Free-floating thrombus (FFT) of the internal carotid artery, which is almost always symptomatic and is usually discovered by ultrasound.

 

The most common characters noted by carotid MRI were rich lipid necrotic core of plaque in18 (90%) and surface ulceration in 18 (90%) patients, followed by thrombosis on top of plaques, calcification of plaque, hemorrhage within plaque in [16 (80%),15 (75%) and 15 (75%) patients] respectively. This matched with Millon A  et al, (2013) [7],  that clarified it was necessary to look beyond the lumen and the degree of stenosis and to identify those imaging Characters by MRI  of vulnerable carotid plaques that are best suited for stroke risk prediction including lipid rich necrotic core with thin fibrous cap, surface irregularity and ulceration, intra plaque hemorrhage to lesser extent calcification.

 

Conclusion

       It was found that ischemic stroke patients had one or more criteria for vulnerable atheromatous plaques detected by carotid MRI. Ultrasound is not considered the best technique

for detection of an irregular plaque surface or ulcerations, but it could detect free floating thrombus on top of atheromatous plaque. MRI has exclusive role in detection of lipid core, fibrous cap of atheromatous plaques, so carotid duplex and MRI had a complementary role in assessment of carotid atheromatous plaques in stroke patients.

Introduction

Stroke is clinically defined as the syndrome of rabidly developing symptoms and signs of focal or global loss of cerebral function with no apparent cause other than of vascular origin. It is the third cause of death after coronary artery disease and all types of cancers. [1, 2].

 

Stroke is a global health problem and is a leading cause of adult disability. Of 35 million deaths attributable to chronic non- communicable diseases that occurred worldwide in 2005, stroke was responsible for 5.7 million (16.6%) deaths, and 87% of these

 

deaths occurred in low-income and middle-income counties. [3, 4]

 

Two-thirds of strokes are ischemic in origin and 50% of these are associated with severe internal carotid artery disease, the underlying, predominant cause of carotid artery disease is atherothrombosis. [5, 6]

 

Vulnerable atheromatous plaques: It is a must to look beyond the lumen and the degree of stenosis and to identify those imaging characters of vulnerable carotid plaques that are best suited for stroke risk prediction including

 

 lipid rich necrotic core with thin fibrous cap, surface irregularity and ulceration, intra plaque hemorrhage, and to lesser extent calcification. All that would lead to thrombus formation on top, then thrombus embolus formation. Finally, stroke occurs. [7]

Criteria of vulnerable atheromatous plaque:

  • Plaque ulceration: it means intimal defect more than 1 mm in width exposing the necrotic core of atheromatous plaque leading to activation of thrombosis cascade with formation of thrombus on top of ulcerating surface with more narrowing of lumen and increase possibility of detachment of the thrombus and embolization to reach cerebral arteries and completely occluding them. [8]
  • Thinned fibrous cap: it is a layer of fibrous connective tissue that cover the lipid core of the atheromatous plaque, it increases risk of rupture of and increase risk of ischemic stroke [9-11]
  • Large lipid rich necrotic core: it increases risk of rupture of and increase risk of ischemic stroke. [9-11]
  • Presence of intra plaque hemorrhage: -as a result of neovascularity or plaque rupture itself [12]

        Carotid Duplex study: is still the basic examination modality in carotid artery assessment as it is simple, cheap, easy to be applied, non-invasive and rapid. It measures the intima-media thickness as well as the heterogeneity or homogeneity of the atheromatous plaque, in addition to degree of luminal stenosis, blood flow parameters. [13]

        MR imaging: it now provides accurate method of detection of the plaque components and intra plaque hemorrhage. This is very important as the effects of atheromatous plaques nowadays depend on the criteria of the vulnerable atheromatous plaques rather than degree of stenosis. [14-15]

 

Aim of the work:

The aim of this study was to assess the criteria of vulnerable atheromatous plaques at ischemic stroke patients using carotid duplex and carotid MRI.

 

Patients and Method:

Twenty patients, with diagnosis of acute anterior circulation cerebral ischemic event, based on both clinical assessment and cerebral imaging findings (MRI), of both sexes were included in the study, with recent history of stroke (within the last 2 weeks) who were referred to radiology department after being diagnosed- at neurology department, Minia university hospital. Age of patients ranged from 40 up to 70 years old.

 

Patients with embolic causes of stroke, hemorrhagic cerebral stroke, posterior circulation ischemic stroke and patients with absolute contra indication to MRI assessment were excluded from the study.

 

Informed consent was taken from all participants in the study or 1st degree relatives. The study was approved by the ethical committee of the Faculty of Medicine.

 

All patients were diagnosed clinically and radiologically by MRI brain to be acute ischemic stroke, then were subjected to carotid Duplex and carotid MRI:

 

  1. Carotid Duplex study for the cervical carotid arteries: using color Duplex machine, using high end Ultrasound machine and linear probe of high frequency 7- 9 MH to assess cervical carotid arteries.

B.MRI (Magnetic resonance imaging) for the cervical carotid arteries: using MRI machine, 1.5 Tesla system using cervical coil. Sequences (T1WI, T2WI, PDW and TOF).

 

 Statistical analysis:

Data entry and analysis was done using SPSS version 21, graphics by Microsoft excel. Data presented as frequency distribution Z test, Chi square test and fisher exact test were used to detect the statistical significance. P value of less than 0.05 considered as a cutoff significance.

 

Results

Twenty acute ischemic anterior circulation stroke patients were included in this study 5 (25%) were females and 15 (75%) were males with age ranged from 40 up to 70 year- old. Elderly patients (61-70) year-old representing most of the studied sample in 12 (75%) of cases, as shown in table (1).

 

Regarding carotid duplex assessment for cervical carotid artery, all 20 patients of the study had carotid atheromatous plauqes. Right carotid arteries (CCA, ICA) were more affected in14 patients (70%), most of the atheromatous plaques were hypoechoic in 12 patients (60%) and had irregular surface in 15 patients (75%) with statistically significant difference (P value 0.01, 0.03, 0.04) respectively. Most atheromatous plaques in9 (45%) of the studied patients caused about 70-90% luminal stenosis, most plaques had calcification in13 (65%) and thrombus on top in12 (60%) of patients with statistically non-significant difference (P value 0.3, 0.2, 0.2) respectively, as shown in table (2).

 

Regarding carotid MRI assessment for cervical carotid artery, all 20 patients of the study had carotid atheromatous plauqes., right carotid arteries (CCA,ICA) were more commonly affected in14 (70%) patients, most of the atheromatous plaques had thin fibrous cap with lipid rich core in18 (90%) patients,  ulcerated surface in18 (90%), calcification in 15 (75%), thrombus on top in16 (80%) and hemorrhage within the plaque in15 (75%) with statistically significant difference (P value 0.01, 0.0001,  0.0001,  0.04, 0.001,0.04) respectively, as shown in table (3). Atheromatous plaques in 10 (50%) of patients caused about 70-90 % luminal stenosis with statistically non-significant difference (P value 0.4).

 

Carotid duplex versus carotid MRI: Carotid MRI could detect surface irregularity of atheromatous plaques and thrombus on top of plaque as well as calcification of plaque more than carotid Duplex (90 % versus 75 %), (80% versus60%) and (75 % versus 65%) respectively. MRI and carotid Duplex had nearly similar results regarding detection of luminal stenosis degree, as shown in table (2) & (3).

 

Only Carotid Duplex could detect free floating thrombus on top of atheromatous plaque. Carotid Duplex is dynamic study, so it could detect movement of thrombus with cardiac cycle. Out of 12(60%) ischemic stroke patients that had thrombus on top of atheromatous plaque [3(15%) of them showed partial free movement with cardiac cycle], as shown in table (2).

Only carotid MRI could detect composition of atheromatous plaques regarding their fibrous cap and lipid core as well as intra plaque hemorrhage, as shown in table (3). 

      

Vulnerable atheromatus plaque: all 20 acute ischemic stroke patients had one or more characters of the vulnerable carotid atheromatous plaques, detected by carotid MRI. The most common characters noted by carotid MRI were rich lipid necrotic core of plaque in18 (90%) and surface ulceration in 18 (90%) patients, followed by thrombosis on top of plaques, calcification of plaque, hemorrhage within plaque in [16 (80%),15 (75%) and 15 (75%) patients] respectively, as shown in figure (1).  These specific criteria of the atheromatous plaque made patients at high risk for developing ischemic anterior cerebrovascular insults, that is called vulnerable criteria of atheromatous plaque other than degree of luminal stenosis.

 

   

 

 

 

Table (1): Demographic distribution within Acute ischemic stroke patients

Age group(years)

Total number

No=20 (100%)

Female

No=5 (25%)

Male

No=15(75%)

40-50

1(5%)

0(0%)

1(5%)

51-60

7(35%)

2(10%)

5(25%)

61-70

12(60%)

3(15%)

9(45%)

 

 

Table (2): Carotid Duplex assessment of atheromatous plaques within CCA and cervical ICA at ischemic stroke patients (N=20)

Atheromatous plaque characters

Number of patients

Site

Right carotid arteries

14(70%)

Left carotid arteries

6(30%)

P-value

0.01*

Stenosis

Less than 70%

4(20%)

70% - 90%

9(45%)

More than 90%

7(35%)

P-value

0.3

Echogenicity of plaque

 

Hyperechoic

3(15%)

Isoechoic

5(25%)

Hypoechoic

12(60%)

P-value

0.03*

Surface of plaque

 Irregular

15(75%)

Smooth

5(25%)

P-value

0.04*

Thrombus on top

Present

-           Fixed thrombus

-           Free floating thrombus

12(60%)

-           9 (45%)

-           3 (15%)

Absent

8(40%)

P-value

0.2

P-value significant if less than 0.05

 Table (3): Carotid MRI assessment of atheromatous plaques within CCA and cervical ICA at ischemic stroke patients (N=20)

Atheromatous plaque characters

Number of patients

Site

Right carotid arteries

14(70%)

Left carotid arteries

6(30%)

P-value

0.01*

Stenosis

Less than 70%

3(15%)

70% - 90%

10(50%)

More than 90%

7(35%)

P-value

0.4

Composition of plaque

Thin fibrous cap, rich lipid core

18(90%)

Thick fibrous cap, poor lipid core

2(10%)

P-value

0.0001*

Surface ulceration of the plaque

Present

18(90%)

Absent

2(10%)

P-value

0.0001*

Thrombus on top of plaque

Present

16(80%)

Absent

4(20%)

P-value

0.0001*

Calcification

 

Present

15(75%)

Absent

5(25%)

P-value

0.04*

Hemorrhage in plaque

Present

15(75%)

Absent

5(25%)

P-value

0.04*

  P-value significant if less than 0.05

 

 

Figure (1): Criteria of vulnerable carotid atheromatous plaques at  acute ischemic stroke patients by carotid MRI (N=20)

 

 

Discussion

In this study, acute ischemic stroke in 20 patients had higher incidence with increased age, (61-70 years old), that was reported in 12 patients (60%), this was in agreement with the study done by Olivia van et al, 2005[16] and Díaz-Guzmán et al, 2008. [17] who revealed that age-specific prevalence rates of CVD, stroke and transient ischemic attacks increased exponentially with advancing age.

 

Regarding carotid MRI characteristics of athermatus plaque:

          18 (90%) of stroke patients showed rich lipid necrotic core of their carotid atheromatous plaques with significant p value =0.0001. This matched with the findings of Kevin DeMarco et al,2014 [18] study of 97 patients with 50%–99% stenosis referred for carotid MRI, there were significant associations between recent ipsilateral carotid stroke and the presence of a

LRNC (lipid rich necrotic core) as well as the presence of a thin or ruptured FC (fibrous cap), with no correlation between carotid artery stenosis and symptoms.

 

Eighteen (90%) of stroke patients showed surface ulceration of their carotid atheromatous plaques with significant p value =0.0001. This matched with Tobias Saam,2007[19] who reported that one of the vulnerable plaques to had fibrous cap rupture and surface ulceration. Also, in agreement with Alistair C. Lindsay et al, 2012 [20], who clarified that carotid plaques seen in 22 of 41patients (54%) in the symptomatic group with neurological manifestation versus 8 of 40 (20%) in the asymptomatic group (p value 0.05). They were caused by surface rupture (24% vs. 5%; p value 0.03).

 

Fifteen (75%) of stroke patients in our study, showed intra plaque hemorrhage of their carotid atheromatous plaques with significant p value =0.04. This was equivalent to the study done by Alistair C. Lindsay et al, 2012[20]. and in agreement with Kevin DeMarco et al, 2014[18] who noted that during a mean follow-up of 38 months in 154 patients with asymptomatic moderate carotid artery stenosis, 12 carotid cerebrovascular events occurred. Both the presence and size of IPH (intra plaque hemorrhage) correlated with a new ipsilateral carotid stroke or TIA.

 

In this study, 16 (80%) of stroke patients showed thrombus on top of their carotid atheromatous plaques with significant p value =0.0001. This matched with Luigi et al, 2004[21] who showed a thrombotically active carotid plaque associated with high inflammatory infiltrate was observed in (74.0%) of patients with ipsilateral major stroke.

 

In this study, Carotid MRI could detect surface irregularity of atheromatous plaques and thrombus on top of plaque as well as calcification of plaque more than carotid Duplex (90 % versus 75 %), (80% versus60%) and (75 % versus 65%) respectively. MRI and carotid Duplex had nearly similar results regarding detection of luminal stenosis degree, this matched with the findings of Paul J. et al, 2003 [22].

 

Regarding carotid duplex ultrasound (DUS) characteristics of carotid atheromatous plaque in our study:

Atheromatous plaques were classified by DUS into three categories, hypoechoic in 18 (60%), isoechoic in 8 (27%) and hyperechoic in 4 (13%) of the studied patients, but there are different studies with conflict to the accurate assessment of plaque echogenicity. This could be explained by David A. Russell et al, 2007 [23] who reported that change in plaque echoegnicity occurred over months from incidence of CVI (cerebrovascular insult), whether Patricia et al,2012 [24] showed that changes in echogenicity occurred over week. Xiaowei et al, 2016 [25] showed that echogenicity depended on its composition, for example hemorrhage and high fibrous content appeared hyperechoic.

 

Carotid Duplex could detect free floating thrombus on top of atheromatous plaque. Out of 12(60%) ischemic stroke patients that had thrombus on top of atheromatous plaque [3(15%) of them showed partial free movement with cardiac cycle], this was supported by CSABA CSOBAY et al, 2011 [26], who clarified the detection of Free-floating thrombus (FFT) of the internal carotid artery, which is almost always symptomatic and is usually discovered by ultrasound.

 

The most common characters noted by carotid MRI were rich lipid necrotic core of plaque in18 (90%) and surface ulceration in 18 (90%) patients, followed by thrombosis on top of plaques, calcification of plaque, hemorrhage within plaque in [16 (80%),15 (75%) and 15 (75%) patients] respectively. This matched with Millon A  et al, (2013) [7],  that clarified it was necessary to look beyond the lumen and the degree of stenosis and to identify those imaging Characters by MRI  of vulnerable carotid plaques that are best suited for stroke risk prediction including lipid rich necrotic core with thin fibrous cap, surface irregularity and ulceration, intra plaque hemorrhage to lesser extent calcification.

 

Conclusion

       It was found that ischemic stroke patients had one or more criteria for vulnerable atheromatous plaques detected by carotid MRI. Ultrasound is not considered the best technique

for detection of an irregular plaque surface or ulcerations, but it could detect free floating thrombus on top of atheromatous plaque. MRI has exclusive role in detection of lipid core, fibrous cap of atheromatous plaques, so carotid duplex and MRI had a complementary role in assessment of carotid atheromatous plaques in stroke patients.

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