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July2007 Vol.44 Issue:      2 Table of Contents
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Is Elevated Blood Pressure Associated with Increase of Plasma C-Reactive Protein Levels in Acute Ischemic Stroke ?

Abo Zaid Abd Allah1, Salah Aaref2

Departments of Neuropsychiatry, Benha University1;

Clinical Pathology, Mansoura University2



ABSTRACT

Background and Purpose: Elevated blood pressure (BP) levels have been associated with an increased risk of stroke and of cardiovascular disease. It is now well established that vascular inflammation is an independent risk factor for the development of atherosclerosis. Furthermore, low grade of inflammation, assessed by C-reactive protein (CRP), significantly predict the risk of future ischemic stroke. Thus, the mechanism underlying the link between elevated blood pressure and an increased risk of stroke may be inflammation. The aim of this work was to study the association between blood pressure and baseline concentrations of c-reactive protein levels in acute ischemic stroke among ischemic stroke patients. Methods: The original inclusion criteria were a diagnosis of first-ever ischemic stroke within 24 hours before enrollment. Sixty four patients (37 men, 27 women, mean age 63.7±11.63 yr) with all forms of ischemic infarctions diagnosed clinically and radiologically by CT and/or MRI were considered for inclusion in the study between February 2004 and October 2005. We excluded patients with diseases that might substantially affect their levels of CRP and who had a cardioembolic etiology. Complete data on systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), pulse pressure (PP) values, plasma levels of CRP, cigarette smoking, total cholesterol levels, neuroradiological findings, neurological deficit severity assessed by the Canadian Neurological Stroke Scale (CNSS) and antihypertensive drugs were collected at the entry. We studied the association between BP and baseline concentrations of CRP within 24 hours after stroke onset. Results: There was a significantly higher levels of CRP levels in patients with arterial hypertension than in patients without arterial hypertension at the entry. Patients without a history of arterial hypertension had a significantly higher levels of CRP at the entry than patients with a documented history. Those with a high CRP levels  had a significant higher mean SBP, DBP, MAP  and PP. Additionally, stroke patients with a high CRP level were significantly older, smokers, had a significantly higher total cholesterol levels with a more severe neurological deficit. CRP levels were significantly lower in patients receiving angiotensin converting enzyme–inhibitors. There was a significant correlation between CRP levels and SBP, DBP, MAP, PP values, total cholesterol levels, but negative with neurological deficit severity assessed by the CNSS.  An increase in SBP, DBP, MAP, or PP was significantly associated with an increase in the odds of having an elevated CRP level(>1.5 mg/dL), independent of other associated study factors. Conclusions: Our results suggested that elevated levels of systolic or diastolic blood pressure in the acute phase after an ischemic stroke are associated with elevated CRP levels. These findings support a possible role of acute hypertension after stroke as an inflammatory stimulus contributing to ischemic brain inflammation.

(Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 517-527)




INTRODUCTION

 

Hypertension is a well-known risk factor for ischemic stroke, and the effect of blood pressure–lowering treatment in preventing first stroke is well established1, but the pathologic and molecular mechanisms by which elevated blood pressure (BP) leads to vascular disease are uncertain: hypertension may promote endothelial expression of cytokines and stimulate inflammation2. These data are particularly intriguing given that inflammation plays a critical role in the pathogenesis of atherosclerosis3.

Prospective data demonstrate that inflammation, particularly C-reactive protein (CRP), appears to predict the risk of cardiovascular events among healthy subjects4, patients with high vascular risk5, those with stable and unstable angina6, and stroke patients7. Signs of an acute inflammatory response are also evident in acute ischemic stroke7. These acute-phase reactants, such as cytokines and CRP may reflect inflammation related to the pathobiology of ischemic stroke8.

Furthermore, low grade of inflammation, assessed by CRP, significantly predict the risk of future ischemic stroke9. Thus, the mechanism underlying the link between elevated blood pressure and an increased risk of stroke may be inflammation. Engström et al.10 demonstrated that increased levels inflammation-sensitive plasma proteins are associated with elevated blood pressure and these proteins are associated with an increased risk of stroke in patient with high blood pressure. The aim of this work was to study the association between blood pressure and baseline concentrations of C-reactive protein levels in acute ischemic stroke among ischemic stroke patients.

 

SUBJECTS AND METHODS

 

The original inclusion criteria were a diagnosis of first-ever ischemic stroke within 24 hours before enrollment. Sixty four patients (37 men, 27 women, mean age 63.7±11.63 yr) with all forms of ischemic infarctions diagnosed clinically and radiologically by CT and/or MRI were considered for inclusion in the study between February 2004 and October 2005. We excluded patients with diseases that might substantially affect their levels of CRP(recent clinical infection, concurrent major renal hepatic or cancerous disease, recent surgery or major trauma, acute osteoarthritis, or inflammatory disease) and who had a probable cardioembolic etiology. They were admitted to the neurology departments of Benha University Hospital and Mansoura International Hospital. The median time from the onset of symptoms to blood pressure measurement and blood sample collection was 13 hours and 14 hours to CT scan or MRI execution. Complete data on systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), pulse pressure (PP)  values, and plasma levels of CRP were collected at the entry.

We obtained 3 sets of blood pressure measurements on each study patients at the entry by using a mercury sphygmomanometer. The first and fifth Korotkoff sounds were recorded and used to determine SBP and DBP respectively. The average of the 3 measurements was used as the SBP and DBP values in the present study. MAP was calculated as (SBP+2DBP)/3, PP was calculated as SBP-DBP. Arterial hypertension was defined as there is a history of hypertension and/or systolic blood pressure >150 mmHg and/or diastolic pressure >90 mmHg, treated or not.

Normal value of C-reactive protein is 0–1.0 milligrams per deciliter (mg/dl) or less than 10 mg/L. Any condition that results in sudden or severe inflammation may increase plasma CRP levels.The CRP test measures the risk for heart or vascular problems.Less than 1.0 mg/dl means that lowest vascular risk,1.0 to 3.0 mg/dl means average risk,while greater than 3.0 mg/dl means highest vascular risk 11.Blood samples were taken at admission, within 24 hours after qualifying stroke. Levels of CRP were determined with a commercially available, high-sensitivity, immunonephelometric, latex-enhanced assay (Dade Behring)12.

Other factors included in this study were age, gender, cerebrovascular risk factors (cigarette smoking status, total cholesterol), and neuroradiological findings (none, single/multiple infarcts, large/small infarcts, leukoaraiosis and brain edema). By definition, large infarcts were so designated when the sum of the largest transverse and sagittal diameter divided by 2 was >1.5 cm, small infarcts;  when the sum of the largest transverse and sagittal diameter divided by 2 was <1.5 cm. The Canadian Neurological Stroke Scale (CNSS) assessed initial stroke severity. Information on current use of antihypertensive medications was also obtained.

 

Statistical analysis:

Differences in proportions were evaluated by 2 analysis, unpaired  t test for continuous normally distributed variables. A Pearson correlation analysis was performed to assess any relationship between log-normalized levels of CRP and blood pressure at the entry. Analysis were designed to assess the association of BP components (SBP, DBP, MAP, and PP) with CRP levels after adjusting for the other study variables. In our analysis, the BP components and other study factors were independent variables, and CRP was the dependent variable. We analyzed CRP as a dichotomous outcome (CRP <1.5 mg/dL or CRP 1.5 mg/dL) in logistic regression models. We chose a cutoff point of 1.5 mg/dL because it has provided better sensitivity and specificity for adverse outcome, based on the receiver operator curves in a previous study31. Individual BP component models assessed the effect of a single BP component (SBP, DBP, MAP, or PP) on CRP, without adjustment for other BP components.

 

RESULTS

 

Table (1) shows descriptive statistics of ischemic stroke patients. The mean (mean ± SD) age of patients was relatively old (63.7±11.6 years), 37(57.8%) subjects were men and 27(42.2%) were women. At the entry, the average CRP level was 4.6±2.4 mg/dL, SBP, DBP, MAP, and PP of the stroke patients were 159±18 mmHg, 99±13 mmHg, 119±14 mmHg, and 58±7 mmHg, respectively. The mean cholesterol level was 203.2±37.6 mg/dl and mean Canadian Neurological Stroke Scale (CNSS) was 6.2±3.2.

Table (2) shows plasma CRP levels of ischemic stroke patients in relation to hypertension at the entry. There was a significantly higher levels  of CRP levels in patients with arterial hypertension (6.5±2.8 mg/dl) than in patients without arterial hypertension (2.4±1.9 mg/dl) at the entry. Patients without a history of arterial hypertension had a significantly higher levels  of CRP at the entry than patients with a documented history (5.2±2.5 versus 3.1±2.1 mg/dL; P<0.05).This means that  an acute increase of blood pressure more than a history of arterial hypertension determine higher levels of CRP after stroke.

Table (3) shows the clinical and laboratory characteristics of ischemic stroke patients according to CRP level (> 1-5 mg/dl or ≥ 1.5 mg/dl). 67.2% (n=43) of the patients had a CRP level of 1.5 mg/dL or higher, and 32.8% (n=21)  had a CRP level of >1.5 mg/dL within 24 hours after stroke. Those with a high CRP level had a significant higher mean SBP (164.9±17.9 versus 145.2±11.8 mmHg), DBP (103.7±13.2 versus 87.1± 6.4 mmHg), MAP (124.1±14.1 versus 106.4±7.4 mmHg) and PP (65.2±10.1 versus 45.1±7.7 mmHg). Additionally, stroke patients with a high CRP level were significantly older (66.1±11.5 versus 57.8±9.6 ys)  smokers (69.4% versus 30.6%), had a significantly higher total cholesterol levels (212.4±38.4 versus 177.9±19.8 mg/dl) with a more severe neurological deficit (5.7±2.8 versus 8.2±2.6) assessed by CNSS. Higher CRP levels were also associated with larger infarcts (37.2% versus 23.8%) but not with other neuroradiological findings, while lower CRP levels were associated with the use of angiotensin-converting-enzyme inhibitors (47.6% versus 11.6%) but not with other antihypertensive drugs.

Table (4) shows the correlation between plasma CRP levels and some variables in ischemic stroke patients. There were a high significant correlations between plasma CRP levels and age (p<0.001), SBP (p<0.001) in (Fig.1), DBP (p<0.001), MBP (p<0.001), total cholesterol level (p<0.001), but  mild with PP (p<0.05). Also there was a negative  significant correlation between stroke  severity assessed by the CNSS (p = 0.01) and plasma CRP levels (Fig. 2).

Table (5) shows the results of multivariable-adjusted logistic regression of increased plasma CRP level on blood pressure components. In model 1, after adjustment for other study factors, SBP showed a persistent, strong, significant association with CRP, for each 10 mm Hg increase in SBP, the odds of having an elevated CRP level increased by 69% (odds ratio[OR] is 1.69, P<0.001). In models 2 and 3, DBP and MAP showed a high significant association with CRP, for each 10 mm Hg increase was associated with an increase in the odds of  having an elevated CRP level by 42% (OR is 1.42, P<0.001), 32% (OR is 1.32, P<0.001), respectively, while in model 4, PP showed a lower significant association with CRP, for each 10 mmHg increase in PP, the odds of having an elevated CRP level increased by 16% (OR is 1.16, P=0.01).

Table 1. Descriptive statistics of ischemic stroke patients.

 

Variable

No

Minimum

Maximum

Mean±SD

Age  (yr)

64

38

84

63.7±11.6

CRP  (mg/dl)

64

1

16.6

4.6±2.4

SBP (mmHg)

64

120

195

159±18

DB (mmHg)

64

80

130

99±13

MBP (mmHg)

64

93

151

119±14

PP (mmHg)

64

40

75

58±7

Cholesterol (mg/dl)

64

107

290

203±37

CNSS

64

4

11

6.2±3.2

CRP: C-reactive protein, BP: blood pressure, SBP: systolic blood  pressure, DBP: diastolic blood pressure,

MBP: mean blood pressure, PP: pulse pressure , CNSS: Canadian neurological stroke scale.

                                                    

 

Table 2. Plasma CRP levels of ischemic stroke patients in relation to hypertension at the entry.

 

History of hypertension

BP at entery

 

Variable

-ve

n=29

+ve

n=35

> 150/90

n=49

< 150/90

n=15

5.2±2.5       

3.1±2.1

6.5±2.8

2.4±1.9

  CRP (mg/dl)

3.379

6.256

t

>0.05

>0.001

P

CRP: C-reactive protein, BP: blood pressure, P: significant at < 0.05 .

 

 

Table 3. Clinical and laboratory characteristics of ischemic stroke patients according to CRP level (> 1-5 mg/dl or ≥ 1.5 mg/dl).

 

Variable

C-reactive  protein

t

p

> 1. 5 mg/dl

n = 21

≥1 . 5 mg/dl

n = 43

Age  ( yr )

57.8±9.6

66.1±11.49

2.832

0.006*

Sex :

       Male n = 37

       Female n = 27

 

12(57.1% )

9(42.9 % )

 

25(61.7%)

16(38.3%)

 

1.098

 

0.19

Blood Pressure (mmHg):    

SBP

DBP

MBP

PP

 

145.2±11.8

87.1±6.4

106.4±7.4

49.1±7.7

 

164.9±17.9

103.7±13.2

124.1±14.1

65.2±10.1

 

4.204

4.696

4.864

2.142

 

<0.001*

<0.001*

<0.001*

0.01*

Cholesterol ( mg/dl )

177.9±19.8

212.4±38.4

3.521

0.01*

Cigarette smoking   n = 36

11(30.6  %  )

25( 69.4 % )

3.896

0.01*

CNSS

8.2±2.6

5.7±2.8

5.226

<0.05*

Radiological findings:

None

Multiple infractions

Small infraction<1.5cm

Large infarction>1.5cm

Leukoaraiosis

Brain edema

 

6 (28.6%)

4 (19%)

6 (28.6%)

5 (23.8%)

4 (19 %)

2 (9.5%)

 

9 ( 20.9%)

11 (25.6%)

6 ( 28.6%)

16 (37.2%)

5 ( 11.6%)

5 (1.6%)

 

1.285

2. 207

1.212

2.195

1.537

1.347

 

0.31

0.08

0.93

<0.05*

0.46

0.17

Antihypertensive drugs:  

 ACE-I

 Ch.Ch.Bl.

 B. Bl.

 Diuretics

 

10 (47.6%)

3 (14.3%)

3 (14.3%)

1 (4.8%)

 

5 (11.6%)

10 (23.3%)

8 (18.6%)

5 (11.6%)

 

2.746

1.247

0.268

0.256

 

<0.05*

0.11

0.17

0.23

CRP: C-reactive protein, SBP: systolic pressure, DBP: diastolic blood pressure, MBP: mean blood pressure, PP:pulse pressure, CNSS: Canadian neurological stroke scale, ACE-I: angiotensin-converting enzyme inhibitors, Ch.Ch.Bl.: calcium channel blocker, B.Bl: beta blocker. P: significant at < 0.05.

 

Table 4. The correlation between plasma CRP levels and some variables in ischemic stroke patients.

 

Variable

C-reactive  protein

r

p

Age

0.539

< 0.001 *

Blood pressure:

     SBP

     DBP

     MBP

     PP

 

0.629

0.712

0.701

0.494

 

< 0.001*

< 0.001*

< 0.001*

< 0.05*

Cholesterol

0.735

< 0.001*

CNSS

- 0.688

< 0.01*

CRP: C-reactive  protein, SBP: systolic blood  pressure, DBP: diastolic blood pressure, MBP: mean blood pressure,

PP: pulse pressure, CNSS: Canadian Neurological Stroke Scale, P : significant at <0.05.

Table 5. Results of multivariable-adjusted logistic regression of increased plasma CRP level on blood pressure components.

 

Models

S.E. of Partial R

Wald 2%

Odds ratio for elevated  CRP

P

value

95 % CI

Model 1

    SBP

0.226

10.735

1.69

1.30-2.08

<0.001*

Model 2

    DBP

0.442

12.384

1.42

1.28-1.56

<0.001*

Model 3

    MAB

0.383

11.808

1.32

1.15-1.49

<0.001*

Model 4

     PP

0.295

5.255

1.16

1.12-1.20

0.01*


 SBP: systolic blood pressure, DBP: diastolic blood pressure, MBP: mean blood pressure, PP: pulse pressure, R: regression coefficient, S.E: standard error. CI: confidence interval, Odds ratio are given per 10 mmHg increase, P: significant at < 0.05.

 

 

Fig. (1): Correlation between plasma C-reactive protein (CRP) levels and systolic blood pressure (SBP).

 

Fig. (2): Correlation between stroke  severity assessed by the Canadian Neurological

Stroke Scale (CNSS) and plasma C-reactive protein (CRP) levels.

 

 


DISCUSSION

 

CRP elevation can result from a variable intensity of the individual acute phase response to cerebral ischemia but it is not known if blood pressure levels in the acute phase after stroke can influence levels of inflammation markers. To verify this hypothesis we analyzed the relationship between blood pressure components and CRP levels within 24 hours after stroke onset.

Di Napoli and Papa13 were the first investigators to address the possible relationship between BP levels and CRP in acute ischemic stroke. Their results were in accordance with our results in table (3) where patients with a high CRP level had a significant higher mean SBP, DBP, MAP  and PP. Table (2) revealed that there was a significantly higher levels  of CRP levels in patients with arterial hypertension at the entry than patients without (6.5±2.8 versus 2.4±1.9 mg/dL; P<0.05). Patients without a history of arterial hypertension had a significantly higher levels  of CRP at the entry than patients with a documented history (5.2±2.5 versus 3.1±2.1mg/dL; P<0.05). These results are in agreement with Di Napoli and Papa13, who showed that an increasing BP is associated with an elevated CRP level in the acute phase after stroke. This means that  an acute increase of blood pressure more than a history of arterial hypertension determine higher levels of CRP after stroke.

The primary finding of the present study was that an increase in BP levels was associated with increased odds of having an elevated CRP level (1.5 mg/dL) among first-ever ischemic stroke patients (Table 5). This association was independent of a number of other factors, including demographic factors, cardiovascular risk factors, and neuroradiological findings. BP elevation may promote inflammation by modulation of the biomechanical stimuli; cyclic strain has been shown to increase soluble intercellular adhesion molecule 1 (sICAM-1) expression and mRNA expression14 and secretion of monocyte chemotactic protein-1 (MCP-1)15. Ischemia in vivo and in vitro have also been shown to upregulate the expression of immunoglobulin-families of adhesion molecules in cerebral endothelial cells and to facilitate leukocyte adhesion and transmigration into the brain16.These data suggest mechanisms by which the increase in pulsatile load and cyclic wall stress imposed by high SBP on the cerebral vasculature may facilitate and increase ischemic brain inflammation13.

Stimulation of human vascular smooth muscle cells by angiotensin (Ang) II, a key regulator of BP, results in inflammatory activation with dose-dependent increases in expression and release of (interleukin) IL-6 2,17. Furthermore, cerebral ischemia induces the expression of IL-6 in neurons and astrocytes, and ischemic brain tissues appear to be a major source of IL-6 in stroke18,19. BP may also have a proinflammatory effect on the arterial wall because of increased oxidative stress20. In addition to its effects on IL-6 expression17, Ang II also stimulates increased sICAM-1 expression and vascular infiltration by monocytes and macrophages, which is reversible by angiotensin-converting-enzyme inhibitors (ACE-I) and Ang type 1 receptor blockade21.This may explain the lack of association between BP and CRP levels in ACE-I–treated patients in our study (Table 3).

Our study revealed that there were a high significant correlations between plasma CRP levels and SBP (p<0.001),DBP (p<0.001), MBP (p<0.001), but  mild with PP (p<0.05). Growing evidence indicates that there are plausible mechanisms by which PP could increase inflammation levels. Ryanet et al.22 have reported that elevated levels of PP are associated with impaired acetylcholine induced endothelium-dependent relaxation, and that this impaired relaxation is prevented by administration of the antioxidant superoxide dismutase. This has led some to believe that a high PP may impair endothelium-dependent relaxation by generating reactive oxygen species (ROS)22. Indeed, there is evidence that in humans, PP is positively associated with increased production of the ROS hydrogen peroxide and that this association is stronger than the association of SBP or DBP with hydrogen peroxide production23. Increased ROS levels, in turn, can stimulate inflammatory signaling pathways24. A wide PP also tends to be associated with greater flow reversals during diastole25. It has been demonstrated that oscillatory shear with flow reversals increases adhesion molecule expression26,which would tend to promote the inflammatory process involved in atherosclerosis. Along these lines, Abramson et al.27 have shown that increases in PP are associated with increased adhesion of monocytes  and elevated levels of the inflammatory marker CRP.

Our results are based on single measurements of BP and CRP, which may not reflect these relationships over time, making it impossible to determine the temporal ordering of the association that we observed between BP and CRP. Cross-sectional independent association of high BP and plasma levels of CRP have been reported28,29. Although the evidence noted above suggests that increases in BP would enhance inflammation, the nature of our data could leave open different possibilities in the relationship between BP and the acute phase response after stroke. One important possibility is that inflammation, reflected by the levels of CRP, is not playing a role in the development of high BP even before the ischemic stroke occurs. However, in our study, an acute increase of BP more than a history of arterial hypertension was associated with higher levels of CRP after stroke. Probably the levels of BP after an ischemic stroke are one of the underlying processes related to inflammation that are relevant in the inflammatory response in ischemic stroke patients, more so than a history of arterial hypertension13. Furthermore, the consistency of the association between SBP, DBP, MBP, PP and CRP across different models indicates that our results may not simply be due to chance.  

An elevated BP may be a predictor of poor outcome after stroke. High BP might promote early recurrence, hemorrhagic transformation, or the formation of cerebral edema, thus increasing the risk of death or new cardiovascular events30. DiNapoli and Papa13 suggested another explanation as to why BP may be predictive of poor outcome, increasing levels of BP were associated with higher odds of having an elevated CRP level, a higher BP, more specifically SBP, thus facilitating or increasing an inflammatory response after stroke, which influences the prognosis of ischemic stroke patients as previously demonstrated31,32. These results were in agreement with our study which showed that stroke patients with a high CRP levels had a significantly more severe neurological deficit assessed by Canadian Neurological Stroke Scale (CNSS) and were also associated with larger infarcts, also, there was a negative  significant correlation between stroke  severity assessed by the CNSS (p = 0.01) and plasma CRP levels.

The relationship between CRP and SBP is probably more complex than we realize. Given the observational nature of our study, our results should not be taken as evidence of a causal relationship and should be interpreted with caution. Patients with high CRP in acute brain ischemia might have a predisposition to the activation of inflammation in response to triggering stimuli in cardiovascular events. Acute brain ischemia increases BP, and ischemia may induce brain inflammation separately.

 

Conclusions:

Our results suggested that elevated levels of systolic or diastolic blood pressure in the acute phase after an ischemic stroke are associated with elevated CRP levels. These findings support a possible role of acute hypertension after stroke as an inflammatory stimulus contributing to ischemic brain inflammation.

 

Recommendations:

Future studies need to clarify whether or not an elevated BP leads to increased inflammatory response after stroke, and whether this effect is more or less pronounced in certain subgroups such as the elderly. Because higher CRP levels are an independent prognostic factor after stroke and high BP is apparently associated with higher CRP levels, the current approach to the treatment of acute hypertension after stroke probably should be revised.

 

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الملخـص العربى

 

هل الارتفاع في ضغط الدم مرتبط بزيادة في بروتين سى المتفاعل في السكتات الدماغية الإنسدادية الحادة

 

وجد أن الزيادة في ضغط الدم مرتبط بزيادة في بروتين سى المتفاعل في البلازما وزيادة في حدوث السكتات الدماغية واعتلال شرايين القلب. ويهدف هذا البحث لدراسة الارتباط بين الارتفاع في ضغط الدم ومستوى بروتين سى المتفاعل في مرضى السكتات الدماغية الإنسدادية الحادة.

اشتملت هذه الدراسة على 64 مريضا بالسكتة الدماغية الإنسدادية الحادة، 37 من الرجال، 27 من الإناث ومتوسط أعمارهم 11.63 ± 63.7 سنة وقد تم تشخيصهم إكلينيكيا وبالأشعة المقطعية أو الرنين المغناطيسي على المخ. وقد تم قياس ضغط الدم بأنواعه الانقباضى والانبساطى وقد تم حساب متوسط ضغط الدم والضغط النبضى وقد تم أخذ عينات الدم في خلال 24 ساعة من حدوث السكتات الدماغية لقياس بروتين سى المتفاعل في البلازما. وقد خضع المرضى لدراسة بعض عوامل الخطر لحدوث السكتات الدماغية الإنسدادية وتم تقييم المرضى إكلينيكيا بواسطة المقياس الكندي للسكتات الدماغية.

وقد أظهرت نتائج البحث ارتفاع ذو دلالة إحصائية لبروتين سى المتفاعل في المرضى ذوو الضغط المرتفع عن المرضى ذوو الضغط الطبيعي عند دخول المرض وارتفاع في المرضى من غير تاريخ مرض للضغط المرتفع عنهم في المرضى ذوو تاريخ إيجابي للضغط المرتفع.

ووجد أيضا ارتفاع ذو دلالة إحصائية في الضغط الانقباضي والانبساطي والمتوسط والضغط النبضى في حالات ارتفاع بروتين سى المتفاعل في البلازما. ووجد ارتباط ذو دلالة إحصائية بين زيادة بروتين سى المتفاعل في البلازما وكبر حجم الأصابه فى الأشعة وبين قلة بروتين سى المتفاعل واستعمال مثبطات أنزيم أنجيوتنسين التحولي لعلاج ضغط الدم المرتفع.

وقد وجد علاقات إيجابية ذات دلالة إحصائية بين بروتين سى المتفاعل وعمر المرضى والضغط الإنقباضي والضغط الانبساطي ومتوسط الضغط و الضغط النبضى ومستوى الكولسترول في الدم. ولكن كانت سالبة مع شدة السكتة الدماغية الإنسدادية عندما قيست بالمقياس الكندي الإكلينيكي. وبإجراء معامل الانحدار الإحصائي وجد ارتباط ذو دلالة إحصائية بين ارتفاع بروتين سى المتفاعل مع زيادة الضغط بأنواعه الإنقباضي والإنبساطي والمتوسط والنبضى.

ونستخلص من هذا البحث أن الزيادة في الضغط الإنقباضي والإنبساطي في مرضى السكته الدماغية الإنسدادية الحادة مرتبط بزيادة في بروتين سى المتفاعل وذلك يسند دور للارتفاع الحاد في ضغط الدم بعد حدوث السكتات الدماغية الإنسدادية كمنبه لحدوث الالتهاب أثناء حدوث السكتة الدماغية الإنسدادية.



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