Introduction
Progressive cerebral infarction (PCI) is a brain
disorder caused by insufficient blood supply. Cerebral infarction
may lead to cerebral ischemia, hypoxia, necrosis and finally
neurological deficit (1).
Recently, studies of cerebral infarction have focused on
identifying risk factors. Multiple measures have also been taken,
including health education, acute-stage patient care, vascular
stenting and surgery, neuroradiology, early rehabilitation.
However, the prevention and treatment of cerebral infarction
remains largely unsuccessful and the prognosis is severe. Between
50 and 70% of surviving patients are left with paralysis, aphasia
and dementia (2). Therefore, it is
particularly important to identify risk factors for the development
of PCI.
At present, there are no ideal strategies that
effectively prevent the progression of cerebral infarction. With
the rapid progress in the treatment of intravascular hydrocephalus
and the continuous improvement of interventional equipment,
stenting and angioplasty are feasible in the treatment of
intracranial vascular stenosis (3). These treatments are recommended for
patients with intracranial arterial stenosis who do not respond
well to medical treatment or whose arterial stenosis is >50%,
according to the guidelines from the American Society of
Interventional and Therapeutic Neuroradiology, the American Society
of Interventional Radiology and the American Society of
Neuroradiology (4). However, the
clinical value of vascular balloon angioplasty and stent
implantation in preventing the progression of cerebral infarction
remains unknown.
The present study enrolled patients with PCI and
those with non-progressive cerebral infarction (NPCI) in order to
compare and analyze the cerebral angiographic characteristics.
Differences in vascular stenosis and vascular morphology were
revealed by cerebral angiography. The aim of the present study was
to provide further theoretical basis for interventional therapy of
cerebrovascular disease.
Materials and methods
Case selection criteria
Data from 608 PCI patients (male 419, female 189)
admitted to the Department of Internal Medicine at Shilong People’s
Hospital (Guangdong, China) were collected between May 2010 and May
2013. The inclusion criteria met the diagnostic criteria set in the
first edition of the Chinese Guidelines for Cerebrovascular Disease
Prevention (5) and were confirmed
by head computed tomography or magnetic resonance imaging
examinations. The patients were divided into two groups: PCI and
NPCI groups. The PCI group included patients who had been admitted
within 24 h after the onset of the disease, but had not been
treated within 6 h of onset. The diseases were progressing and the
patients scored ≥2 points according to the United States National
Institute of Health Stroke Scale (NIHSS) (6). The NPCI group (control group)
included patients who were admitted within 24 h after onset and
whose diseases had reached the peak, thus progression had stopped 6
h after onset. These patients scored <2 points on the NIHSS. The
study protocol was approved by the Institutional Ethical Committee
for Research on Human Subjects (Guangzhou, China) and informed
written consent was obtained from each patient.
Carotid artery ultrasonography
To examine the extent of common carotid artery
atherosclerosis, the intima media thickness (IMT) and the vessel
diameters were measured by ultrasonography. The severity of the
carotid artery lesions was classified into four groups: Normal (IMT
≤0.9 mm), hardening (0.9 mm<IMT≤1.5 mm), plaque formation
(IMT>1.5 mm) and stenosis (narrowing, >30%).
Cerebral angiography
A Seldinger puncture was created in the femoral
arteries of patients from the two groups. Angiography was performed
using catheters at the aortic arch, bilateral common carotid
arteries and vertebral arteries. Based on the North America
Symptomatic Carotid Endarterectomy Trial method (7), vascular stenosis was assessed by
doctors experienced in neurointervention. The degree of cerebral
artery stenosis was classified into two groups based on the
reduction in vessel diameter: Mild stenosis (≤50%) and severe
stenosis (>50%). The severity of arterial lesions was
evaluated.
Statistical analysis
Continuous data are presented as mean ± SD and were
analyzed with a Student’s t-test or one-way analysis of variance
(when the variance was irregular Welch correction was used).
Categorical data were analyzed with a χ2 test. To
identify the potential risk factors for the development of PCI, the
linear regression method and multivariate logistic regression
analyses were used. P<0.05 was considered to indicate a
statistically significant difference.
Results
Single factor analysis
Associations between multiple potential risk factors
and carotid artery atherosclerosis were firstly analyzed. As shown
in Table I, the incidence rate of
diabetes was significantly higher in patients with carotid artery
atherosclerosis when compared with those with normal carotid
arteries (χ2=18.988; P<0.01). As the severity of
atherosclerosis increased, the diabetes incidence also increased,
indicating the involvement of diabetes in the pathogenesis of
carotid artery atherosclerosis. Similarly to diabetes, the
incidence of hypertension was also significantly higher in patients
with carotid artery atherosclerosis when compared with those with
normal carotid arteries (χ2=82.107; P<0.01). The
incidence of hypertension increased to 90% in patients with carotid
artery stenosis, demonstrating the effect of hypertension on
carotid artery stenosis. Hyperlipidemia was more common among
patients with impaired carotid arteries, despite the less evident
difference in the incidence (χ2=10.312; P=0.016).
Notably, other factors, including smoking, alcohol consumption,
cholesterol and lipoprotein, were not significantly different
between the normal carotid artery and the dysfunctional carotid
artery groups. The ages of the patients varied among the groups
with different carotid artery lesions. Stenosis occurred more
frequently in older patients.
| Table IAssociation of potential risk factors
with severity of carotid atherosclerosis. |
Table I
Association of potential risk factors
with severity of carotid atherosclerosis.
Risk factor | Carotid
atherosclerosis | Total | Test statistic | P-value |
---|
|
---|
Normal | Hardening | Plaque | Stenosis |
---|
Gender, n (%) |
Male | 60 (69.0) | 67 (67.7) | 197 (69.6) | 62 (74.7) | 386 (69.9) | 1.189 | 0.756 |
Female | 27 (31.0) | 32 (32.3) | 86 (30.4) | 21 (25.3) | 166 (30.1) | | |
Diabetes, n (%) |
No | 75 (86.2) | 75 (75.8) | 185 (65.4) | 50 (60.2) | 385 (69.7) | 18.988 | <0.01 |
Yes | 12 (13.8) | 24 (24.2) | 98 (34.6) | 33 (39.8) | 167 (30.3) | | |
Hypertension, n
(%) |
No | 49 (56.3) | 24 (24.2) | 37 (13.1) | 8 (9.6) | 118 (21.4) | 82.107 | <0.01 |
Yes | 38 (43.7) | 75 (75.8) | 246 (86.9) | 75 (90.4) | 434 (78.6) | | |
Hyperlipidemia, n
(%) |
No | 56 (64.4) | 51 (51.5) | 127 (45.0) | 39 (47.0) | 273 (49.5) | 10.312 | 0.016 |
Yes | 31 (35.6) | 48 (48.5) | 155 (55.0) | 44 (53.0) | 278 (50.5) | | |
Smoking, n (%) |
No | 60 (69.0) | 58 (58.6) | 172 (60.8) | 43 (51.8) | 333 (60.3) | 5.379 | 0.146 |
Yes | 27 (31.0) | 41 (41.4) | 111 (39.2) | 40 (48.2) | 219 (39.7) | | |
Wine consumption, n
(%) |
No | 78 (89.7) | 87 (87.9) | 241 (85.2) | 71 (85.5) | 477 (86.4) | 1.393 | 0.707 |
Yes | 9 (10.3) | 12 (12.1) | 42 (14.8) | 12 (14.5) | 75 (13.6) | | |
Age, yearsa | 53.2±11.6 | 62.3±11.3 | 66.4±10.0 | 68.6±8.3 | | 43.4 | <0.01 |
Systolic blood
pressure, mmHga | 136.3±21.3 | 151.3±23.8 | 153.2±23.5 | 153.6±22.1 | | 12.9 | <0.01 |
Diastolic blood
pressure, mmHga | 81.2±12.8 | 85.3±13.3 | 85.2±12.3 | 83.7±9.1 | | 2.6 | 0.049 |
Platelet count
(109/l)a | 235.788±67.761 | 253.153±95.158 | 237.735±76.974 | 236.602±70.103 | | 1.135 | 0.334 |
International
normalized ratioa | 1.001±0.080 | 1.006±0.088 | 1.033±0.109 | 1.041±0.170 | | 2.911 | 0.034 |
Plasma fibrinogen
(g/l) a | 3.301±0.789 | 3.564±0.796 | 3.805±0.990 | 3.862±1.011 | | 7.297 | <0.01 |
Total cholesterol
(mmol/l)a | 4.675±1.208 | 4.959±1.137 | 4.980±1.156 | 5.043±1.499 | | 1.639 | 0.179 |
Triglyceride
(mmol/l)a | 1.661±1.165 | 1.741±1.112 | 1.738±1.069 | 1.643±0.937 | | 0.254 | 0.859 |
HDL (mmol/l)a | 1.087±0.334 | 1.226±0.508 | 1.135±0.549 | 1.114±0.340 | | 1.451 | 0.227 |
LDL (mmol/l)a | 2.596±0.992 | 2.905±0.993 | 2.773±1.002 | 2.936±1.123 | | 2.039 | 0.107 |
HLRa | 0.480±0.253 | 0.492±0.405 | 0.478±0.330 | 0.451±0.397 | | 0.219 | 0.883 |
Fasting blood glucose
(mmol/l)a | 5.878±1.691 | 6.222±2.006 | 6.698±3.055 | 6.866±3.622 | | 2.640 | 0.049 |
Glycated hemoglobin
(%)a | 6.233±1.948 | 6.197±1.415 | 6.942±2.016 | 6.970±1.881 | | 4.122 | 0.007 |
Homocysteine
(μmol/l)a | 13.574±5.586 | 13.941±4.898 | 14.849±6.470 | 15.002±5.258 | | 1.031 | 0.379 |
In addition, whether the factors listed in Table I contributed to the development of
cerebral artery stenosis was investigated. As shown in Table II, diabetes, hypertension,
hyperlipidemia and age were associated with the severity of
cerebral artery stenosis, exhibiting a similar pattern to carotid
artery atherosclerosis. However, smoking and alcohol consumption
was also demonstrated to affect the narrowing of cerebral arteries,
contrary to carotid arteries.
| Table IIAssociation between potential risk
factors with the severity of cerebral artery stenosis. |
Table II
Association between potential risk
factors with the severity of cerebral artery stenosis.
| Cerebral artery
stenosis | | | |
---|
|
| | | |
---|
Risk factor | Narrowing ≤50% | Narrowing
>50% | Total | Test statistic | P-value |
---|
Gender, n (%) |
Male | 185 (68.0) | 234 (69.6) | 419 (68.9) | 0.186 | 0.666 |
Female | 87 (32.0) | 102 (30.4) | 189 (31.1) | | |
Diabetes, n
(%) |
No | 221 (81.3) | 209 (62.2) | 430 (70.7) | 26.339 | <0.001 |
Yes | 51 (18.8) | 127 (37.8) | 178 (29.3) | | |
Hypertension, n
(%) |
No | 79 (29.0) | 50 (14.9) | 129 (21.2) | 18.039 | <0.001 |
Yes | 193 (71.0) | 286 (85.1) | 479 (78.8) | | |
Hyperlipidemia, n
(%) |
No | 154 (56.6) | 149 (44.5) | 303 (49.9) | 8.850 | 0.003 |
Yes | 118 (43.4) | 186 (55.5) | 304 (50.1) | | |
Smoking, n (%) |
No | 185 (68.0) | 195 (58.0) | 380 (62.5) | 6.387 | 0.011 |
Yes | 87 (32.0) | 141 (42.0) | 228 (37.5) | | |
Wine consumption, n
(%) |
No | 246 (90.4) | 281 (83.6) | 527 (86.7) | 6.037 | 0.014 |
Yes | 26 (9.6) | 55 (16.4) | 81 (13.3) | | |
Age, yearsa | 60.7±12.1 | 65.8±10.4 | | −5.6 | <0.01 |
Systolic blood
pressure, mmHga | 147.9±24.9 | 151.4±22.7 | | −1.8 | 0.065 |
Diastolic blood
pressure, mmHga | 84.0±12.7 | 84.0±12.0 | | 0.026 | 0.979 |
Platelet count
(109/l)a | 237.345±78.032 | 245.263±78.838 | | −1.229 | 0.220 |
International
normalized ratioa | 1.029±0.101 | 1.020±0.118 | | 0.884 | 0.377 |
Plasma fibrinogen
(g/l)a | 3.460±0.859 | 3.871±1.045 | | −5.124 | <0.001 |
Total cholesterol
(mmol/l)a | 4.862±1.199 | 5.023±1.206 | | −1.632 | 0.103 |
Triglyceride
(mmol/l)a | 1.642±0.996 | 1.753±1.140 | | −1.27 | 0.204 |
HDL
(mmol/l)a | 1.191±0.447 | 1.116±0.491 | | 1.942 | 0.053 |
LDL
(mmol/l)a | 2.715±1.011 | 2.846±0.990 | | −1.598 | 0.111 |
HLRa | 0.520±0.408 | 0.444±0.252 | | 2.686 | 0.008 |
Fasting blood
glucose (mmol/l)a | 6.000±2.149 | 6.846±3.188 | | −3.874 | <0.001 |
Glycated hemoglobin
(%)a | 6.415±1.837 | 7.009±1.985 | | −3.115 | 0.002 |
Homocysteine
(μmol/l)a | 14.084±4.669 | 14.992±6.561 | | −1.615 | 0.107 |
Furthermore, whether these factors were involved in
the development of neurological deficits, including stroke and
progressive stroke, was investigated. The factors that contributed
to the severity of cerebral stenosis (Table II) also affected the incidence of
stroke (Table III) in a similar
manner. This observation also enhances the correlation of stroke
and cerebral artery stenosis. However, the data showed that only
hyperlipidemia, alcohol consumption and age were significantly
different between the patients with or without progressive stroke
(Table IV; P<0.05).
| Table IIIAssociation between potential risk
factors and the severity of stroke. |
Table III
Association between potential risk
factors and the severity of stroke.
Risk factor | No stroke | Stroke with large
artery atherosclerosis | Stroke with small
artery atherosclerosis | Total | Test statistic | P-value |
---|
Gender, n (%) |
Male | 113 (64.6) | 154 (70.0) | 109 (73.6) | 376 (69.2) | 3.201 | 0.202 |
Female | 62 (35.4) | 66 (30.0) | 39 (26.4) | 167 (30.8) | | |
Diabetes, n
(%) |
No | 140 (80.0) | 131 (59.5) | 109 (73.6) | 380 (70.0) | 20.714 | <0.001 |
Yes | 35 (20.0) | 89 (40.5) | 39 (26.4) | 163 (30.0) | | |
Hypertension, n
(%) |
No | 59 (33.7) | 34 (15.5) | 19 (12.8) | 112 (20.6) | 27.388 | <0.001 |
Yes | 116 (66.3) | 186 (84.5) | 129 (87.2) | 431 (79.4) | | |
Hyperlipidemia, n
(%) |
No | 104 (59.4) | 88 (40.2) | 75 (50.7) | 267 (49.3) | 14.578 | 0.001 |
Yes | 71 (40.6) | 131 (59.8) | 73 (49.3) | 275 (50.7) | | |
Smoking, n (%) |
No | 128 (73.1) | 119 (54.1) | 90 (60.8) | 337 (62.1) | 15.161 | 0.001 |
Yes | 47 (26.9) | 101 (45.9) | 58 (39.2) | 206 (37.9) | | |
Wine consumption, n
(%) |
No | 167 (95.4) | 175 (79.5) | 126 (85.1) | 468 (86.2) | 20.845 | <0.01 |
Yes | 8 (4.6) | 45 (20.5) | 22 (14.9) | 75 (13.6) | | |
Age, yearsa | 61.7±11.3 | 65.5±11.1 | 62.6±11.6 | | 6.2 | 0.002 |
Systolic blood
pressure, mmHga | 140.7±21.4 | 152.54±22.9 | 157.3±23.0 | | 24.1 | <0.01 |
Diastolic blood
pressure, mmHga | 79.6±9.8 | 85.7±12.4 | 88.2±12.7 | | 27.5 | <0.01 |
Platelet count
(109/l)a | 233.751±72.418 | 244.735±76.258 | 247.944±83.259 | | 1.559 | 0.211 |
International
normalized ratioa | 1.031±0.094 | 1.013±0.094 | 1.011±0.087 | | 2.097 | 0.124 |
Plasma fibrinogen
(g/l)a | 3.368±0.879 | 3.984±1.103 | 3.659±0.835 | | 17.363 | <0.001 |
Total cholesterol
(mmol/l)a | 4.742±1.142 | 5.082±1.228 | 4.909±1.113 | | 4.039 | 0.018 |
Triglyceride
(mmol/l)a | 1.677±1.236 | 1.762±1.071 | 1.719±0.972 | | 0.291 | 0.748 |
HDL
(mmol/l)a | 1.192±0.407 | 1.114±0.566 | 1.142±0.463 | | 1.189 | 0.305 |
LDL
(mmol/l)a | 2.542±0.907 | 2.936±0.997 | 2.796±0.984 | | 7.966 | <0.001 |
HLRa | 0.542±0.357 | 0.418±0.212 | 0.498±0.454 | | 8.833 | <0.001 |
Fasting blood
glucose (mmol/l)a | 5.765±2.347 | 7.166±3.402 | 6.414±2.354 | | 11.659 | <0.001 |
Glycated hemoglobin
(%)a | 6.243±1.376 | 7.219±2.189 | 6.613±1.879 | | 10.379 | <0.001 |
Homocysteine
(μmol/l)a | 14.301±4.473 | 15.051±6.512 | 14.640±6.106 | | 0.500 | 0.607 |
| Table IVAssociation between potential risk
factors and progressive stroke. |
Table IV
Association between potential risk
factors and progressive stroke.
| Progressive
stroke | | | |
---|
|
| | | |
---|
Risk factor | No (n=368) | Yes (n=60) | Total | Test statistic | P-value |
---|
Gender, n (%) |
Male | 262 (71.2) | 43 (71.7) | 305 (71.3) | 0.006 | 0.940 |
Female | 106 (28.8) | 17 (28.3) | 123 (28.7) | | |
Diabetes, n
(%) |
No | 248 (67.4) | 40 (66.7) | 288 (67.3) | 0.012 | 0.912 |
Yes | 120 (32.6) | 20 (33.3) | 140 (32.7) | | |
Hypertension, n
(%) |
No | 58 (15.8) | 13 (21.7) | 71 (16.6) | 1.300 | 0.254 |
Yes | 310 (84.2) | 47 (78.3) | 357 (83.4) | | |
Hyperlipidemia, n
(%) |
No | 179 (48.8) | 21 (35.0) | 200 (46.8) | 3.929 | 0.047 |
Yes | 188 (51.2) | 39 (65.0) | 227 (53.2) | | |
Smoking, n (%) |
No | 217 (59.0) | 29 (48.3) | 246 (57.5) | 2.387 | 0.122 |
Yes | 151 (41.0) | 31 (51.7) | 182 (42.5) | | |
Wine consumption, n
(%) |
No | 318 (86.4) | 37 (61.7) | 355 (82.9) | 22.331 | <0.01 |
Yes | 50 (13.6) | 23 (38.3) | 73 (17.1) | | |
Age, yearsa | 63.5±11.1 | 68.8±12.0 | | −3.4 | <0.01 |
Systolic blood
pressure, mmHga | 153.6±24.1 | 152.8±19.0 | | 0.3 | 0.766 |
Diastolic blood
pressure, mmHga | 85.7±12.9 | 87.1±11.7 | | −0.8 | 0.432 |
Platelet count
(109/l)a | 244.019±79.526 | 246.967±89.006 | | −0.261 | 0.794 |
International
normalized ratioa | 1.031±0.118 | 0.975±0.099 | | 3.46 | <0.01 |
Plasma fibrinogen
(g/l)a | 3.789±0.982 | 3.964±1.135 | | −1.234 | 0.218 |
Total cholesterol
(mmol/l)a | 4.980±1.229 | 5.278±1.148 | | −1.756 | 0.080 |
Triglyceride
(mmol/l)a | 1.706±1.022 | 1.686±0.923 | | 0.14 | 0.889 |
HDL
(mmol/l)a | 1.121±0.355 | 1.204±0.998 | | −0.635 | 0.528 |
LDL
(mmol/l)a | 2.840±1.032 | 3.032±0.935 | | −1.349 | 0.178 |
HLRa | 0.458±0.298 | 0.453±0.459 | | 0.083 | 0.934 |
Fasting blood
glucose (mmol/l)a | 6.610±2.599 | 7.782±4.420 | | −1.997 | 0.050 |
Glycated hemoglobin
(%)a | 7.073±2.108 | 6.494±1.995 | | 1.917 | 0.056 |
Homocysteine
(μmol/l)a | 14.847±6.432 | 13.731±5.049 | | 1.429 | 0.156 |
Multivariate logistic regression
analysis
Multiple linear regression analysis revealed that
multicollinearity existed between systolic and diastolic pressure,
total cholesterol and LDL. Due to extensive variance, two factors
(diastolic blood pressure and total cholesterol) were rejected in
the model and the results are shown in Table V. The results demonstrated that
these factors exhibited significant differences at various levels
of carotid artery atherosclerosis (hardened, hardened plaque and
stenosis groups), when compared with the normal group. The odds
ratio was set at >1 for risk factors and otherwise protective
factors. As shown in Table VI,
the influencing factors of cerebral artery stenosis included age,
diabetes, plasma fibrinogen and HLR (HDL/LDL ratio), among which
age, diabetes mellitus and plasma fibrinogen were identified as
risk factors, whereas HLR was a protective factor. As shown in
Table VII, risk factors were
also identified for stroke. These included fasting blood glucose
and smoking. However, multivariate analysis of the bivariate
correlation between progressive stroke and cerebral artery
atherosclerosis exhibited no significant correlation (Table VIII). For effects of fasting
blood glucose and plasma fibrinogen (FIB) classification, as shown
in Table IX, age, diabetes and
smoking were important factors for carotid atherosclerosis.
Similarly, age and diabetes were also the important factors in FIB
classification of cerebral artery stenosis (Table X).
| Table VLogistic regression analysis of
factors affecting carotid atherosclerosis. |
Table V
Logistic regression analysis of
factors affecting carotid atherosclerosis.
| | | | | | 95% CI of OR
value |
---|
| | | | | |
|
---|
Risk factor | B | SE | Wald | P-value | OR value | Lower limit | Upper limit |
---|
Hardening |
Intercept | −10.138 | 6.565 | 2.385 | 0.123 | | | |
Age | 0.063 | 0.030 | 4.445 | 0.035 | 1.066 | 1.004 | 1.130 |
Systolic blood
pressure | 0.029 | 0.016 | 3.045 | 0.081 | 1.029 | 0.996 | 1.063 |
Platelet
count | 0.003 | 0.004 | 0.338 | 0.561 | 1.003 | 0.994 | 1.011 |
International
normalized ratio | 4.015 | 3.747 | 1.148 | 0.284 | 55.413 | 0.036 | 85,759.316 |
Plasma
fibrinogen | 0.386 | 0.406 | 0.901 | 0.342 | 1.471 | 0.663 | 3.260 |
Triglyceride | 0.542 | 0.408 | 1.763 | 0.184 | 1.720 | 0.772 | 3.830 |
HDL | 1.878 | 0.947 | 3.932 | 0.047 | 6.540 | 1.022 | 41.851 |
LDL | 0.441 | 0.397 | 1.232 | 0.267 | 1.554 | 0.714 | 3.382 |
HLR | −0.269 | 1.235 | 0.048 | 0.827 | 0.764 | 0.068 | 8.601 |
Fasting blood
glucose | 0.197 | 0.172 | 1.314 | 0.252 | 1.218 | 0.870 | 1.705 |
Glycated
hemoglobin | −0.929 | 0.363 | 6.546 | 0.011 | 0.395 | 0.194 | 0.805 |
Homocysteine | 0.037 | 0.065 | 0.314 | 0.576 | 1.037 | 0.912 | 1.179 |
Gender | −0.319 | 0.781 | 0.167 | 0.683 | 0.727 | 0.157 | 3.356 |
Diabetes | 2.322 | 1.161 | 3.999 | 0.046 | 10.195 | 1.047 | 99.254 |
Hypertension | 0.887 | 0.742 | 1.428 | 0.232 | 2.427 | 0.567 | 10.390 |
Hyperlipidemia | 0.640 | 0.806 | 0.629 | 0.428 | 1.896 | 0.390 | 9.203 |
Smoking | 1.522 | 0.777 | 3.839 | 0.050 | 4.582 | 1.000 | 21.002 |
Wine
consumption | −0.232 | 0.926 | 0.063 | 0.802 | 0.793 | 0.129 | 4.868 |
Plaque
formation |
Intercept | −13.361 | 6.013 | 4.938 | 0.026 | | | |
Age | 0.092 | 0.028 | 10.952 | 0.001 | 1.096 | 1.038 | 1.157 |
Systolic blood
pressure | 0.023 | 0.015 | 2.369 | 0.124 | 1.024 | 0.994 | 1.055 |
Platelet
count | 0.004 | 0.004 | 0.785 | 0.376 | 1.004 | 0.996 | 1.012 |
International
normalized ratio | 6.320 | 3.414 | 3.428 | 0.064 | 555.608 | 0.690 | 447,157.189 |
Plasma
fibrinogen | 0.454 | 0.377 | 1.449 | 0.229 | 1.574 | 0.752 | 3.296 |
Triglyceride | 0.248 | 0.393 | 0.400 | 0.527 | 1.282 | 0.594 | 2.768 |
HDL | 1.874 | 0.929 | 4.070 | 0.044 | 6.512 | 1.055 | 40.209 |
LDL | −0.220 | 0.377 | 0.341 | 0.559 | 0.802 | 0.383 | 1.681 |
HLR | −1.205 | 1.166 | 1.068 | 0.301 | 0.300 | 0.030 | 2.946 |
Fasting blood
glucose | 0.143 | 0.152 | 0.886 | 0.346 | 1.154 | 0.856 | 1.556 |
Glycated
hemoglobin | −0.367 | 0.288 | 1.628 | 0.202 | 0.693 | 0.394 | 1.218 |
Homocysteine | 0.056 | 0.061 | 0.844 | 0.358 | 1.058 | 0.938 | 1.193 |
Gender | 0.092 | 0.702 | 0.017 | 0.896 | 1.096 | 0.277 | 4.341 |
Diabetes | 2.163 | 1.092 | 3.921 | 0.048 | 8.700 | 1.022 | 77.035 |
Hypertension | 1.147 | 0.635 | 3.269 | 0.071 | 3.150 | 0.908 | 10.927 |
Hyperlipidemia | 1.236 | 0.730 | 2.864 | 0.091 | 3.441 | 0.822 | 14.393 |
Smoking | 1.006 | 0.698 | 2.077 | 0.150 | 2.735 | 0.696 | 10.749 |
Wine
consumption | 0.337 | 0.840 | 0.160 | 0.689 | 01.400 | 0.270 | 7.267 |
Stenosis |
Intercept | −12.001 | 6.638 | 3.268 | 0.071 | | | |
Age | 0.104 | 0.033 | 10.273 | 0.001 | 1.110 | 1.041 | 1.183 |
Systolic blood
pressure | 0.016 | 0.016 | 0.898 | 0.343 | 1.016 | 0.983 | 1.049 |
Platelet
count | 0.000 | 0.005 | 0.000 | 0.996 | 1.000 | 0.991 | 1.009 |
International
normalized ratio | 5.469 | 3.692 | 2.194 | 0.139 | 237.189 | 0.171 | 329,261.826 |
Plasma
fibrinogen | 0.539 | 0.403 | 1.787 | 0.181 | 1.713 | 0.778 | 3.773 |
Triglyceride | −0.067 | 0.461 | 0.021 | 0.884 | 0.935 | 0.379 | 2.307 |
HDL | 1.833 | 1.100 | 2.780 | 0.095 | 6.256 | 0.725 | 53.975 |
LDL | −0.072 | 0.460 | 0.025 | 0.875 | 0.930 | 0.378 | 2.291 |
HLR | −2.148 | 1.809 | 1.410 | 0.235 | 0.117 | 0.003 | 4.047 |
Fasting blood
glucose | 0.133 | 0.165 | 0.647 | 0.421 | 1.142 | 0.827 | 1.577 |
Glycated
hemoglobin | −0.406 | 0.317 | 1.637 | 0.201 | 0.666 | 0.358 | 1.241 |
Homocysteine | 0.059 | 0.066 | 0.800 | 0.371 | 1.061 | 0.932 | 1.209 |
Gender | 0.276 | 0.801 | 0.118 | 0.731 | 1.317 | 0.274 | 6.332 |
Diabetes | 2.237 | 1.151 | 3.778 | 0.052 | 9.362 | 0.982 | 89.303 |
Hypertension | 1.654 | 0.789 | 4.387 | 0.036 | 5.225 | 1.112 | 24.552 |
Hyperlipidemia | 0.947 | 0.804 | 1.387 | 0.239 | 2.577 | 0.533 | 12.450 |
Smoking | 1.449 | 0.767 | 3.570 | 0.059 | 4.259 | 0.947 | 19.142 |
Wine
consumption | 0.161 | 0.929 | 0.030 | 0.862 | 1.175 | 0.190 | 7.251 |
| Table VILogistic regression analysis of
factors affecting cerebral artery stenosis (significant
factors). |
Table VI
Logistic regression analysis of
factors affecting cerebral artery stenosis (significant
factors).
| | | | | | 95% CI of OR
value |
---|
| | | | | |
|
---|
Risk factor | B | SE | Wald | P-value | OR value | Lower limit | Upper limit |
---|
Age | 0.030 | 0.012 | 6.174 | 0.013 | 1.031 | 1.006 | 1.056 |
Diabetes | 1.054 | 0.295 | 12.772 | 0.000 | 2.869 | 1.609 | 5.133 |
Plasma
fibrinogen | 0.299 | 0.147 | 4.148 | 0.042 | 1.348 | 1.011 | 1.797 |
HLR | −0.925 | 0.420 | 4.841 | 0.028 | 0.396 | 0.174 | 0.904 |
| Table VIILogistic regression analysis of
factors affecting stroke. |
Table VII
Logistic regression analysis of
factors affecting stroke.
| | | | | | 95% CI of OR
value |
---|
| | | | | |
|
---|
Risk factor | B | SE | Wald | P-value | OR value | Lower limit | Upper limit |
---|
Large artery
atherosclerosis |
Intercept | −6.995 | 3.664 | 3.645 | 0.056 | | | |
Age | 0.010 | 0.019 | 0.262 | 0.609 | 1.010 | 0.972 | 1.049 |
Systolic blood
pressure | 0.013 | 0.009 | 1.763 | 0.184 | 1.013 | 0.994 | 1.031 |
Platelet
count | −0.001 | 0.003 | 0.153 | 0.696 | 0.999 | 0.994 | 1.004 |
International
normalized ratio | −1.453 | 2.100 | 0.479 | 0.489 | 0.234 | 0.004 | 14.348 |
Plasma
fibrinogen | 0.356 | 0.235 | 2.294 | 0.130 | 1.427 | 0.901 | 2.261 |
Triglyceride | −0.048 | 0.208 | 0.053 | 0.817 | 0.953 | 0.635 | 1.432 |
HDL | 0.021 | 0.750 | 0.001 | 0.978 | 1.021 | 0.235 | 4.441 |
LDL | 0.381 | 0.411 | 0.858 | 0.354 | 1.464 | 0.654 | 3.279 |
HLR | −0.690 | 1.890 | 0.133 | 0.715 | 0.502 | 0.012 | 20.399 |
Fasting blood
glucose | 0.400 | 0.174 | 5.302 | 0.021 | 1.492 | 1.061 | 2.097 |
Glycated
hemoglobin | 0.308 | 0.259 | 1.419 | 0.234 | 1.361 | 0.819 | 2.261 |
Homocysteine | −0.020 | 0.038 | 0.271 | 0.602 | 0.981 | 0.910 | 1.056 |
Gender | 0.296 | 0.479 | 0.383 | 0.536 | 1.345 | 0.526 | 3.439 |
Diabetes | 0.111 | 0.552 | 0.040 | 0.841 | 1.117 | 0.379 | 3.294 |
Hypertension | 0.293 | 0.530 | 0.306 | 0.580 | 1.341 | 0.474 | 3.789 |
Hyperlipidemia | 0.505 | 0.454 | 1.239 | 0.266 | 1.657 | 0.681 | 4.034 |
Smoking | 0.183 | 0.464 | 0.155 | 0.694 | 1.200 | 0.483 | 2.983 |
Wine
consumption | 1.635 | 0.728 | 5.041 | 0.025 | 5.127 | 1.231 | 21.358 |
Small artery
occlusion |
Intercept | −5.180 | 3.822 | 1.837 | 0.175 | | | |
Age | −0.005 | 0.020 | 0.063 | 0.802 | 0.995 | 0.956 | 1.035 |
Systolic blood
pressure | 0.019 | 0.010 | 3.312 | 0.069 | 1.019 | 0.999 | 1.039 |
Platelet
count | 0.003 | 0.003 | 1.292 | 0.256 | 1.003 | 0.998 | 1.008 |
International
normalized ratio | −3.342 | 2.372 | 1.985 | 0.159 | 0.035 | 0.000 | 3.697 |
Plasma
fibrinogen | 0.061 | 0.250 | 0.060 | 0.806 | 1.063 | 0.652 | 1.735 |
Triglyceride | −0.018 | 0.212 | 0.007 | 0.932 | 0.982 | 0.648 | 1.489 |
HDL | −1.230 | 0.926 | 1.763 | 0.184 | 0.292 | 0.048 | 1.796 |
LDL | 0.803 | 0.422 | 3.626 | 0.057 | 2.232 | 0.977 | 5.100 |
HLR | 2.486 | 1.812 | 1.881 | 0.170 | 12.010 | 0.344 | 418.996 |
Fasting blood
glucose | 0.361 | 0.180 | 4.022 | 0.045 | 1.434 | 1.008 | 2.041 |
Glycated
hemoglobin | 0.196 | 0.271 | 0.523 | 0.469 | 1.217 | 0.715 | 2.069 |
Homocysteine | −0.054 | 0.042 | 1.671 | 0.196 | 0.947 | 0.873 | 1.028 |
Gender | 0.285 | 0.510 | 0.312 | 0.577 | 1.330 | 0.489 | 3.615 |
Diabetes | 0.005 | 0.607 | 0.000 | 0.994 | 1.005 | 0.306 | 3.302 |
Hypertension | 0.736 | 0.593 | 1.542 | 0.214 | 2.088 | 0.653 | 6.679 |
Hyperlipidemia | −0.128 | 0.495 | 0.067 | 0.796 | 0.880 | 0.333 | 2.322 |
Hyperlipidemia | 0.068 | 0.501 | 0.018 | 0.892 | 1.070 | 0.401 | 2.855 |
Smoking | 1.513 | 0.768 | 3.886 | 0.049 | 4.542 | 1.009 | 20.455 |
| Table VIIILogistic regression analysis of
factors affecting progressive stroke. |
Table VIII
Logistic regression analysis of
factors affecting progressive stroke.
| | | | | | 95% CI of OR
value |
---|
| | | | | |
|
---|
Risk factor | B | SE | Wald | P-value | OR value | Lower limit | Upper limit |
---|
Age | 0.067 | 0.018 | 14.401 | <0.001 | 1.070 | 1.033 | 1.108 |
Wine
consumption | 1.724 | 0.400 | 18.570 | 0.001 | 5.608 | 2.560 | 12.286 |
International
normalized ratio | −6.955 | 2.292 | 9.203 | 0.002 | 0.001 | 0.000 | 0.085 |
Fasting blood
glucose | 0.314 | 0.079 | 15.916 | <0.001 | 1.369 | 1.173 | 1.598 |
Glycated
hemoglobin | −0.553 | 0.158 | 12.290 | <0.001 | 0.575 | 0.423 | 0.784 |
| Table IXEffect of fasting blood glucose and
FIB classification on carotid atherosclerosis. |
Table IX
Effect of fasting blood glucose and
FIB classification on carotid atherosclerosis.
| | | | | | 95% CI of OR
value |
---|
| | | | | |
|
---|
Risk factor | B | SE | Wald | P-value | OR value | Lower limit | Upper limit |
---|
Hardening |
Intercept | −13.523 | 6.101 | 4.912 | 0.027 | | | |
Age | 0.066 | 0.031 | 4.533 | 0.033 | 1.069 | 1.005 | 1.136 |
Systolic blood
pressure | 0.028 | 0.017 | 2.821 | 0.093 | 1.029 | 0.995 | 1.063 |
Platelet
count | 0.002 | 0.004 | 0.236 | 0.627 | 1.002 | 0.993 | 1.011 |
International
normalized ratio | 4.318 | 3.937 | 1.202 | 0.273 | 75.015 | 0.033 | 168,551.521 |
Triglyceride | 0.732 | 0.445 | 2.708 | 0.100 | 2.079 | 0.870 | 4.971 |
HDL | 1.812 | 1.011 | 3.215 | 0.073 | 6.124 | 0.845 | 44.394 |
LDL | 0.551 | 0.413 | 1.780 | 0.182 | 1.735 | 0.772 | 3.898 |
HLR | −0.175 | 1.264 | 0.019 | 0.890 | 0.839 | 0.070 | 10.005 |
Glycated
hemoglobin | −0.872 | 0.345 | 6.381 | 0.012 | 0.418 | 0.212 | 0.822 |
Homocysteine | 0.025 | 0.065 | 0.150 | 0.698 | 1.026 | 0.902 | 1.166 |
Diabetes | 2.883 | 1.210 | 5.681 | 0.017 | 17.875 | 1.669 | 191.421 |
Hypertension | 0.906 | 0.801 | 1.280 | 0.258 | 2.474 | 0.515 | 11.888 |
Hyperlipidemia | 0.283 | 0.835 | 0.115 | 0.735 | 1.327 | 0.258 | 6.816 |
Smoking | 1.578 | 0.796 | 3.934 | 0.047 | 4.845 | 1.019 | 23.043 |
Wine
consumption | −0.026 | 0.989 | 0.001 | 0.979 | 0.974 | 0.140 | 6.761 |
Gender | −0.274 | 0.816 | 0.113 | 0.737 | 0.760 | 0.154 | 3.760 |
Fasting blood
glucose 1 | 0.313 | 1.013 | 0.096 | 0.757 | 1.368 | 0.188 | 9.965 |
Fasting blood
glucose 2 | 0.133 | 1.014 | 0.017 | 0.896 | 1.142 | 0.157 | 8.328 |
Fasting blood
glucose 3 | −0.260 | 0.992 | 0.069 | 0.793 | 0.771 | 0.110 | 5.388 |
Plasma fibrinogen
1 | −1.408 | 1.031 | 1.865 | 0.172 | 0.245 | 0.032 | 1.846 |
Plasma fibrinogen
2 | 0.242 | 0.978 | 0.061 | 0.805 | 1.273 | 0.187 | 8.654 |
Plasma fibrinogen
3 | −0.125 | 0.936 | 0.018 | 0.893 | 0.882 | 0.141 | 5.523 |
Plaque
formation |
Intercept | −17.606 | 5.621 | 9.811 | 0.002 | | | |
Age | 0.094 | 0.029 | 10.782 | 0.001 | 1.099 | 1.039 | 1.162 |
Systolic blood
pressure | 0.023 | 0.016 | 2.254 | 0.133 | 1.024 | 0.993 | 1.055 |
Platelet
count | 0.004 | 0.004 | 0.795 | 0.373 | 1.004 | 0.996 | 1.012 |
International
normalized ratio | 6.246 | 3.601 | 3.009 | 0.083 | 516.125 | 0.444 | 599,451.170 |
Triglyceride | 0.358 | 0.423 | 0.717 | 0.397 | 1.431 | 0.624 | 3.280 |
HDL | 1.847 | 0.989 | 3.490 | 0.062 | 6.343 | 0.913 | 44.055 |
LDL | −0.133 | 0.394 | 0.113 | 0.736 | 0.876 | 0.405 | 1.896 |
HLR | −1.207 | 1.202 | 1.010 | 0.315 | 0.299 | 0.028 | 3.151 |
Glycated
hemoglobin | −0.275 | 0.259 | 1.122 | 0.289 | 0.760 | 0.457 | 1.263 |
Homocysteine | 0.054 | 0.061 | 0.769 | 0.381 | 1.055 | 0.936 | 1.190 |
Diabetes | 2.713 | 1.146 | 5.609 | 0.018 | 15.076 | 1.596 | 142.377 |
Hypertension | 1.384 | 0.692 | 3.998 | 0.046 | 3.991 | 1.028 | 15.500 |
Hyperlipidemia | 0.877 | 0.753 | 1.355 | 0.244 | 2.403 | 0.549 | 10.518 |
Smoking | 1.105 | 0.719 | 2.364 | 0.124 | 3.019 | 0.738 | 12.350 |
Wine
consumption | 0.727 | 0.892 | 0.664 | 0.415 | 2.069 | 0.360 | 11.890 |
Gender | 0.033 | 0.737 | 0.002 | 0.964 | 1.034 | 0.244 | 4.385 |
Fasting blood
glucose 1 | 0.582 | 0.915 | 0.404 | 0.525 | 1.790 | 0.298 | 10.766 |
Fasting blood
glucose 2 | 0.422 | 0.916 | 0.212 | 0.645 | 1.525 | 0.253 | 9.172 |
Fasting blood
glucose 3 | −0.182 | 0.904 | 0.040 | 0.841 | 0.834 | 0.142 | 4.902 |
Plasma fibrinogen
1 | −1.163 | 0.929 | 1.568 | 0.211 | 0.313 | 0.051 | 1.930 |
Plasma fibrinogen
2 | 0.262 | 0.893 | 0.086 | 0.769 | 1.300 | 0.226 | 7.476 |
Plasma fibrinogen
3 | −0.938 | 0.879 | 1.137 | 0.286 | 0.392 | 0.070 | 2.194 |
Stenosis |
Intercept | −17.095 | 6.254 | 7.471 | 0.006 | | | |
Age | 0.094 | 0.033 | 7.945 | 0.005 | 1.099 | 1.029 | 1.173 |
Systolic blood
pressure | 0.013 | 0.017 | 0.603 | 0.437 | 1.013 | 0.980 | 1.048 |
Platelet
count | −0.001 | 0.005 | 0.041 | 0.839 | 0.999 | 0.990 | 1.008 |
International
normalized ratio | 6.102 | 3.870 | 2.487 | 0.115 | 446.693 | 0.227 | 878,531.134 |
Triglyceride | −0.010 | 0.480 | 0.000 | 0.984 | 0.990 | 0.387 | 2.535 |
HDL | 1.555 | 1.182 | 1.729 | 0.189 | 4.733 | 0.466 | 48.022 |
LDL | −0.034 | 0.492 | 0.005 | 0.945 | 0.966 | 0.368 | 2.536 |
HLR | −1.891 | 1.908 | 0.982 | 0.322 | 0.151 | 0.004 | 6.353 |
Glycated
hemoglobin | −0.157 | 0.288 | 0.295 | 0.587 | 0.855 | 0.486 | 1.504 |
Homocysteine | 0.060 | 0.067 | 0.799 | 0.371 | 1.062 | 0.931 | 1.210 |
Diabetes | 2.665 | 1.215 | 4.808 | 0.028 | 14.367 | 1.327 | 155.573 |
Hypertension | 1.943 | 0.861 | 5.091 | 0.024 | 6.979 | 1.291 | 37.737 |
Hyperlipidemia | 0.685 | 0.827 | 0.686 | 0.407 | 1.985 | 0.392 | 10.048 |
Smoking | 1.584 | 0.787 | 4.055 | 0.044 | 4.874 | 1.043 | 22.773 |
Wine
consumption | 0.555 | 0.974 | 0.326 | 0.568 | 1.743 | 0.259 | 11.746 |
Gender | 0.161 | 0.846 | 0.036 | 0.849 | 1.174 | 0.224 | 6.161 |
Fasting blood
glucose 1 | 1.193 | 1.063 | 1.260 | 0.262 | 3.298 | 0.411 | 26.501 |
Fasting blood
glucose 2 | 0.979 | 1.089 | 0.808 | 0.369 | 2.663 | 0.315 | 22.524 |
Fasting blood
glucose 3 | 1.366 | 1.009 | 1.835 | 0.176 | 3.921 | 0.543 | 28.311 |
Plasma fibrinogen
1 | −1.024 | 0.994 | 1.061 | 0.303 | 0.359 | 0.051 | 2.521 |
Plasma fibrinogen
2 | −1.151 | 1.053 | 1.194 | 0.275 | 0.316 | 0.040 | 2.492 |
Plasma fibrinogen
3 | −0.871 | 0.936 | 0.866 | 0.352 | 0.418 | 0.067 | 2.620 |
| Table XEffect of fasting blood glucose and
FIB classification on cerebral artery stenosis. |
Table X
Effect of fasting blood glucose and
FIB classification on cerebral artery stenosis.
| | | | | | 95% CI of OR
value |
---|
| | | | | |
|
---|
Factors | B | SE | Wald | P-value | OR value | Lower limit | Upper limit |
---|
Gender | 0.033 | 0.361 | 0.009 | 0.926 | 1.034 | 0.509 | 2.100 |
Age | 0.031 | 0.014 | 4.796 | 0.029 | 1.032 | 1.003 | 1.061 |
Diabetes | 0.946 | 0.415 | 5.186 | 0.023 | 2.574 | 1.141 | 5.809 |
Hypertension | 0.185 | 0.404 | 0.210 | 0.647 | 1.203 | 0.545 | 2.659 |
Hyperlipidemia | 0.585 | 0.352 | 2.759 | 0.097 | 1.794 | 0.900 | 3.576 |
Smoking | 0.265 | 0.346 | 0.586 | 0.444 | 1.303 | 0.662 | 2.565 |
Wine
consumption | 0.239 | 0.437 | 0.300 | 0.584 | 1.270 | 0.540 | 2.990 |
Systolic blood
pressure | 0.002 | 0.007 | 0.110 | 0.740 | 1.002 | 0.989 | 1.015 |
Platelet count | 0.000 | 0.002 | 0.035 | 0.852 | 1.000 | 0.997 | 1.004 |
International
normalized ratio | −0.400 | 1.450 | 0.076 | 0.783 | 0.671 | 0.039 | 11.492 |
Triglyceride | −0.142 | 0.162 | 0.772 | 0.380 | 0.868 | 0.632 | 1.191 |
HDL | −0.006 | 0.345 | 0.000 | 0.985 | 0.994 | 0.505 | 1.953 |
LDL | −0.055 | 0.203 | 0.074 | 0.785 | 0.946 | 0.636 | 1.408 |
HLR | −0.788 | 0.666 | 1.403 | 0.236 | 0.455 | 0.123 | 1.676 |
Glycated
hemoglobin | 0.009 | 0.128 | 0.005 | 0.946 | 1.009 | 0.785 | 1.295 |
Homocysteine | 0.033 | 0.029 | 1.255 | 0.263 | 1.033 | 0.976 | 1.094 |
Fasting blood
glucose | | | 1.497 | 0.683 | | | |
Fasting blood
glucose 1 | −0.480 | 0.470 | 1.040 | 0.308 | 0.619 | 0.246 | 1.556 |
Fasting blood
glucose 2 | −0.276 | 0.477 | 0.335 | 0.563 | 0.759 | 0.298 | 1.932 |
Fasting blood
glucose 3 | −0.060 | 0.457 | 0.018 | 0.895 | 0.941 | 0.385 | 2.304 |
Plasma
fibrinogen | | | 1.967 | 0.579 | | | |
Plasma fibrinogen
1 | −0.269 | 0.415 | 0.421 | 0.516 | 0.764 | 0.339 | 1.723 |
Plasma fibrinogen
2 | −0.427 | 0.402 | 1.129 | 0.288 | 0.653 | 0.297 | 1.434 |
Plasma fibrinogen
3 | 0.058 | 0.398 | 0.022 | 0.883 | 1.060 | 0.486 | 2.311 |
Discussion
PCI is a refractory cerebral vascular disease with
an incidence rate of 20–30% in patients with cerebral infarction.
PCI often leads to brain deterioration and thereby significantly
increases the mortality rate (8–10).
The occurrence and development of PCI are affected by a number of
factors and mechanisms. Among the numerous risk factors,
atherosclerosis, stenosis or occlusion of the trunk and main
branches of cerebral arteries are major independent risk factors
(11). Consistent with a previous
study (12), the data of the
present study demonstrated that the corresponding vessels in the
infarction region had various degrees of vascular sclerosis and
stenosis.
Multiple mechanisms of cerebral infarction caused by
atherosclerosis have been proposed, including intravascular
thrombosis, vascular stenosis and reduced perfusion pressure in
terminal cerebral vessels (8).
When intravascular plaques detach from the arterial thrombus or
atherosclerosis directly involves the perforator vessels, cerebral
infarction may occur. The atherosclerotic vessels are more prone to
thrombosis, which aggravates the preexisting vascular stenosis or
occlusion (13). Thrombosis may
exacerbate cerebral ischemia unless collateral circulation is
formed in time. When collateral circulation does not form, cerebral
infarction becomes progressive. Stenosis of the cerebral vessels is
an additional mechanism underlying the progression of infarction
(14). The narrowed cerebral
vessels are more likely to have local thrombosis. Thrombosis may
extend to the distal vessels resulting in stenosis, and detachment
of the thrombus from the wall may also cause an arterial embolism
(15,16). When stenosis occurs in the internal
carotid, vertebral basilar or other medium-sized arteries, blood
flow to the distal branches decreases. With low perfusion, the
distal narrowed vessels fail to form effective collateral
circulation to bypass the blockage. The results of the present
study revealed that atherosclerotic plaques and stenosis existed in
the corresponding vessels of cerebral infarction. These
observations indicate that cerebral vascular lesions play an
important role in the pathogenesis of PCI. In addition, the current
study identified that numerous factors, including age, HDL,
glycosylated hemoglobin and blood parameters, correlated with the
severity of atherosclerosis, plaque formation and stenosis in the
carotid artery. Factors affecting cerebral artery stenosis were
also identified, including age, diabetes, plasma fibrinogen and
HLR, among which age, diabetes mellitus and plasma fibrinogen were
risk factors, while HLR was a protective factor. Therefore, in
patients with acute cerebral infarction, early treatment of
vascular stenosis and cerebral artery recanalization may improve
cerebral perfusion, thus, prevent the progression and recurrence of
cerebral infarction. A previous study demonstrated that placing a
stent in the narrowed vessels of patients with PCI, particularly in
those with artery stenosis when performed within 16 h of disease
onset and treated within 8 h, achieves favorable effects (17). In conclusion, the results of the
present study indicate that the lesions of responsible blood
vessels play an important role in PCI. The observations provide
supporting evidence for interventional therapy for cerebrovascular
disease.
Acknowledgements
This study was supported by the Science and
Technology Program for Dongguan Higher Education, Science, Research
and Health Care (grant number 201010515000333). The authors would
like to thank Forevergen Biosciences for assistance with the
experiments and for valuable discussion and 91SCI Company for
language editing assistance.
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