Open Access

Analysis of multiple factors involved in acute progressive cerebral infarction and extra‑ and intracranial arterial lesions

  • Authors:
    • Yuefu Chen
    • Yajie Liu
    • Chenghong Luo
    • Weiheng Lu
    • Binru Su
  • View Affiliations

  • Published online on: March 14, 2014     https://doi.org/10.3892/etm.2014.1624
  • Pages: 1495-1505
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Abstract

In order to identify the potential factors involved in the development of acute progressive cerebral infarction (PCI), the association between potential risk factors and extra‑ and intracranial arterial lesions was investigated. A total of 608 patients underwent cerebral angiography to analyze the morphological characteristics between the PCI and NPCI groups. In addition, data from numerous cases of extra‑ and intracranial arterial lesions were collected and compared with the control groups, and the associations between the severity of arterial lesions and the potential influential factors were analyzed. In the blood vessels responsible for cerebral infarction, various degrees of atherosclerotic plaques and stenosis were observed. Age, high‑density lipoprotein (HDL) levels, glycosylated hemoglobin and blood pressure affected the degrees of hardening, plaques and stenosis. Analysis of cerebral artery stenosis revealed that age, diabetes mellitus and plasma fibrinogen were risk factors for cerebral artery stenosis, while the HDL/low density lipoprotein ratio was a protective factor. Therefore, the results of the present study indicate that the lesions of blood vessels are a major pathological change in PCI and multiple factors are involved in the pathogenesis.

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 I

Association of potential risk factors with severity of carotid atherosclerosis.

Table I

Association of potential risk factors with severity of carotid atherosclerosis.

Risk factorCarotid atherosclerosisTotalTest statisticP-value

NormalHardeningPlaqueStenosis
Gender, n (%)
 Male60 (69.0)67 (67.7)197 (69.6)62 (74.7)386 (69.9)1.1890.756
 Female27 (31.0)32 (32.3)86 (30.4)21 (25.3)166 (30.1)
Diabetes, n (%)
 No75 (86.2)75 (75.8)185 (65.4)50 (60.2)385 (69.7)18.988<0.01
 Yes12 (13.8)24 (24.2)98 (34.6)33 (39.8)167 (30.3)
Hypertension, n (%)
 No49 (56.3)24 (24.2)37 (13.1)8 (9.6)118 (21.4)82.107<0.01
 Yes38 (43.7)75 (75.8)246 (86.9)75 (90.4)434 (78.6)
Hyperlipidemia, n (%)
 No56 (64.4)51 (51.5)127 (45.0)39 (47.0)273 (49.5)10.3120.016
 Yes31 (35.6)48 (48.5)155 (55.0)44 (53.0)278 (50.5)
Smoking, n (%)
 No60 (69.0)58 (58.6)172 (60.8)43 (51.8)333 (60.3)5.3790.146
 Yes27 (31.0)41 (41.4)111 (39.2)40 (48.2)219 (39.7)
Wine consumption, n (%)
 No78 (89.7)87 (87.9)241 (85.2)71 (85.5)477 (86.4)1.3930.707
 Yes9 (10.3)12 (12.1)42 (14.8)12 (14.5)75 (13.6)
Age, yearsa53.2±11.662.3±11.366.4±10.068.6±8.343.4<0.01
Systolic blood pressure, mmHga136.3±21.3151.3±23.8153.2±23.5153.6±22.112.9<0.01
Diastolic blood pressure, mmHga81.2±12.885.3±13.385.2±12.383.7±9.12.60.049
Platelet count (109/l)a235.788±67.761253.153±95.158237.735±76.974236.602±70.1031.1350.334
International normalized ratioa1.001±0.0801.006±0.0881.033±0.1091.041±0.1702.9110.034
Plasma fibrinogen (g/l) a3.301±0.7893.564±0.7963.805±0.9903.862±1.0117.297<0.01
Total cholesterol (mmol/l)a4.675±1.2084.959±1.1374.980±1.1565.043±1.4991.6390.179
Triglyceride (mmol/l)a1.661±1.1651.741±1.1121.738±1.0691.643±0.9370.2540.859
HDL (mmol/l)a1.087±0.3341.226±0.5081.135±0.5491.114±0.3401.4510.227
LDL (mmol/l)a2.596±0.9922.905±0.9932.773±1.0022.936±1.1232.0390.107
HLRa0.480±0.2530.492±0.4050.478±0.3300.451±0.3970.2190.883
Fasting blood glucose (mmol/l)a5.878±1.6916.222±2.0066.698±3.0556.866±3.6222.6400.049
Glycated hemoglobin (%)a6.233±1.9486.197±1.4156.942±2.0166.970±1.8814.1220.007
Homocysteine (μmol/l)a13.574±5.58613.941±4.89814.849±6.47015.002±5.2581.0310.379

a Mean ± SD.

{ label (or @symbol) needed for fn[@id='tfn2-etm-07-06-1495'] } HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

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 II

Association 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 factorNarrowing ≤50%Narrowing >50%TotalTest statisticP-value
Gender, n (%)
 Male185 (68.0)234 (69.6)419 (68.9)0.1860.666
 Female87 (32.0)102 (30.4)189 (31.1)
Diabetes, n (%)
 No221 (81.3)209 (62.2)430 (70.7)26.339<0.001
 Yes51 (18.8)127 (37.8)178 (29.3)
Hypertension, n (%)
 No79 (29.0)50 (14.9)129 (21.2)18.039<0.001
 Yes193 (71.0)286 (85.1)479 (78.8)
Hyperlipidemia, n (%)
 No154 (56.6)149 (44.5)303 (49.9)8.8500.003
 Yes118 (43.4)186 (55.5)304 (50.1)
Smoking, n (%)
 No185 (68.0)195 (58.0)380 (62.5)6.3870.011
 Yes87 (32.0)141 (42.0)228 (37.5)
Wine consumption, n (%)
 No246 (90.4)281 (83.6)527 (86.7)6.0370.014
 Yes26 (9.6)55 (16.4)81 (13.3)
Age, yearsa60.7±12.165.8±10.4−5.6<0.01
Systolic blood pressure, mmHga147.9±24.9151.4±22.7−1.80.065
Diastolic blood pressure, mmHga84.0±12.784.0±12.00.0260.979
Platelet count (109/l)a237.345±78.032245.263±78.838−1.2290.220
International normalized ratioa1.029±0.1011.020±0.1180.8840.377
Plasma fibrinogen (g/l)a3.460±0.8593.871±1.045−5.124<0.001
Total cholesterol (mmol/l)a4.862±1.1995.023±1.206−1.6320.103
Triglyceride (mmol/l)a1.642±0.9961.753±1.140−1.270.204
HDL (mmol/l)a1.191±0.4471.116±0.4911.9420.053
LDL (mmol/l)a2.715±1.0112.846±0.990−1.5980.111
HLRa0.520±0.4080.444±0.2522.6860.008
Fasting blood glucose (mmol/l)a6.000±2.1496.846±3.188−3.874<0.001
Glycated hemoglobin (%)a6.415±1.8377.009±1.985−3.1150.002
Homocysteine (μmol/l)a14.084±4.66914.992±6.561−1.6150.107

a Mean ± SD.

{ label (or @symbol) needed for fn[@id='tfn4-etm-07-06-1495'] } HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

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 III

Association between potential risk factors and the severity of stroke.

Table III

Association between potential risk factors and the severity of stroke.

Risk factorNo strokeStroke with large artery atherosclerosisStroke with small artery atherosclerosisTotalTest statisticP-value
Gender, n (%)
 Male113 (64.6)154 (70.0)109 (73.6)376 (69.2)3.2010.202
 Female62 (35.4)66 (30.0)39 (26.4)167 (30.8)
Diabetes, n (%)
 No140 (80.0)131 (59.5)109 (73.6)380 (70.0)20.714<0.001
 Yes35 (20.0)89 (40.5)39 (26.4)163 (30.0)
Hypertension, n (%)
 No59 (33.7)34 (15.5)19 (12.8)112 (20.6)27.388<0.001
 Yes116 (66.3)186 (84.5)129 (87.2)431 (79.4)
Hyperlipidemia, n (%)
 No104 (59.4)88 (40.2)75 (50.7)267 (49.3)14.5780.001
 Yes71 (40.6)131 (59.8)73 (49.3)275 (50.7)
Smoking, n (%)
 No128 (73.1)119 (54.1)90 (60.8)337 (62.1)15.1610.001
 Yes47 (26.9)101 (45.9)58 (39.2)206 (37.9)
Wine consumption, n (%)
 No167 (95.4)175 (79.5)126 (85.1)468 (86.2)20.845<0.01
 Yes8 (4.6)45 (20.5)22 (14.9)75 (13.6)
Age, yearsa61.7±11.365.5±11.162.6±11.66.20.002
Systolic blood pressure, mmHga140.7±21.4152.54±22.9157.3±23.024.1<0.01
Diastolic blood pressure, mmHga79.6±9.885.7±12.488.2±12.727.5<0.01
Platelet count (109/l)a233.751±72.418244.735±76.258247.944±83.2591.5590.211
International normalized ratioa1.031±0.0941.013±0.0941.011±0.0872.0970.124
Plasma fibrinogen (g/l)a3.368±0.8793.984±1.1033.659±0.83517.363<0.001
Total cholesterol (mmol/l)a4.742±1.1425.082±1.2284.909±1.1134.0390.018
Triglyceride (mmol/l)a1.677±1.2361.762±1.0711.719±0.9720.2910.748
HDL (mmol/l)a1.192±0.4071.114±0.5661.142±0.4631.1890.305
LDL (mmol/l)a2.542±0.9072.936±0.9972.796±0.9847.966<0.001
HLRa0.542±0.3570.418±0.2120.498±0.4548.833<0.001
Fasting blood glucose (mmol/l)a5.765±2.3477.166±3.4026.414±2.35411.659<0.001
Glycated hemoglobin (%)a6.243±1.3767.219±2.1896.613±1.87910.379<0.001
Homocysteine (μmol/l)a14.301±4.47315.051±6.51214.640±6.1060.5000.607

a Mean ± SD.

{ label (or @symbol) needed for fn[@id='tfn6-etm-07-06-1495'] } HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

Table IV

Association between potential risk factors and progressive stroke.

Table IV

Association between potential risk factors and progressive stroke.

Progressive stroke

Risk factorNo (n=368)Yes (n=60)TotalTest statisticP-value
Gender, n (%)
 Male262 (71.2)43 (71.7)305 (71.3)0.0060.940
 Female106 (28.8)17 (28.3)123 (28.7)
Diabetes, n (%)
 No248 (67.4)40 (66.7)288 (67.3)0.0120.912
 Yes120 (32.6)20 (33.3)140 (32.7)
Hypertension, n (%)
 No58 (15.8)13 (21.7)71 (16.6)1.3000.254
 Yes310 (84.2)47 (78.3)357 (83.4)
Hyperlipidemia, n (%)
 No179 (48.8)21 (35.0)200 (46.8)3.9290.047
 Yes188 (51.2)39 (65.0)227 (53.2)
Smoking, n (%)
 No217 (59.0)29 (48.3)246 (57.5)2.3870.122
 Yes151 (41.0)31 (51.7)182 (42.5)
Wine consumption, n (%)
 No318 (86.4)37 (61.7)355 (82.9)22.331<0.01
 Yes50 (13.6)23 (38.3)73 (17.1)
Age, yearsa63.5±11.168.8±12.0−3.4<0.01
Systolic blood pressure, mmHga153.6±24.1152.8±19.00.30.766
Diastolic blood pressure, mmHga85.7±12.987.1±11.7−0.80.432
Platelet count (109/l)a244.019±79.526246.967±89.006−0.2610.794
International normalized ratioa1.031±0.1180.975±0.0993.46<0.01
Plasma fibrinogen (g/l)a3.789±0.9823.964±1.135−1.2340.218
Total cholesterol (mmol/l)a4.980±1.2295.278±1.148−1.7560.080
Triglyceride (mmol/l)a1.706±1.0221.686±0.9230.140.889
HDL (mmol/l)a1.121±0.3551.204±0.998−0.6350.528
LDL (mmol/l)a2.840±1.0323.032±0.935−1.3490.178
HLRa0.458±0.2980.453±0.4590.0830.934
Fasting blood glucose (mmol/l)a6.610±2.5997.782±4.420−1.9970.050
Glycated hemoglobin (%)a7.073±2.1086.494±1.9951.9170.056
Homocysteine (μmol/l)a14.847±6.43213.731±5.0491.4290.156

a Mean ± SD.

{ label (or @symbol) needed for fn[@id='tfn8-etm-07-06-1495'] } HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

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 V

Logistic regression analysis of factors affecting carotid atherosclerosis.

Table V

Logistic regression analysis of factors affecting carotid atherosclerosis.

95% CI of OR value

Risk factorBSEWaldP-valueOR valueLower limitUpper limit
Hardening
 Intercept−10.1386.5652.3850.123
 Age0.0630.0304.4450.0351.0661.0041.130
 Systolic blood pressure0.0290.0163.0450.0811.0290.9961.063
 Platelet count0.0030.0040.3380.5611.0030.9941.011
 International normalized ratio4.0153.7471.1480.28455.4130.03685,759.316
 Plasma fibrinogen0.3860.4060.9010.3421.4710.6633.260
 Triglyceride0.5420.4081.7630.1841.7200.7723.830
 HDL1.8780.9473.9320.0476.5401.02241.851
 LDL0.4410.3971.2320.2671.5540.7143.382
 HLR−0.2691.2350.0480.8270.7640.0688.601
 Fasting blood glucose0.1970.1721.3140.2521.2180.8701.705
 Glycated hemoglobin−0.9290.3636.5460.0110.3950.1940.805
 Homocysteine0.0370.0650.3140.5761.0370.9121.179
 Gender−0.3190.7810.1670.6830.7270.1573.356
 Diabetes2.3221.1613.9990.04610.1951.04799.254
 Hypertension0.8870.7421.4280.2322.4270.56710.390
 Hyperlipidemia0.6400.8060.6290.4281.8960.3909.203
 Smoking1.5220.7773.8390.0504.5821.00021.002
 Wine consumption−0.2320.9260.0630.8020.7930.1294.868
Plaque formation
 Intercept−13.3616.0134.9380.026
 Age0.0920.02810.9520.0011.0961.0381.157
 Systolic blood pressure0.0230.0152.3690.1241.0240.9941.055
 Platelet count0.0040.0040.7850.3761.0040.9961.012
 International normalized ratio6.3203.4143.4280.064555.6080.690447,157.189
 Plasma fibrinogen0.4540.3771.4490.2291.5740.7523.296
 Triglyceride0.2480.3930.4000.5271.2820.5942.768
 HDL1.8740.9294.0700.0446.5121.05540.209
 LDL−0.2200.3770.3410.5590.8020.3831.681
 HLR−1.2051.1661.0680.3010.3000.0302.946
 Fasting blood glucose0.1430.1520.8860.3461.1540.8561.556
 Glycated hemoglobin−0.3670.2881.6280.2020.6930.3941.218
 Homocysteine0.0560.0610.8440.3581.0580.9381.193
 Gender0.0920.7020.0170.8961.0960.2774.341
 Diabetes2.1631.0923.9210.0488.7001.02277.035
 Hypertension1.1470.6353.2690.0713.1500.90810.927
 Hyperlipidemia1.2360.7302.8640.0913.4410.82214.393
 Smoking1.0060.6982.0770.1502.7350.69610.749
 Wine consumption0.3370.8400.1600.68901.4000.2707.267
Stenosis
 Intercept−12.0016.6383.2680.071
 Age0.1040.03310.2730.0011.1101.0411.183
 Systolic blood pressure0.0160.0160.8980.3431.0160.9831.049
 Platelet count0.0000.0050.0000.9961.0000.9911.009
 International normalized ratio5.4693.6922.1940.139237.1890.171329,261.826
 Plasma fibrinogen0.5390.4031.7870.1811.7130.7783.773
 Triglyceride−0.0670.4610.0210.8840.9350.3792.307
 HDL1.8331.1002.7800.0956.2560.72553.975
 LDL−0.0720.4600.0250.8750.9300.3782.291
 HLR−2.1481.8091.4100.2350.1170.0034.047
 Fasting blood glucose0.1330.1650.6470.4211.1420.8271.577
 Glycated hemoglobin−0.4060.3171.6370.2010.6660.3581.241
 Homocysteine0.0590.0660.8000.3711.0610.9321.209
 Gender0.2760.8010.1180.7311.3170.2746.332
 Diabetes2.2371.1513.7780.0529.3620.98289.303
 Hypertension1.6540.7894.3870.0365.2251.11224.552
 Hyperlipidemia0.9470.8041.3870.2392.5770.53312.450
 Smoking1.4490.7673.5700.0594.2590.94719.142
 Wine consumption0.1610.9290.0300.8621.1750.1907.251

[i] CI, confidence interval; SE, standard error; OR, odds ratio; HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

Table VI

Logistic 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 factorBSEWaldP-valueOR valueLower limitUpper limit
Age0.0300.0126.1740.0131.0311.0061.056
Diabetes1.0540.29512.7720.0002.8691.6095.133
Plasma fibrinogen0.2990.1474.1480.0421.3481.0111.797
HLR−0.9250.4204.8410.0280.3960.1740.904

[i] HLR, high-density lipoprotein/low-density lipoprotein ratio; CI, confidence interval; OR, odds ratio; SE, standard error.

Table VII

Logistic regression analysis of factors affecting stroke.

Table VII

Logistic regression analysis of factors affecting stroke.

95% CI of OR value

Risk factorBSEWaldP-valueOR valueLower limitUpper limit
Large artery atherosclerosis
 Intercept−6.9953.6643.6450.056
 Age0.0100.0190.2620.6091.0100.9721.049
 Systolic blood pressure0.0130.0091.7630.1841.0130.9941.031
 Platelet count−0.0010.0030.1530.6960.9990.9941.004
 International normalized ratio−1.4532.1000.4790.4890.2340.00414.348
 Plasma fibrinogen0.3560.2352.2940.1301.4270.9012.261
 Triglyceride−0.0480.2080.0530.8170.9530.6351.432
 HDL0.0210.7500.0010.9781.0210.2354.441
 LDL0.3810.4110.8580.3541.4640.6543.279
 HLR−0.6901.8900.1330.7150.5020.01220.399
 Fasting blood glucose0.4000.1745.3020.0211.4921.0612.097
 Glycated hemoglobin0.3080.2591.4190.2341.3610.8192.261
 Homocysteine−0.0200.0380.2710.6020.9810.9101.056
 Gender0.2960.4790.3830.5361.3450.5263.439
 Diabetes0.1110.5520.0400.8411.1170.3793.294
 Hypertension0.2930.5300.3060.5801.3410.4743.789
 Hyperlipidemia0.5050.4541.2390.2661.6570.6814.034
 Smoking0.1830.4640.1550.6941.2000.4832.983
 Wine consumption1.6350.7285.0410.0255.1271.23121.358
Small artery occlusion
 Intercept−5.1803.8221.8370.175
 Age−0.0050.0200.0630.8020.9950.9561.035
 Systolic blood pressure0.0190.0103.3120.0691.0190.9991.039
 Platelet count0.0030.0031.2920.2561.0030.9981.008
 International normalized ratio−3.3422.3721.9850.1590.0350.0003.697
 Plasma fibrinogen0.0610.2500.0600.8061.0630.6521.735
 Triglyceride−0.0180.2120.0070.9320.9820.6481.489
 HDL−1.2300.9261.7630.1840.2920.0481.796
 LDL0.8030.4223.6260.0572.2320.9775.100
 HLR2.4861.8121.8810.17012.0100.344418.996
 Fasting blood glucose0.3610.1804.0220.0451.4341.0082.041
 Glycated hemoglobin0.1960.2710.5230.4691.2170.7152.069
 Homocysteine−0.0540.0421.6710.1960.9470.8731.028
 Gender0.2850.5100.3120.5771.3300.4893.615
 Diabetes0.0050.6070.0000.9941.0050.3063.302
 Hypertension0.7360.5931.5420.2142.0880.6536.679
 Hyperlipidemia−0.1280.4950.0670.7960.8800.3332.322
 Hyperlipidemia0.0680.5010.0180.8921.0700.4012.855
 Smoking1.5130.7683.8860.0494.5421.00920.455

[i] CI, confidence interval; OR, odds ratio; SE, standard error; HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

Table VIII

Logistic regression analysis of factors affecting progressive stroke.

Table VIII

Logistic regression analysis of factors affecting progressive stroke.

95% CI of OR value

Risk factorBSEWaldP-valueOR valueLower limitUpper limit
Age0.0670.01814.401<0.0011.0701.0331.108
Wine consumption1.7240.40018.5700.0015.6082.56012.286
International normalized ratio−6.9552.2929.2030.0020.0010.0000.085
Fasting blood glucose0.3140.07915.916<0.0011.3691.1731.598
Glycated hemoglobin−0.5530.15812.290<0.0010.5750.4230.784

[i] International normalized ratio and glycated hemoglobin were protective factors (P<0.05), fasting blood glucose, age and alcohol consumption were risk factors (P<0.05). In total factor model, only 57 cases occurred progressive stroke so the single factor was age, hyperlipidemia, drinking, international normalized ratio, fasting blood glucose, glycated hemoglobin (P=0.057). CI, confidence interval; OR, odds ratio; SE, standard error.

Table IX

Effect 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 factorBSEWaldP-valueOR valueLower limitUpper limit
Hardening
 Intercept−13.5236.1014.9120.027
 Age0.0660.0314.5330.0331.0691.0051.136
 Systolic blood pressure0.0280.0172.8210.0931.0290.9951.063
 Platelet count0.0020.0040.2360.6271.0020.9931.011
 International normalized ratio4.3183.9371.2020.27375.0150.033168,551.521
 Triglyceride0.7320.4452.7080.1002.0790.8704.971
 HDL1.8121.0113.2150.0736.1240.84544.394
 LDL0.5510.4131.7800.1821.7350.7723.898
 HLR−0.1751.2640.0190.8900.8390.07010.005
 Glycated hemoglobin−0.8720.3456.3810.0120.4180.2120.822
 Homocysteine0.0250.0650.1500.6981.0260.9021.166
 Diabetes2.8831.2105.6810.01717.8751.669191.421
 Hypertension0.9060.8011.2800.2582.4740.51511.888
 Hyperlipidemia0.2830.8350.1150.7351.3270.2586.816
 Smoking1.5780.7963.9340.0474.8451.01923.043
 Wine consumption−0.0260.9890.0010.9790.9740.1406.761
 Gender−0.2740.8160.1130.7370.7600.1543.760
 Fasting blood glucose 10.3131.0130.0960.7571.3680.1889.965
 Fasting blood glucose 20.1331.0140.0170.8961.1420.1578.328
 Fasting blood glucose 3−0.2600.9920.0690.7930.7710.1105.388
 Plasma fibrinogen 1−1.4081.0311.8650.1720.2450.0321.846
 Plasma fibrinogen 20.2420.9780.0610.8051.2730.1878.654
 Plasma fibrinogen 3−0.1250.9360.0180.8930.8820.1415.523
Plaque formation
 Intercept−17.6065.6219.8110.002
 Age0.0940.02910.7820.0011.0991.0391.162
 Systolic blood pressure0.0230.0162.2540.1331.0240.9931.055
 Platelet count0.0040.0040.7950.3731.0040.9961.012
 International normalized ratio6.2463.6013.0090.083516.1250.444599,451.170
 Triglyceride0.3580.4230.7170.3971.4310.6243.280
 HDL1.8470.9893.4900.0626.3430.91344.055
 LDL−0.1330.3940.1130.7360.8760.4051.896
 HLR−1.2071.2021.0100.3150.2990.0283.151
 Glycated hemoglobin−0.2750.2591.1220.2890.7600.4571.263
 Homocysteine0.0540.0610.7690.3811.0550.9361.190
 Diabetes2.7131.1465.6090.01815.0761.596142.377
 Hypertension1.3840.6923.9980.0463.9911.02815.500
 Hyperlipidemia0.8770.7531.3550.2442.4030.54910.518
 Smoking1.1050.7192.3640.1243.0190.73812.350
 Wine consumption0.7270.8920.6640.4152.0690.36011.890
 Gender0.0330.7370.0020.9641.0340.2444.385
 Fasting blood glucose 10.5820.9150.4040.5251.7900.29810.766
 Fasting blood glucose 20.4220.9160.2120.6451.5250.2539.172
 Fasting blood glucose 3−0.1820.9040.0400.8410.8340.1424.902
 Plasma fibrinogen 1−1.1630.9291.5680.2110.3130.0511.930
 Plasma fibrinogen 20.2620.8930.0860.7691.3000.2267.476
 Plasma fibrinogen 3−0.9380.8791.1370.2860.3920.0702.194
Stenosis
 Intercept−17.0956.2547.4710.006
 Age0.0940.0337.9450.0051.0991.0291.173
 Systolic blood pressure0.0130.0170.6030.4371.0130.9801.048
 Platelet count−0.0010.0050.0410.8390.9990.9901.008
 International normalized ratio6.1023.8702.4870.115446.6930.227878,531.134
 Triglyceride−0.0100.4800.0000.9840.9900.3872.535
 HDL1.5551.1821.7290.1894.7330.46648.022
 LDL−0.0340.4920.0050.9450.9660.3682.536
 HLR−1.8911.9080.9820.3220.1510.0046.353
 Glycated hemoglobin−0.1570.2880.2950.5870.8550.4861.504
 Homocysteine0.0600.0670.7990.3711.0620.9311.210
 Diabetes2.6651.2154.8080.02814.3671.327155.573
 Hypertension1.9430.8615.0910.0246.9791.29137.737
 Hyperlipidemia0.6850.8270.6860.4071.9850.39210.048
 Smoking1.5840.7874.0550.0444.8741.04322.773
 Wine consumption0.5550.9740.3260.5681.7430.25911.746
 Gender0.1610.8460.0360.8491.1740.2246.161
 Fasting blood glucose 11.1931.0631.2600.2623.2980.41126.501
 Fasting blood glucose 20.9791.0890.8080.3692.6630.31522.524
 Fasting blood glucose 31.3661.0091.8350.1763.9210.54328.311
 Plasma fibrinogen 1−1.0240.9941.0610.3030.3590.0512.521
 Plasma fibrinogen 2−1.1511.0531.1940.2750.3160.0402.492
 Plasma fibrinogen 3−0.8710.9360.8660.3520.4180.0672.620

[i] FIB, fibrinogen; CI, confidence interval; OR, odds ratio; SE, standard error; HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio.

Table X

Effect 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

FactorsBSEWaldP-valueOR valueLower limitUpper limit
Gender0.0330.3610.0090.9261.0340.5092.100
Age0.0310.0144.7960.0291.0321.0031.061
Diabetes0.9460.4155.1860.0232.5741.1415.809
Hypertension0.1850.4040.2100.6471.2030.5452.659
Hyperlipidemia0.5850.3522.7590.0971.7940.9003.576
Smoking0.2650.3460.5860.4441.3030.6622.565
Wine consumption0.2390.4370.3000.5841.2700.5402.990
Systolic blood pressure0.0020.0070.1100.7401.0020.9891.015
Platelet count0.0000.0020.0350.8521.0000.9971.004
International normalized ratio−0.4001.4500.0760.7830.6710.03911.492
Triglyceride−0.1420.1620.7720.3800.8680.6321.191
HDL−0.0060.3450.0000.9850.9940.5051.953
LDL−0.0550.2030.0740.7850.9460.6361.408
HLR−0.7880.6661.4030.2360.4550.1231.676
Glycated hemoglobin0.0090.1280.0050.9461.0090.7851.295
Homocysteine0.0330.0291.2550.2631.0330.9761.094
Fasting blood glucose1.4970.683
Fasting blood glucose 1−0.4800.4701.0400.3080.6190.2461.556
Fasting blood glucose 2−0.2760.4770.3350.5630.7590.2981.932
Fasting blood glucose 3−0.0600.4570.0180.8950.9410.3852.304
Plasma fibrinogen1.9670.579
Plasma fibrinogen 1−0.2690.4150.4210.5160.7640.3391.723
Plasma fibrinogen 2−0.4270.4021.1290.2880.6530.2971.434
Plasma fibrinogen 30.0580.3980.0220.8831.0600.4862.311

[i] HDL, high-density lipoprotein; LDL, low-density lipoprotein; HLR, HDL/LDL ratio; CI, confidence interval; OR, odds ratio; SE, standard error.

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 (810). 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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June 2014
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APA
Chen, Y., Liu, Y., Luo, C., Lu, W., & Su, B. (2014). Analysis of multiple factors involved in acute progressive cerebral infarction and extra‑ and intracranial arterial lesions. Experimental and Therapeutic Medicine, 7, 1495-1505. https://doi.org/10.3892/etm.2014.1624
MLA
Chen, Y., Liu, Y., Luo, C., Lu, W., Su, B."Analysis of multiple factors involved in acute progressive cerebral infarction and extra‑ and intracranial arterial lesions". Experimental and Therapeutic Medicine 7.6 (2014): 1495-1505.
Chicago
Chen, Y., Liu, Y., Luo, C., Lu, W., Su, B."Analysis of multiple factors involved in acute progressive cerebral infarction and extra‑ and intracranial arterial lesions". Experimental and Therapeutic Medicine 7, no. 6 (2014): 1495-1505. https://doi.org/10.3892/etm.2014.1624