A total of 116 patients with cerebral infarction were selected (32–74 years old; 78 males, 38 females). The patients had been hospitalized between August 2005 and December 2008 in the Neurology Department of Baotou Central Hospital, Inner Mongolia Autonomous Region, China. All patients had symptoms and signs of nervous system alterations such as hemiplegia or aphasia, confirmed by brain CT or MRI. The levels of muscle strength were graded between 0 and 4. Of the 116 patients, 59 had hypertension, 29 had hyperlipidemia, 36 had diabetes and 43 had hyperhomocysteinemia. The heart valves, heart cavity with or without mural thrombus, ascending aorta, aortic arch and descending aorta of all patients were assessed using transesophageal ultrasound. CAPs were examined using color Doppler ultrasound, and intracranial hemodynamics were determined by TCD ultrasound. The exclusion criteria were as follows: i) history of heart disease, heart valve disease and intracardiac mural thrombus; ii) moyamoya disease, Takayasu’s arteritis and embolism; iii) intracranial vascular stenosis examined by TCD ultrasound; iv) massive cerebral infarction; and v) blood system diseases. This study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of Baotou Central Hospital. All patients provided written informed consent.

A lacunar cerebral infarction has an infarct diameter of ≤15 mm. Small/medium-sized areas of infarction refer to an infarct between the lacunar cerebral and large cerebral infarction. Multiple cerebral infarctions referred to multiple ischemic infarct in brain. In total, lacunar cerebral infarctions were identified in the basal ganglia in 48 cases and in the pontine area in 10 cases; small/medium-sized areas of infarction were noted in 5 cases in the temporal lobe, 12 in the parietal lobe, 7 in the frontal lobe and 2 in the cerebellum; and 32 cases had multiple cerebral infarctions in the basal ganglia, temporal lobe, parietal lobe and cerebellum. Of the 32 cases of multiple cerebral infarctions, 20 were acute multiple cerebral infarctions, confirmed by NMR diffusion imaging.

All patients diagnosed by a neurologist were examined with TCD, color Doppler ultrasound and TEE using a GE Vivid3 dual-function color ultrasound diagnostic apparatus (GE Instruments Inc., Aurora, OH, USA) with a 3.5 MHz esophageal probe.

The following criteria were used for AAP grading: normal, the aortic inner wall was smooth and complete; mild, <1.0 mm of mildly thickened intima; moderate, 1.0–3.9 mm of moderately thickened intima; and severe, ≥4 mm of irregular or active atherosclerotic plaque was prominent in the lumen.

Statistical significance was determined using the χ² test for χ-list data using SPSS software version 12.0 (SPSS, Inc., Chicago, IL, USA). P<0.05 was considered to indicate a statistically significant difference.

AAP lesions were observed in 70 cases of cerebral infarction (Table I). Plaques in the ascending aorta, aortic arch and descending aorta accounted for 5.7% (n=4), 77.1% (n=54) and 17.1% (n=12) of the 70 AAP cases, respectively. The degree of severity of the atherosclerotic plaques differed between the sites. The atherosclerotic plaques in the four ascending aorta cases were graded as moderate. In the aortic arch, mild, moderate and severe changes to the aortic plaques were observed in 10, 24 and 20 cases, respectively, whereas mild, moderate and severe changes to aortic plaques in the descending aorta were observed in 4, 6 and 2 cases, respectively. Moderate/severe atherosclerotic changes were detected in 48.3% of the patients with cerebral infarction.

Of all cases, CAPs and unstable plaques accounted for 55.2% (64/116) and 39.7% (46/116), respectively. Bilateral unstable plaques were observed in 28 cases, bilateral stable plaques in 10, unilateral unstable plaques in 18 and unilateral stable plaques in 8.

The TCD ultrasound examination did not identify any changes in the patients that were sufficient for diagnosis as vascular stenosis.

Of the 70 cases of AAP, 64 were accompanied by CAP. Of the 56 cases with moderate/severe AAP, 42 cases were accompanied by unstable CAP, and 14 cases were accompanied by stable CAP. Of the 14 cases with mild AAP, 8 cases were accompanied by CAP, including 4 cases with stable plaque and 4 cases with unstable plaque.

Of the patients with cerebral infarction, lacunar cerebral infarction, multiple cerebral infarction and small/medium areas of infarction were observed in 58, 32 and 26 cases, respectively.

Mild, moderate and severe AAP in patients with lacunar cerebral infarction were observed in 8, 8 and 5 cases, respectively; in patients with multiple cerebral infarctions they were observed in 4, 14 and 6 cases, respectively, and in patients with a small/medium area of infarction, they were observed in 2, 12 and 11 cases, respectively. The results of statistical analysis by χ² test revealed that the difference in the incidence of various types of infarction between APP severity levels was significant (χ²=39.52, P<0.01; Table II). With normal or mild AAP, the incidence of lacunar cerebral infarction was higher than that of small/medium area infarction. The incidence of small/medium area infarction in patients with moderate/severe AAP was higher than in those with mild or normal AAP.

Stable and unstable CAPs in patients with lacunar cerebral infarctions were observed in 12 and 6 cases, respectively. Stable and unstable CAPs in patients with multiple cerebral infarctions were observed in 4 and 20 cases, respectively. Stable and unstable CAPs in patients with small/medium area of infarctions were observed in 2 and 20 cases, respectively. The results of statistical analysis by χ² test revealed that the difference in the incidence of various types of infarction between the two CAP stability levels was significant (χ²=43.47, P<0.01; Table III). The incidence of embolic cerebral infarction in patients with unstable CAP is higher than in those with stable CAP.