Fetal congenital heart diseases: Diagnosis by anatomical scans, echocardiography and genetic tests.

Objective: To determine the distribution of major fetal congenital heart diseases (CHDs) diagnosed antenatally during routine second-trimester obstetric anatomical scans in an unselected population at a single tertiary centre and to characterise and stratify risk factors, genetic diagnosis and long-term health at 4 years old. Method: A single-centre cohort study of all major fetal CHDs detected on routine obstetric fetal anatomical ultrasound scans between January 2014 and December 2017 was performed in an unselected population. Demographic details, fetal echocardiogram reports, genetic test results, delivery outcomes and postnatal progress were stratified by CHD subtype. Results: Of 20,031 screened pregnancies, 109 pregnancies (0.53%) had major fetal CHDs. The most common subtypes were coarctation of aorta (17.4%), transposition of great arteries (16.5%), and tetralogy of Fallot and univentricular hearts (13.8% each). Of the 60.5% that underwent confirmatory genetic testing-mostly conventional karyotyping and testing for 22q11 microdeletion-about a quarter had abnormalities, of which 22q microdeletion was the most common. We had complete obstetric data in 85 pregnancies (78%), of which 76.5% progressed to live birth. Among these, 92.1% of postnatal echocardiograms concurred with antenatal ones. At 4 years old, 43.2% of offspring had no medical or developmental issues, 20.0% had mild medical or developmental issues, 21.5% had major medical or developmental issues, and 12.3% had deceased. Conclusion: Fetal echocardiograms accurately diagnose CHDs. Future studies should evaluate the roles of chromosomal microarray and next-generation sequencing in diagnosing CHD.

Long-term survival after immunotherapy and targeted therapy without chemotherapy in an elderly patient with HER2-positive gastroesophageal junction cancer: A case report.

A 74-yr-old man underwent thoracic laparoscopy combined with radical gastrectomy, and the postoperative pathological diagnosis was esophageal and gastric cardia cancer pT3N1M0, pStage IIB. Immunohistochemical staining for HER2 (3+) and PD-L1 (<5%) was positive. Adjuvant chemotherapy was not performed because the patient developed severe thrombocytopenia (platelet counts <30 × 109/L), which was never cured throughout the reporting period. At 10.7 months post-surgery, he suffered metastases in multiple organs, including the peritoneum, liver, lung, and bone. Following two cycles of first-line trastuzumab and pembrolizumab (200 mg), he developed immune-related myositis (G2), myocarditis (G2), and hepatitis (G1). Therefore, pembrolizumab was discontinued. Trastuzumab was administered as a monotherapy; meanwhile, adoptive cytokine-induced killer (CIK) cell infusions were initiated. Eight months after the initial immunotherapy, a solitary brain metastasis was detected, and the patient underwent CyberKnife radiosurgery. For second-line therapy, adoptive CIK cell immunotherapy plus trastuzumab was still used. At the time of reporting, the patient had achieved a complete response (CR) in the brain and liver and a partial response (PR) in the ilium, and he had been followed-up for 36.6 months, much longer than the median survival time for patients with advanced GEJ cancer. We suggest that HER2-targeted therapy and immunotherapy with pembrolizumab or CIK adoptive cell infusions prolonged the overall survival of an elderly patient with HER2-positive GEJ cancer with multiple metastases.

A difficult-to-diagnose pericardial fistula.

Pericardial fistula is a rare complication. Generally, the diagnosis can be confirmed by imaging examination, but our patient was an exception. We present a 71-year-old female patient that complained of remnant gastric cancer for five months and dyspnea for seven days; the dyspnea became aggravated during the last two days. After admission, emergency thoracic computed tomography and echocardiography showed pericardial effusion, and pericardiocentesis was performed. After conventional treatment, the pericardial effusion was unchanged and no cancer cells were found in the pericardial drainage. However, the color changed from turbid to golden yellow and, finally, to green. After 20 days of repeated laboratory, imaging, and gastrointestinal contrast examinations, no cause was found. Moreover, a clinical diagnosis could not be obtained following numerous comprehensive clinical analyses. Given the color change of the pericardial drainage, we strongly suspected pericardial fistula, but the imaging examinations were negative. Finally, a methylene blue test confirmed the existence of a pericardial fistula. When the color of the pericardial effusion changes, the existence of a pericardial fistula must be considered in advance, and other methods should be evaluated if imaging cannot assist in the diagnosis.

MMP-10 rs17435959 Polymorphism is Associated with the Formation and Stability of Carotid Atherosclerosis Plaque: A Case-Control Study.

BACKGROUND: Matrix metalloproteinase 10 (MMP-10) has a close relationship with carotid atherosclerosis (CAS) and cerebral infarction. The MMP-10 rs17435959 polymorphism causes a leucine to valine transition at codon 4 in exon 1 of the MMP-10 gene and may have functional effects. OBJECTIVES: To investigate the relationship between the MMP-10 rs17435959 polymorphism and the formation and stability of CAS plaques. MATERIALS AND METHODS: The present case-control study contains 738 visitors who came to our health examination center for the first time. According to the carotid ultrasound examinations, visitors were classified into the vulnerable plaque group (41-86 years old, 141 male, 105 female), the stable plaque group (41-86 years old, 141 male, 105 female) and the no plaque group (41-85 years old, 141 male, 105 female). All visitors in the three groups were sex- and- age-matched, and cardiovascular and cerebrovascular diseases were absent. The polymorphism was genotyped by real-time polymerase chain reaction- restriction. RESULTS: Compared to the GG genotype, the frequency of the CC and CG genotypes was significantly more common in the vulnerable plaque group than in the no plaque group (18.7% vs. 7.7%, unadjusted P = 0.002). Moreover, compared to the G allele, the frequency of the C allele was significantly more common in the vulnerable plaque group than in the no plaque group (10.4% vs. 3.9%, unadjusted P = 0.000) and in the vulnerable plaque group than in the stable plaque group (10.4% vs. 5.1%, unadjusted P = 0.008). Binary logistic regression showed that the CC and CG genotype was independent risk factor for the formation (P = 0.019, OR = 1.961, 95% CI [1.117, 3.444]) and vulnerability (P = 0.035, OR = 1.842, 95% CI [1.045, 3.247]) of CAS plaques. Moreover, individuals who have the C allele showed a higher level of fibrinogen, which was an independent risk factor for the formation of CAS plaques (P = 0.000, OR = 2.425, 95% CI [1.475, 3.985]). CONCLUSIONS: The rs17435959 polymorphism was associated with the formation and vulnerability of CAS plaques. Individuals who had variant-type MMP-10 showed higher levels of fibrinogen, which promoted the formation of CAS plaques.

Transmission of wireless signals using space division multiplexing in few mode fibers.

Evolution of next generation wireless networks brings challenges to efficiently transmit a large amount of data from a base station to a remote antenna unit. We investigate a space division multiplexing technique that employs few mode fibers (FMFs) to transmit 3 × 3 MIMO wireless signals, aiming to employ a common digital signal processing (DSP) unit to equalize both the fiber and wireless channel. We optimize system parameters and obtain above 28 dB and 23 dB signal-to-interference and noise ratio (SINR) for 3 meters wireless systems with 500 m and 2 km FMF, which correspond to the transmission capacity of 578 Mb/s and 468 Mb/s using a 20 MHz bandwidth, respectively. Moreover, we analyze that the nonlinear spectrum distortion due to the combined effect of nonlinearity in the directly modulated laser and the differential mode delay in multimode fibers and validate it by simulations.

Voltage-gated potassium channel blocker 4-aminopyridine induces glioma cell apoptosis by reducing expression of microRNA-10b-5p.

Accumulating evidence has demonstrated that voltage-gated potassium channels (Kv channels) were associated with regulating cell proliferation and apoptosis in tumor cells. Our previous study proved that the Kv channel blocker 4-aminopyridine (4-AP) could inhibit cell proliferation and induce apoptosis in glioma. However, the precise mechanisms were not clear yet. MicroRNAs (miRNAs) are small noncoding RNAs that act as key mediators in the progression of tumor, so the aim of this study was to investigate the role of miRNAs in the apoptosis-promoting effect of 4-AP in glioma cells. Using a microRNA array, we found that 4-AP altered the miRNA expression in glioma cells, and the down-regulation of miR-10b-5p induced by 4-AP was verified by real-time PCR. Transfection of miR-10b-5p mimic significantly inhibited 4-AP-induced caspases activation and apoptosis. Moreover, we verified that apoptosis-related molecule Apaf-1 was the direct target of miR-10b-5p. Furthermore, miR-10b-5p mimic significantly inhibited 4-AP-induced up-regulation of Apaf-1 and its downstream apoptosis-related proteins, such as cleaved caspase-3. In conclusion, Kv channel blocker 4-AP may exert its anti-tumor effect by down-regulating the expression of miR-10b-5p and then raised expression of Apaf-1 and its downstream apoptosis-related proteins. Current data provide evidence that miRNAs play important roles in Kv channels-mediated cell proliferation and apoptosis.

Serum levels of galectin-1, galectin-3, and galectin-9 are associated with large artery atherosclerotic stroke.

The aim of this study was to assess the expression patterns of serum galectin-1 (Gal-1), galectin-3 (Gal-3), galectin-9 (Gal-9), and galectin-3 binding protein (Gal-3BP) and their associations with stroke outcome in large artery atherosclerotic (LAA) stroke. The serum levels of Gal-1, Gal-3, Gal-9, and Gal-3BP were measured by ELISA in 130 patients with LAA stroke and 130 age- and sex-matched controls. Serum samples were collected from the patients on day 1, day 6, and in the 4th week after ischaemic stroke (IS). An unfavourable outcome was defined as a modified Rankin Scale score of >2 on day 90 after IS. Our results indicated that the Gal-3 and Gal-9 levels were higher in patients with LAA stroke than in controls. A higher Gal-3 level was independently associated with an unfavourable outcome both on day 1 and day 6 after IS. In addition, Gal-9 and Gal-1 levels were upregulated on day 6 and in the 4th week after IS, respectively. For Gal-3BP, no difference was detected between patients and controls and no predictive value was found in patients. In conclusion, these findings suggest that the serum levels of Gal-1, Gal-3, and Gal-9 may be associated with LAA stroke.

Grafting of mesenchymal stem cell-seeded small intestinal submucosa to repair the deep partial-thickness burns.

PURPOSE: Regenerative medicine provides many treatments for burn wounds, of which cell-seeded substitutes are encouraging for large and deep burns. To assess the feasibility of mesenchymal stem cell (MSC)-seeded small intestinal submucosa (SIS) to repair the deep partial-thickness burns, a rat study was performed. MATERIALS & METHODS: The burn model was created by contacting the dorsal surface directly with boiled water for 10 seconds. MSCs at passage 3 were seeded on the SIS before implantation. Three days after burn injury, the grafts were implanted onto the burn area. At 3, 7, 14 and 21 days post implantation, gross observation and histological assessments were performed. RESULTS: SIS alone and MSC-seeded SIS were able to accelerate the burn wound closure by enhancing granulation tissue formation, increasing wound maturity, improving revascularization, and inducing the proliferation of neo-epidermal cells. Additionally, MSC-seeded SIS was much more effective than SIS alone for the repair of deep partial-thickness burns. CONCLUSION: Both SIS and MSC-seeded SIS were able to repair the large and deep burn wounds and the loaded MSCs possessed positive effects to accelerate the wound closure in a rat model.

Anti-atherosclerotic potential of baicalin mediated by promoting cholesterol efflux from macrophages via the PPARγ-LXRα-ABCA1/ABCG1 pathway.

BACKGROUND: Atherosclerosis (AS) is associated with severe cardiovascular disease. The anti-inflammatory, anti-oxidation, and lipid regulating properties of baicalin suggest potential as an anti-atherosclerotic agent. We therefore investigated whether baicalin can protect against the development of atherosclerosis in an AS rabbit model and explored the underling mechanisms in THP-1 macrophages. METHODS AND RESULTS: In vivo, treatment with baicalin markedly decreased atherosclerotic lesion sizes and lipid accumulation in AS rabbit carotid arteries. Western blotting revealed that the protein expression levels of both peroxisome proliferator-activated receptor gamma (PPARγ) and liver X receptor alpha (LXRα) were up-regulated in the baicalin group compared with the model group. In vitro, baicalin restricted oxidized-low density lipoprotein (ox-LDL)-induced intracellular lipid accumulation and foam cell formation in THP-1 macrophages. Molecular data showed that baicalin significantly increased the expression levels of PPARγ, LXRα, ATP binding cassette transporters (ABC) A1 and ABCG1. Cell transfection experiments (including PPARγ and LXRα siRNAs) suggested that the effects of baicalin are mediated by the PPARγ-LXRα signalling pathway, which stimulates the expression of ABCA1 and ABCG1. CONCLUSION: These results suggest that baicalin potentially exerts anti-atherosclerosis effects, possibly through the PPARγ-LXRα-ABCA1/ABCG1 pathway, by promoting efflux of cholesterol from macrophages and delaying the formation of foam cells.

Preliminary study of brain glucose metabolism changes in patients with lung cancer of different histological types.

BACKGROUND: Cerebral glucose metabolism changes are always observed in patients suffering from malignant tumors. This preliminary study aimed to investigate the brain glucose metabolism changes in patients with lung cancer of different histological types. METHODS: One hundred and twenty patients with primary untreated lung cancer, who visited People's Hospital of Zhengzhou University from February 2012 to July 2013, were divided into three groups based on histological types confirmed by biopsy or surgical pathology, which included adenocarcinoma (52 cases), squamous cell carcinoma (43 cases), and small-cell carcinoma (25 cases). The whole body 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/computed tomography (CT) of these cases was retrospectively studied. The brain PET data of three groups were analyzed individually using statistical parametric maps (SPM) software, with 50 age-matched and gender-matched healthy controls for comparison. RESULTS: The brain resting glucose metabolism in all three lung cancer groups showed regional cerebral metabolic reduction. The hypo-metabolic cerebral regions were mainly distributed at the left superior and middle frontal, bilateral superior and middle temporal and inferior and middle temporal gyrus. Besides, the hypo-metabolic regions were also found in the right inferior parietal lobule and hippocampus in the small-cell carcinoma group. The area of the total hypo-metabolic cerebral regions in the small-cell carcinoma group (total voxel value 3255) was larger than those in the adenocarcinoma group (total voxel value 1217) and squamous cell carcinoma group (total voxel value 1292). CONCLUSIONS: The brain resting glucose metabolism in patients with lung cancer shows regional cerebral metabolic reduction and the brain hypo-metabolic changes are related to the histological types of lung cancer.

Celastrol may have an anti-atherosclerosis effect in a rabbit experimental carotid atherosclerosis model.

BACKGROUND: Celastrol may have an anti-atherosclerosis effect. This study aimed to investigate if celastrol had an anti-AS effect using a rabbit experimental carotid atherosclerosis model. METHODS: Forty male Japanese white rabbits were divided into the sham group (normal diet), the model group (high fat diet), the group treated with celastrol (high fat diet) and the group treated with atorvastatin (high fat diet) randomly. The rabbits fed a high fat diet underwent balloon injury of the right common carotid artery and were treated with dimethyl sulfoxide (DMSO) (the model group, 3.5 ml/kg/d), celastrol and its dissolvent DMSO (the celastrol group, 1 mg/kg/d and 3.5 ml/kg/d) and atorvastatin and its dissolvent DMSO (the atorvastatin group, 2.5 mg/kg/d and 3.5 ml/kg/d) for 12 weeks by gavage. RESULTS: The ratio of the plaque area and the arterial wall cross-section area in the celastrol group was significantly less than the model group (P < 0.001), and there was no significant difference compared with the atorvastatin group. The serum level of LDL-C of the celastrol group was significantly lower than the model group (P = 0.014), and there was no significant difference compared with the atorvastatin group. The expression of VEGF in the celastrol group was significantly less compared with the model group (P = 0.014), whereas the expression of VEGF in the atorvastatin group and the model group showed no significant differences. CONCLUSION: Our findings suggest that celastrol effectively reduced the plaque ratio, decreased the serum levels of LDL and downregulated the expression of VEGF, suggesting an anti-AS effect of celastrol.

Positive association of MMP 14 gene polymorphism with vulnerable carotid plaque formation in a Han Chinese population.

BACKGROUND: MMP 14 is expressed in atherosclerotic plaques and potentially plays an important role in the development of vulnerable carotid plaques. MMP 14 gene polymorphisms can influence the bioactivity or expression of MMP 14. OBJECTIVE: The aim of this study was to investigate the association between MMP 14 position + 7096 T > C (NM_004995.2:c.855T> C, rs2236307) polymorphism and vulnerable carotid plaque formation. METHODS: 1370 patients with ischemic cerebral infarctions were enrolled and divided into three groups according to their carotid ultrasound examination: No plaque group (n = 346), stable plaque group (n = 695) and vulnerable plaque group (n = 329). The traditional atherosclerosis risk factors were recorded, and the MMP 14 polymorphism were genotyped by Applied Biosystems 7300 Real-Time PCR System using the TaqMan assay. RESULTS: In the multiple logistic regression analysis done among the sub-groups, compared to no carotid plaque group, individuals with the MMP 14 position + 7096 TC+ CC genotype showed a significantly (p = 0.009) lower risk for vulnerable plaque (AOR = 0.675; 95% CI, 0.568-0.922) formation compared with subjects of the TT genotype; however, no relation between TC+ CC genotype and stable carotid plaque was observed (p > 0.125). Age was a risk factor for both stable plaque (p = 0.000; AOR = 3.732; 95% CI: 2.496-5.58) and vulnerable plaque formation (p = 0.001; AOR = 2.234; 95% CI: 1.387-3.597). Meanwhile, fibrinogen (> 4.0 g/L) was a risk factor for stable plaque (p = 0.004; AOR = 2.313; 95% CI: 1.308-4.091). CONCLUSIONS: The MMP 14 position + 7096 TC+ CC genotype might lower the risk of vulnerable carotid plaque formation. Fibrinogen (> 4.0 g/L) was a risk factor for stable plaque.

Inhibition of metastasis and invasion of ovarian cancer cells by crude polysaccharides from rosa roxburghii tratt in vitro.

BACKGROUND: Rosa Roxburghii Tratt is a promising wild fruit crop in Southwest China. Its extracts have been used as traditional Chinese medicine, which benefit immune responses and cure various health disorders. However, whether Rosa Roxburghii Tratt polysaccharides could inhibit metastasis and invasion of ovarian cancer cells remains unknown. MATERIALS AND METHODS: Effects of crude polysaccharides from Rosa Roxburghii Tratt on the viability of ovarian cancer A2780 cells were detected by MTT assay. Ovarian carcinoma cell migration and invasion after exposure to Rosa Roxburghii Tratt polysaccharides were quantified by wound healing and Transwell assays, respectively. Western blotting was applied to assess protein levels of MMP-9. RESULTS: The results indicated that Rosa Roxburghii Tratt polysaccharides significantly reduced wound closure rate of A2780 cells, inhibited their migration and invasion, and suppressed the expression of MMP-9. CONCLUSIONS: Our findings indicated that Rosa Roxburghii Tratt polysaccharides have potential for develop as anti-metastatic cancer drug preparations for ovarian cancer patients.

[Association between matrix metalloproteinase-10 gene polymorphisms and instability of carotid plaque].

OBJECTIVE: To assess the association between 2 single nucleotide polymorphisms (SNPs) located in exonic regions of matrix metalloproteinase-10 (MMP-10) gene and instability of carotid plaques in a Han Chinese population. METHODS: Five hundred and eighty-five patients were divided into carotid vulnerable plaque group (n=206) and stable plaque group (n=379) based on results of carotid B-mode ultrasonography. The SNPs were genotyped by real-time polymerase chain reaction using an ABI 7300 TaqMan platform. RESULTS: The distribution of rs17435959 between the two groups was significantly different at both genotypic (GC+CC vs. GG, P=0.006, OR=2.012) and allelic levels (C vs. G, P=0.001,OR=2.160). Above differences have remained significant with binary logistic regression analysis (P=0.007, OR=2.022; P=0.002, OR=2.104). The minor allele frequency of rs17293607 was 0.56%. CONCLUSION: Above findings suggested that rs17435959 of the MMP-10 gene is associated with carotid vulnerable plaque in ethnic Chinese Hans. The C allele may be a susceptible predictor for carotid vulnerable plaque.

Matrix metalloproteinase 10 gene polymorphism and atherothrombotic cerebral infarction risk in a Han Chinese population.

BACKGROUND: Matrix metalloproteinase 10 (MMP10) plays an important role in ischemic stroke and has a close relationship with some stroke risk factors. The aim of this study was to investigate the relationship between two single nucleotide polymorphisms (SNP) in the exon regions of the MMP10 gene and atherothrombotic cerebral infarction risk. METHODS: Five hundred and thirty-seven hospital-based patients who had suffered first atherothrombotic cerebral infarction and 580 unrelated healthy controls were enrolled. Demographic and clinical features of the subjects were recorded, and two polymorphisms, rs17435959 (G>C), rs17293607 (C>T) were chosen to be genotyped by real-time polymerase chain reaction-restriction TaqMan probes using the ABI 7300 TaqMan platform. RESULTS: There were several clinical parameters, such as blood pressure, fasting blood glucose, total cholesterol, homocysteine, as well as carotid plaque and smoking, but not average age and sex ratios that showed significant differences between patients and control subjects. For rs17435959, there was no significant difference between the ischemic stroke group and the healthy control group in genotype frequency (OR=1.295, P=0.187, 95% CI (0.882-1.899)) or allele frequency (OR=1.267, P=0.202, 95% CI (0.881-1.823)). Moreover, in smoking, none smoking, having carotid plaque, no carotid plaque, male or female subtypes, there was significant difference between patients and control subjects in genotype frequencies or allele frequencies. The minor allele frequency of rs17293607 was 0.92%, prohibiting further study of this allele. CONCLUSIONS: These findings suggest that the rs17435959 SNP may not associated with atherothrombotic cerebral infarction risk. We also found that rs17293607 is not polymorphic in our study population.

[Association between matrix metalloproteinase-8 -799C/T polymorphism and instability of carotid plaque].

OBJECTIVE: To investigate the association between a -799C/T polymorphism in the promotor region of matrix metalloproteinase-8 (MMP-8) gene and instability of carotid plaque in Chinese Han population. METHODS: A total of 451 acute infarction patients from the Department of Neurology of Taizhou Hospital were divided into carotid vulnerable plaque group and carotid stable plaque group according to the results of carotid B-mode ultrasonography. Serum MMP -8 level was measured by the means of enzyme-linked immunosorbent assay (ELISA). At the same time, the MMP-8 -799C/T polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: Serum level of MMP-8 in the carotid vulnerable plaque group was higher than that in the carotid stable plaque group (t= 2.894, P= 0.004). The genotype distribution of -799C/T polymorphism between the two groups was significantly different (Chi-square = 13.65, P= 0.000). Serum level of MMP-8 in patients with TT genotype was higher than that in patients with CC genotype (t= 3.141, P= 0.001). CONCLUSION: The present study suggested that serum level of MMP-8 and the -799C/T polymorphism of MMP-8 gene are associated with carotid vulnerable plaque in Chinese Han population, and the T allele may be a predictor for the susceptibility of carotid vulnerable plaque.

Association of a functional polymorphism in the MMP7 gene promoter with susceptibility to vulnerable carotid plaque in a Han Chinese population.

BACKGROUND: Matrix metalloproteinase-7 (MMP-7) may play an important role in the development of vulnerable carotid plaque. An A-to-G transition (-181A/G) in the promoter region of MMP7 is functional in vitro by altering the transcriptional activity of the gene. The aim of this study was to investigate the association between the MMP7 -181A/G polymorphism and vulnerable carotid plaque formation. METHODS: The authors enrolled 641 patients and divided them into three groups according to the carotid ultrasound examination: vulnerable plaque group (n=118), stable plaque group (n=385) and no plaque group (n=138). Traditional atherosclerosis risk factors were recorded and the MMP7 -181A/G polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: In the multinomial logistic regression analysis, compared to the no plaque group, no relationship between MMP7 -181AG+GG genotypes and stable carotid plaque was observed [odds ratio (OR) 1.50; p=0.239]. However, the frequency of AG+GG genotypes was significantly higher in the vulnerable plaque group (OR 2.74; p=0.008). Age was a risk factor for plaque formation, while statin treatment can reduce the prevalence of atherosclerotic plaque. Additionally, using binary logistic regression analysis between the stable and vulnerable plaque groups, this MMP7 polymorphism was associated with vulnerable plaque independently of other factors [OR 1.83; 95% confidence interval 1.08- 3.11; p=0.026]. CONCLUSIONS: The MMP7 -181A/G polymorphism is associated with the development of vulnerable carotid plaques. Age is a risk factor for plaque formation, while statin therapy is associated with a decreased prevalence of carotid atheromatous plaques.