Atherosclerotic plaque rupture is the main cause of many cardiovascular diseases, and biomechanical factors play an important role in the process of plaque rupture. In the study of plaque biomechanics, there are relatively few studies based on fatigue fracture failure theory, and most of them mainly focus on the whole fatigue propagation process from crack initiation to plaque rupture, while there are few studies on the influence of crack on plaque rupture at a certain time in the process of fatigue propagation. In this paper, a two-dimensional plaque model with crack was established. Based on the theory of fracture mechanics and combined with the finite element numerical simulation method, the stress intensity factor (SIF) and related influencing factors at the crack tip in the plaque were studied. The SIF was used to measure the influence of crack on plaque rupture. The results show that the existence of crack can lead to local stress concentration, which increases the risk of plaque rupture. The SIF at the crack tip in the plaque was positively correlated with blood pressure, but negatively correlated with fibrous cap thickness and lipid pool stiffness. The effect of the thickness and angle of lipid pool on the SIF at the crack tip in the plaque was less than 4%, which could be ignored. This study provides a theoretical basis for the risk assessment of plaque rupture with cracks.
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
ObjectiveTo summarize the progress on the injury mechanism of vascular endothelial cells in atherosclerosis.MethodsThe latest progress was reviewed in recent literatures.ResultsAll kinds of etiological factors have activated NF-kappa B and cytokines in the development of atherosclerosis, which lead to expression of cell adhesive molecules and adhesion of monocytes to vascular endothelial cells.A variety of inflammatory mediums are released, which can directly damage endothelial cells.Besides, the inflammatory mediums make monocytes and neutrophils attach to endothelial cells by immune mechanisms, which injure the endothelial cells more severely. Meanwhile the damaged membrance structure leads to the production of AECA which activates the complementary system. Then the vascular endothelial cell injury is aggravated and the development of atherosclerosis accelerated. ConclusionIt is very important to recognize the injury mechanism of vascular endothelial cells in the development of atherosclerosis for prevention and treatment of atherosclerosis.
Objective To explore the factors affecting the operation of coronary artery bypass grafting with heart beating and improve the effect of the operation. MethodsFrom January 2012 to June 2016, 898 patients with coronary heart disease who received cardiovascular surgery in the Second Affiliated Hospital of Jilin University were analyzed retrospectively. All patients only underwent coronary artery bypass grafting with beating heart. Among them, 797 patients underwent the off-pump coronary artery bypass grafting (an OPCABG group, 592 males and 205 females, with an average age of 60.5±8.4 years); another 101 patients received on-pump beating heart coronary artery bypass grafting (an OPBH group, 77 males and 24 females, with an average age of 61.5±8.2 years). ResultsThe average number of grafts in the OPCABG group was 3.36±0.74, and in the OPBH group was 3.71±0.69 (P<0.05). The postoperative ventilation time (10.8±9.5 h vs. 20.6±12.3 h), ICU stay (28.8±15.5 h vs. 37.4±30.8 h), hospital stay (10.9±4.8 d vs. 14.8±8.6 d), mortality (1.1% vs. 3.0%), the utilization rate of intra-aortic balloon pump (2.4% vs. 8.9%) and extracorporeal membrane oxygenation (0.5% vs. 5.0%) were significantly different between the OPCABG group and OPBH group (all P<0.05). Twelve patients died after surgery, and the total bloodless operation ratio was 91.3%. ConclusionThe results show that most patients can achieve good results with the help of apical fixation and myocardial fixator, improved surgical techniques and methods, good anesthesia management as well as flexible and accurate use of vasoactive drugs. But extracorporeal circulation is necessary in the patients with large left ventricle, low ejection fraction and hemodynamic instability after intraoperatively moving the heart.
Obesity, sleep disorders, psychological stress, sedentary are modifiable cardiovascular risk factors. There is growing evidence that these risk factors may accelerate the chronic inflammatory process of atherosclerosis and lead to myocardial infarction. Studies on the role of immune cells and their related immune mechanisms in atherosclerosis have shown that the above modifiable risk factors can affect the hematopoiesis of the bone marrow system, affect the production of immune cells and phenotypes, and then affect the progress of atherosclerosis. This review will focus on the effects of modifiable cardiovascular risk factors on the progression of atherosclerosis through the role of the innate immune system.
Objective To review research advances in atherosclerosis of removal mechanisms of apoptotic cells.Method The literatures about the removal mechanisms of the apoptotic cells were reviewed．Results The removal factors of apoptotic cells， such as transglutaminase 2， milk fat globule-EGF-factor 8， complement system，c-Mer proto-oncogene tyrosine protein kinase，and Fas，might cause the lipid core of the atherosclerotic plaque if one of them was defective phagocytic clearance．Conclusion How to remove the surplus of the phagocytosis and study the common pathways of the downstream signal of its receptor were the future direction of development．
In June 2022, the American Lipid Society released "NLA scientific statement on statin intolerance: a new definition and key considerations for ASCVD risk reduction in the statin intolerant patient", which provides the latest definition, modifiable factors, and treatment strategies of statin intolerance. According to the guidelines, for statin intolerance, the statin medication regimen should be adjusted first (reducing the dose, switching to another statin, reducing the frequency of medication), and if the patient is still intolerant, non-statin drugs should be considered to reduce the risk of ASCVD in the patient. The interpretation of this guideline will help clinicians and researchers identify, manage and intervene in the statin intolerance syndrome.
【Abstract】ObjectiveTo investigate the effects of CO2 pneumoperitoneum on blood flow of carotid arteries in atherosclerosis rabbits.MethodsFifty Japan white rabbits were randomly divided into control group and three atherosclerosis groups. In atherosclerosis group, the rabbits were randomly subjected to CO2 pneumoperitoneum with an intraabdominal pressure of 0 mm Hg, 10 mm Hg or 15 mm Hg for 2 hours, after the model were created by feeding the rabbits with high fatty diet. The blood flow of the common carotid arteries were measured by electromagnetic blood flowmeter. Artery blood samples were collected for blood gas analysis at 30 minute intervals. ResultsHigher insufflation pressures and longer duration of CO2 pneumoperitoneum were associated with greater increase in blood flow of common carotid arteries. Compared with those in control group and atherosclerosis group with 0 mm Hg CO2 pneumoperitoneum, there were statistically significant increases in blood flow of the common carotid arteries during CO2 pneumoperitoneum in 10 mm Hg and 15 mm Hg pneumoperitoneum group, the changes in 15 mm Hg pneumoperitoneum group were more significant than those in 10 mm Hg pneumoperitoneum group (Plt;0.05). When compared with the blood flow before insufflation, those in 10 mm Hg and 15 mm Hg pneumoperitoneum group also increased significantly during CO2 pneumoperitoneum, even at 30 minute after desufflation (Plt;0.05). However, those in control group and 0 mm Hg pneumoperitoneum group did not change significantly (Pgt;0.05). There were significant decrease in pH and significant increase in PCO2 in both 10 mm Hg and 15 mm Hg groups, when compared with presufflation values or those in control group and 0 mm Hg pneumoperitoneum group(Plt;0.05). The changes in pH and PCO2, however, were no significant at any time point in control group and 0 mm Hg pneumoperitoneum group (Pgt;0.05). HCO3- did not change significantly in either group(Pgt;0.05).ConclusionUnder atherosclerosis conditions, CO2 pneumoperitoneum has an adverse influence on the blood flow of the common carotid arteries which may be associated with increased intrabdominal pressure,absorbed CO2 gas.
Objective To investigate the effectiveness of percutaneous transluminal renal artery stenting (PTRAS) in treating atherosclerotic renal artery stenosis (ARAS). Methods A total of 69 patients with severe ARAS were treated with PTRAS between January 2002 and December 2008. There were 47 males and 22 females with an average age of 66.2 years(range, 42-88 years), including 66 cases of unilateral ARAS (single functional kidney, 1 case) and 3 cases of bilateral ARAS. Renal angiography revealed that the degree of renal artery stenosis was 70%-99%. Concomitant diseases included hypertension (67 cases), atherosclerosis obl iterans (69 cases), coronary heart disease (34 cases), diabetes (44 cases), and hyperl ipidemia (36 cases). Blood pressure, serum creatinine (sCr), and patency of the renal artery were measured to assess the effectiveness of PTRAS after 12 months. Results The renal artery stent was successfully implanted in 68 patients and the technical success rate was 98.6%. One patient was converted to il io-renal bypass because of intra-operative acute renal artery occlusion. One patient died of heart failure at 6 months after PTRAS, and 1 patient was lost at 3 months after PTRAS. The other 66 patients were followed up 32 months on average (range, 13-60 months). The blood pressure decreased significantly at 1 month and gained a further decrease at 12 months after PTRAS when compared with the preoperative ones [systol ic blood pressure: (132 ± 24) mm Hg vs (163 ± 34) mm Hg, P lt; 0.05; diastol ic blood pressure: (78 ± 11) mm Hg vs (89 ± 17) mm Hg, P lt; 0.05; 1 mm Hg=0.133 kPa]. Hypertension was cured in 4 cases (6.3%), improved in 52 cases (81.2%), failure in 8 cases (12.5%), and the overall benefit rate was87.5%. The sCr level was stable after 12 months of PTRAS, showing no significant difference when compared with preoperative basel ine [(107.8 ± 35.4) μmol/L vs (104.1 ± 33.8) μmol/L, P gt; 0.05]. Renal function was improved in 9 cases (13.6%), stable in 48 cases (72.8%), deterioration in 9 cases (13.6%), and the overall benefit rate was 86.4%. Instent restenosis found in 2 patients (3.0%) at 12 months after operation. Conclusion PTRAS is a safe and effective method to treat ARAS. It can control the blood pressure and stabil ize the renal function in most ARAS patients. Long-term efficacy needs further investigation.