Liraglutide downregulates hepatic LDL receptor and PCSK9 expression in HepG2 cells and db/db mice through a HNF-1a dependent mechanism.

BACKGROUND: Proprotein convertase subtilisin/kexin type 9 (PCSK9), a major regulator of cholesterol homeostasis, is associated with glucose metabolism. Liraglutide, a glucagon-like peptide-1 receptor agonist, can increase insulin secretion in a glucose-dependent manner and lower blood glucose. We aimed to investigate the relationship between liraglutide and PCSK9. METHODS: At the cellular level, the expressions of PCSK9 and hepatocyte nuclear factor 1 alpha (HNF1α) protein in HepG2 cells stimulated by liraglutide was examined using Western blot. Seven-week old db/db mice and wild type (WT) mice were administered either liraglutide (200 µg/kg) or equivoluminal saline subcutaneously, twice daily for 7 weeks. Fasting glucose level, food intake and body weight were measured every week. After the 7-week treatment, the blood was collected for lipid and PCSK9 levels detection and the liver was removed from the mice for oil red O staining, immunohistochemical analysis, immunofluorescence test and Western bolt. RESULTS: Firstly, liraglutide suppressed both PCSK9 and HNF1α expression in HepG2 cells in a time and concentration dependent manner. Secondly, liraglutide induced weight loss in WT and db/db mice, decreased serum PCSK9, glucose and lipid levels and improved hepatic accumulation in db/db but not WT mice. Thirdly, liraglutide reduced both hepatic PCSK9 and low-density lipoprotein receptor (LDLR) expression with a decrease in HNF1α in db/db mice but not in WT mice. CONCLUSIONS: Liraglutide suppressed PCSK9 expression through HNF1α-dependent mechanism in HepG2 cells and db/db mice, and decreased LDLR possibly via PCSK9-independent pathways in db/db mice.

Electrocardiogram in patients with acute inferior myocardial infarction due to occlusion of circumflex artery.

To investigate the diagnostic value of electrocardiographic (ECG) ST-segment in acute inferior myocardial infarction (AIMI) caused by the left circumflex branch (LCX).A total of 240 clinical cases with AIMI in our hospital were retrospectively analyzed. All of them had received percutaneous coronary intervention (PCI) within 12 hours after symptom onset. The clinical features, ECG manifestations, and coronary artery lesion characteristics of the patients were collected.The right coronary artery (RCA) was shown to be the infarct-related artery (IRA) in 177 patients, while LCX was responsible for AIMI in 63 cases. There was no significant difference in the risk factors of coronary heart disease (CHD) (P > .05 for all) between the 2 groups. ST-segment elevation in lead II, III, and AVF could be found in all patients. Moreover, ST-segment depression in lead I (STD I), ST-segment elevation in lead III (STE III), STE III-STE II, STE AVF, STD AVL, STD AVL-STD I and STE v6 lead ST-segment deviation exhibited significant difference in 2 groups (P < .05 for all). The changes of STD I, STE III < STEII, STD AVL < STD I could discriminate between LCX and RCA in AIMI patients with high sensitivity and specificity.ECG may be an effective tool to predict the IRA in patient with AIMI.

Association Between Helicobacter Pylori Infection and Long-term Outcome in Patients with Drug-eluting Stent Implantation.

To investigate the relationship between Helicobacter pylori (Hp) infection and the long-term outcome in acute coronary syndrome (ACS) patients with drug-eluting stent (DES) implantation and so as to explore the significance of Hp eradication therapy in preventing major adverse cardiac events (MACE) and upper gastrointestinal bleeding (UGIB). 539 ACS patients with DES implantation from January 1, 2010 to December 31, 2012 were analyzed. All the patients were divided into two groups according to the result of 13C urea breath test. 253 patients with Hp infection were put into group A (Hp+), and 286 cases without Hp infection were put into group B (Hp-). Demographic data was collected and all patients went through biochemical indicators and other routine blood examinations. We explored the correlations of Hp infection with MACE and UGIB after 3 to 5 years of follow-up using survival analysis. Survival analysis showed that Hp infection was a predictor of MACE and UGI. Sub-group analysis showed that patients with Hp eradication therapy had no relationship with MACE but had a lower rate of UGIB than those without Hp eradication therapy.

Relationship of coronary collateral circulation with eosinophils in patients with unstable angina pectoris.

BACKGROUND: Eosinophils (EOS) have been associated with prognosis of patients with coronary artery disease, and those who showed plenitudinous coronary collateral circulation (CCC) often have good clinical consequences. However, the relationship between EOS and CCC was seldom reported. OBJECTIVE: To investigate the relationship between EOS and CCC development in patients with unstable angina pectoris (UAP). METHODS: The study population consisted of 502 consecutive patients with UAP who underwent coronary angiography and coronary stenosis ≥80%. CCC was graded according to the Rentrop grading system of 0-3. Rentrop grades of 0 and 1 indicated low-grade CCC group, whereas grades 2 and 3 indicated high-grade CCC group. RESULTS: The EOS was significantly higher in the high-grade CCC group compared with the low-grade CCC group. In multiple logistic regression analysis, EOS (odds ratio: 1.969; 95% confidence interval [CI]: 1.210-3.3205; P=0.006) and neutrophil count (odds ratio: 0.757; 95% CI: 0.584-0.981; P=0.035) were predictors of high-grade CCC development. EOS of >0.12×10(9)/L could independently predict high-grade CCC with 72.5% sensitivity and 58.4% specificity (area under the curve: 0.681; 95% CI: 0.632-0.729). CONCLUSION: EOS were associated with high-grade CCC in patients with UAP with coronary stenosis ≥80%. Increased EOS count may play an important role in the development of CCC in patients with UAP.

Soluble receptor for advanced glycation end-products protects against ischemia/reperfusion-induced myocardial apoptosis via regulating the ubiquitin proteasome system.

AIM: Apoptosis participated in the pathological process of myocardial ischemia/reperfusion (I/R) injury. Previous studies have reported that endogenous substance sRAGE protect against I/R injury through inhibiting myocardial apoptosis. But the mechanisms are currently unknown. Prior work has demonstrated that ubiquitin proteasome system (UPS) dysfunction is closely related to apoptosis. We explored the potential role of UPS in the effect of sRAGE inhibition on I/R-induced myocardial apoptosis. METHODS AND RESULTS: Adult male C57BL mice treated with sRAGE (100µg/day, i.p.) or saline were performed to ligate left anterior descending coronary artery (LAD) as an in vivo model. As an in vitro model, primary murine cardiomyocytes pretreated with sRAGE or sRAGE-containing adenovirus were simulated I/R by "ischemia buffer". The TUNEL and caspase-3 activity were assessed. Also the activity and expression of proteasome were detected. sRAGE decreased the number of TUNEL-positive cardiomyocytes and caspase-3 activity, however, the inhibition of sRAGE on I/R-induced apoptosis was abolished by proteasome inhibitor Bortezimb (BTZ). sRAGE inhibited the decreased proteasome activity, also the reduction in protein and gene levels of ß1i and ß5i following I/R. Suppression of STAT3 blocked the inhibition of sRAGE on apoptosis induced by I/R. The chromatin immunoprecipitation (CHIP) results confirmed that sRAGE promoted activating STAT3 binding to ß1i and ß5i promoter. CONCLUSIONS: Our data suggest that the inhibition of sRAGE on I/R-induced apoptosis is associated with activation and expression of proteasome, including improved proteasome activity and elevated ß1i and ß5i expression mediated by STAT3 activation. We predict that sRAGE is a novel intervention to target UPS activation for preventing and treating myocardial apoptosis.

Helicobacter pylori infection in Chinese patients with atrial fibrillation.

OBJECTIVE: To explore the relationship between Helicobacter pylori (Hp) infection and atrial fibrillation (AF) in Chinese patients. METHODS: A total of 285 hospitalized patients with AF and 300 patients from Health Screening Center who matched age and sex with AF group were enrolled. AF patients were divided into two groups: the short-standing AF category (less than a year) and the long-standing AF category (more than a year). All patients had laboratory testing of (13)C urea breath test, high-sensitive C-reactive protein (hs-CRP) and left atrial diameter (LAD). We analyzed the difference of these factors in all groups and explored the correlation between Hp infection and AF using logistic regression analysis. RESULTS: Both AF groups had more hypertension, diabetes, and Hp infection than the control group. The Hp value and the hs-CRP level in patients with long-standing AF were higher than those in the short-standing AF and the control groups (for Hp value: P<0.001 for both and for hs-CRP level: P=0.003, 0.002, respectively). The LAD of patients in the long-standing AF group was significantly larger than those in the short-standing AF group and control group (P=0.001 and P<0.001, respectively). The values of Hp, hs-CRP, and LAD in the long-standing AF category were significantly higher than those in the short-standing AF category (all P<0.05). After controlling the potential confounders, Hp value ≥4‰, hs-CRP >5 mg/L, and LAD >36 mm were significantly related to long-standing AF. CONCLUSION: The values of Hp in patients with long-standing AF were significantly higher than those in short-standing AF and control groups. Hp δ value ≥4‰ is an independent predictor for long-standing AF.

A soluble receptor for advanced glycation end-products inhibits myocardial apoptosis induced by ischemia/reperfusion via the JAK2/STAT3 pathway.

sRAGE can protect cardiomyocytes from apoptosis induced by ischemia/reperfusion (I/R). However, the signaling mechanisms in cardioprotection by sRAGE are currently unknown. We investigated the cardioprotective effect and potential molecular mechanisms of sRAGE inhibition on apoptosis in the mouse myocardial I/R as an in vivo model and neonatal rat cardiomyocyte subjected to ischemic buffer as an in vitro model. Cardiac function and myocardial infarct size following by I/R were evaluated with echocardiography and Evans blue/2,3,5-triphenyltetrazolium chloride. Apoptosis was detected by TUNEL staining and caspase-3 activity. Expression of the apoptosis-related proteins p53, Bax, Bcl-2, JAK2/p-JAK2, STAT3/p-STAT3, AKT/p-AKT, ERK/p-ERK, STAT5A/p-STAT5A and STAT6/p-STAT6 were detected by western blot analysis in the presence and absence of the JAK2 inhibitor AG 490. sRAGE (100 µg/day) improved the heart function in mice with I/R: the left ventricular ejection fraction and fractional shortening were increased by 42 and 57%, respectively; the infarct size was decreased by 52%, the TUNEL-positive myocytes by 66%, and activity of caspase-3 by 24%, the protein expression of p53 and ratio of Bax to Bcl-2 by 29 and 88%, respectively; protein expression of the p-JAK2, p-STAT3 and p-AKT were increased by 92, 280 and 31%, respectively. sRAGE have no effect on protein expression of p-ERK1/2, p-STAT5A and p-STAT6 following by I/R. sRAGE (900 nmol/L) exhibited anti-apoptotic effects in cardiomyocytes by decreasing TUNEL-positive myocytes by 67% and caspase-3 activity by 20%, p53 protein level and the Bax/Bcl-2 ratio by 58 and 86%, respectively; increasing protein expression of the p-JAK2 and p-STAT3 by 26 and 156%, respectively, p-AKT protein level by 33%. The anti-apoptotic effects of sRAGE following I/R were blocked by JAK2 inhibitor AG 490. The effect of sRAGE reduction on TUNEL-positive myocytes and caspase-3 activity were abolished by PI3K inhibitor LY294002, but not ERK 1/2 inhibitor PD98059. These results suggest that sRAGE protects cardiomyocytes from apoptosis induced by I/R in vitro and in vivo by activating the JAK2/STAT3 signaling pathway.

Significance of eosinophil accumulation in the thrombus and decrease in peripheral blood in patients with acute coronary syndrome.

BACKGROUND AND AIMS: It is well known that the interaction between platelets (PLTs), endothelial cells, and leukocytes contributes to thrombosis in patients with acute coronary syndrome. The aim of this study was to investigate the significance of PLTs and eosinophils (EOS) in coronary arterial thrombi. METHODS: PLT count, mean PLT volume, PLT mass, EOS count, EOS percentage, and troponin I level in peripheral blood were determined in 81 patients with angina pectoris (AP) and 49 patients with acute myocardial infarction (AMI). A total of 12 thrombus specimens from AMI patients were submitted for histopathological analysis. EOS presence in thrombectomy specimens were checked by hematoxylin-eosin staining and confirmed by Luna staining. RESULTS: Results showed that EOS were present in all 12 samples (100%). Cell count and percentage of EOS in peripheral blood of patients with AMI were lower than those in patients with AP (both P<0.00001). A higher PLT count was observed in AMI patients (243±70), especially among female patients or those who were older than 60 years, when compared with AP patients (216±60; all P<0.05). According to the troponin I level, we divided AMI patients into groups I (≥20 ng/ml) and II (<20 ng/ml). Group I had a lower EOS percentage compared with group II (P=0.0496). PLT count was also lower in group I with no statistical difference found (P=0.1202). Moreover, there was an inverse correlation between the EOS percentage and the troponin I level (r=-0.434). CONCLUSION: In conclusion, patients with AMI presented with a decreased EOS percentage and an increased PLT count. The decreased EOS percentage suggested serious myocardial damage. The study indicated that EOS play an important role in thrombosis in patients with acute coronary syndrome.

Echo-tracking technology assessment of carotid artery stiffness in patients with coronary slow flow.

Coronary slow flow (CSF) in coronary angiography (CAG) is a well-recognized clinical entity. Previous studies have suggested that microvascular abnormalities and endothelial dysfunction are responsible for CSF. Accordingly, we hypothesized that the CSF phenomenon is a form of atherosclerosis including both small vessels and epicardial coronary arteries. The echo-tracking (ET) technique is a non-invasive detection method for early prediction of arterial atherosclerosis. Therefore, we investigated carotid elasticity with the ET technique in patients with CSF. Fifty patients with CSF and 50 patients with normal coronary artery blood flow, as determined by CAG, with a similar distribution of risk factors were recruited. The stiffness parameter (ß), pressure-strain elastic modulus (Ep), arterial compliance (AC), augmentation index (AIx) and local pulse-wave velocity (PWV) were determined at the level of the bilateral common carotid artery (CCA) with using the ET technique. Levels of serum high-sensitivity C-reactive protein (hs-HSCRP) were determined for the two groups. ß, Ep and PWV were significantly higher in the CSF group than in the control group (ß: 11.4 ± 3.76 vs. 9.22 ± 3.28, p < 0.01; Ep: 153.44 ± 47.85 vs. 126.40 ± 43.32, p < 0.01; PWV: 7.26 ± 1.10 vs. 6.55 ± 1.02, p < 0.01), but AC was lower in the CSF group than in the control group (0.62 ± 0.20 vs. 0.74 ± 0.24, p < 0.01). The elasticity parameters of the bilateral common carotid artery did not significantly differ. The level of hs-HSCRP was correlated positively with ß (r = 0.306, p = 0.015), Ep (r = 0.358, p = 0.005) and PWV (r = 0.306, p = 0.015), but negatively with AC (r = -0.236, p = 0.049). In conclusion, the ET technique is a simple practical method for evaluating carotid artery elasticity, and there is a significant correlation between carotid artery stiffness and level of hs-HSCRP in patients with CSF.

Effect of blood pressure variability on cardiovascular outcome in diabetic and nondiabetic patients with stroke.

BACKGROUND: The association between blood pressure (BP) variability and stroke outcome is controversial, and there are few studies that have focused on the impact of BP variability in diabetic patients with stroke. Therefore, we aimed to examine the impact of BP variability on cardiovascular outcome in diabetic and nondiabetic patients with stroke. METHODS: A total of 373 ischemic stroke patients with large artery atherosclerosis were recruited and followed up. Ambulatory BP monitoring was performed in all patients and divided according to the 25th and 75th percentiles interval of SD of daytime systolic BP (SBP). Kaplan-Meier analysis and Cox regression were used to assess the relationship between BP variability and cardiovascular outcomes including stroke recurrence, vascular events and cardiovascular death. RESULTS: The 339 patients were included in the final analysis. During an average follow-up of 19.0 ± 5.1 months (.6-26.8 months), 69 (20.4%) cardiovascular events occurred in all patients. Kaplan-Meier analysis found that there were no differences in cardiovascular events-free survival among the different BP variability groups in diabetic patients (P = .995); however, nondiabetic patients with greater BP variability showed a lesser cardiovascular events-free survival (P = .039). Through Cox regression we found the SD of daytime SBP (hazard ratio 1.103; 95% CI 1.011-1.203) was associated with cardiovascular outcomes in nondiabetic patients with stroke. CONCLUSIONS: We show that SBP variability is associated with cardiovascular outcomes in stroke patients without diabetes, but we didn't find a correlation between SBP variability and cardiovascular outcomes in stroke patients with diabetes.

Diagnostic value of combined parameters derived from ambulatory electrocardiography for detecting coronary artery disease in non-active chest pain patients.

BACKGROUND AND OBJECTIVE: The diagnostic value of ST-segment deviation detected by ambulatory electrocardiography (AECG) is controversial in identifying coronary artery disease (CAD) referred for coronary angiography (CAG). Recently, many parameters which evaluate CAD can be derived from AECG. Therefore, we aimed to investigate the diagnostic value of AECG in screening CAD referred for CAG when several parameters were combined. METHODS: We studied the 104 chest pain inpatients. All patients received the CAG and AECG. A lumen diameter reduction of ≥ 50% was considered CAD according to CAG. The parameters derived from AECG included ST-segment deviation, apnea hypopnea index (AHI), QT interval dispersion (QTd) and heart rate variability (HRV). The diagnostic value of AECG in screening CAD was evaluated. RESULTS: Of the 104 patients, 57 (54.8%) had CAD according to CAG. The sensitivity of ST-segment deviation in screening CAD was 64.9%; the specificity was 89.4%; and the Kappa value was 0.528. The sensitivity of at least three combined parameters including ST-segment deviation, AHI, QTd and HRV was 89.5%; the specificity was 87.2%; and the Kappa value was 0.767. CONCLUSION: AECG is very useful in screening CAD referred for CAG, especially while several parameters including ST-segment deviation, AHI, HRV and QTd are combined.

Left main coronary artery spasm in a hyperthyroid patient with suspected acute coronary syndrome.

The left main coronary artery (LMCA) vasospasm is rare. We report a suspected acute coronary syndrome patient with hyperthyroidism who had LMCA vasospasm. Coronary angiogram showed 60% stenosis at LMCA. After administering nitroglycerin, re-angiography showed no significant stenosis. Then we evaluated LMCA lesion using intravascular ultrasound (IVUS) showing no significant stenosis. We considered that it was a LMCA vasospasm and may be assosiated with hyperthyroid state. After anti-thyroid and anti-spasm treatment, chest pain subsided. In conclusion, hyperthyroidism induced coronary hypersensitivity may contribute to LMCA vasospasm as seen in this case. IVUS may be useful to identify coronary vasospasm.

Performance measures for management of chronic heart failure patients with acute coronary syndrome in China: results from the Bridging the Gap on Coronary Heart Disease Secondary Prevention in China (BRIG) Project.

BACKGROUND: Chronic heart failure (CHF) is a severe clinical syndrome associated with high morbidity and mortality, and with high health care expenditures. No nationwide data are currently available regarding the quality of clinical management of CHF patients in China. The aim of this study was to assess the quality of care of CHF inpatients in China. METHODS: The American College of Cardiology/American Heart Association Clinical Performance Measures for Adults with Chronic Heart Failure (Inpatient Measurement Set) with slight modifications was used to measure the performance status in 612 CHF patients with acute coronary syndrome (ACS) from 65 hospitals across all regions of China. RESULTS: The implementation rates of guideline recommended strategies for CHF management were low. Only 57.5% of the CHF patients received complete discharge instructions, 53.6% of the patients received evaluation of left ventricular systolic function, 62.8% received an angiotensin-converting enzyme inhibitor/angiotensin receptor blocker at discharge, and 52.7% received a ß-blocker at discharge, 56.3% of the smokers received smoking cessation counseling. The rate of warfarin utilization was only 9.7% in CHF patients with atrial fibrillation. Most patients (81.4%) did not receive all the first four treatments. There were marked differences in the quality of CHF management among patients with different characteristics. CONCLUSIONS: Performance measures provide a standardized method of assessing quality of care, and can thus highlight problems in disease management in clinical practice. The quality of care for CHF patients with ACS in China needs to be improved.

[Using the combination of traditional risk factors and quantitative coronary angiography (QCA) in predicting the risk of individuals with subclinical artherosclerosis].

OBJECTIVE: To determine whether the combination of traditional risk factors and quantitative coronary angiography (QCA) assessment could provide accurate prognostic information on a population-based study including 1137 adults with subclinical artherosclerosis and with coronary risk factors. METHODS: Participants underwent coronary angiography examination before the minimal stenotic diameters, segment diameters, percent stenosis, plaque areas. Other parameters were analyzed by the computer-assisted Coronary Angiography Analysis System. The Framingham Risk Score for each participant was assessed. During the 1 year follow-up period, all kinds of endpoint cardiovascular events were screened. Endpoint events were defined as death from coronary heart disease, nonfatal myocardial infarction (MI) or unstable angina pectoris. RESULTS: During the 1 year of follow-up period, a total of 124 participants developed an endpoint event, which was significantly associated with the Framingham Risk Score, calcium of plaques and the plaque areas (all Ps<0.05). The QCA score incorporated with the QCA parameters was related to the endpoint events. The Framingham Risk Score was combined with QCA score through logistic regression for prediction of end-point events. Data from the ROC analysis showed the accuracy of this prediction algorithm was superior to the accuracy when variables themselves were used. The event-free survival rate was inferior to the control group in participates under high risk, when being screened with this prediction algorithm (P<0.05). CONCLUSION: The risk of cardiovascular attack in subclinical artherosclerosis individual seemed to be associated with the Framingham Risk Score, calcium of plaques and the plaque areas. When the traditional risk factors (the Framingham Risk Score) were combined with QCA, the new method could provide more prognostic information on those adults with subclinical artherosclerosis.

[Characterization of atherosclerotic plaque in patients with unstable angina pectoris and stable angina pectoris by optical coherence tomography].

OBJECTIVE: To compare the characterization of coronary atherosclerotic plaques in patients with unstable angina pectoris (UAP) and stable angina pectoris (SAP) by optical coherence tomography (OCT). METHODS: OCT was performed in 47 patients (23 UAP and 24 SAP) undergoing coronary angiography. Lipid-rich plaque (defined by > or = 2 quadrants of the cross-section area), thin cap fibroatheroma (TCFA), thickness of fibrous cap, plaque rupture, calcification and thrombus visualized by OCT were compared between UAP and SAP patients. RESULTS: OCT imaging was successfully in 44 out of 47 patients (22 UAP, 22 SAP). Proportion of lipid-rich plaques was similar between UAP and SAP groups [91% (20/22) vs. 73% (16/22), P = 0.741]. The minimum thickness of fibrous cap in the UAP group was significantly thinner than that in SAP group [(69.5 +/- 34.7) microm vs. (141.1 +/- 68.5) microm, P = 0.000] and the rate of fibrous cap erosion in the UAP group was significantly higher than that in the SAP group [59% (13/22) vs. 9% (2/22), P = 0.000]. Percents of TCFA [73% (16/22) vs. 14% (3/22), P = 0.000] and plaque rupture [50% (11/22) vs. 9% (2/22), P = 0.003] were significantly higher in UAP group compared those in SAP group. Incidence of thrombus and calcification were similar between two groups. CONCLUSIONS: OCT imaging can clearly define plaque characterization of coronary atherosclerosis. UAP patients have thinner fibrous cap, higher incidences of fibrous cap erosion, plaque rupture and TCFA compared patients with SAP.

[Diagnostic value of 128-slice CT coronary angiography in comparison with invasive coronary angiography].

OBJECTIVE: To observe the diagnostic value of non-invasive 128-slice computed tomography coronary angiography (CTA) in comparison with invasive coronary angiography. METHODS: 128-slice CTA and invasive coronary angiography were performed in 78 unselected consecutive patients (63 patients with suspected coronary artery disease and 15 patients with previous coronary stenting, 56 males, mean age 61 +/- 10 years) and > 50% reduction of minimal lumen diameter was defined as significant coronary stenosis. RESULTS: Fifty-eight out of 879 segments (7%) from CTA were not assessable because of irregular rhythm, vessel calcification or tachycardia. Compared with invasive coronary angiography, segment-based analysis from the 821 segments showed the sensitivity by CTA was 87%, specificity 97%, PPV 83% and NPV 97%. Four out of 22 stents implanted in 15 patients were not assessable by CTA because of poor image quality. Compared with invasive coronary angiography, the sensitivity of diagnosing in-stent restenosis by CTA was 100%, specificity 77%, PPV 63% and NPV 100% for the remaining 18 stents. CONCLUSIONS: One hundred and twenty-eight-slice CTA has a high accuracy for detecting coronary artery disease and in-stent restenosis after coronary stenting and could be considered as a valuable noninvasive technique for screening coronary artery disease in suspected patients.

[Visualization of intimal proliferation of drug-eluting stent and bare mental stent by use of optical coherence tomography].

OBJECTIVE: To compare neointimal proliferation of drug-eluting stent (DES) with bare mental stent (BMS) by optical coherence tomography (OCT). METHODS: OCT images were obtained in 21 diseased coronary vessels with 23 stents in 19 patients with coronary artery disease at 5 - 93 months post DES or BMS stents. Twenty-two stents of all 23 stents were divided into three groups. Nine DES stents at 6 - 10 months post stenting were considered as group A, 8 BMS stents at 5 - 10 months post stenting as group B, and 5 BMS stents at 23 - 93 months post stenting as group C. OCT images were quantitatively analyzed to compare neointimal proliferation of three groups after stenting. RESULTS: All 21 vessels and 23 stents OCT images were successfully acquired. The maximal neointima, luminal loss in diameter and cross sectional area (CSA), and restenosis in diameter and CSA were significantly statistically different within three groups. The maximal intimal proliferations post stenting in group A were significantly lower than group B (0.20 mm +/- 0.13 mm vs 0.81 mm +/- 0.46 mm, P = 0.019) or group C (0.91 mm +/- 0.27 mm, P = 0.007), luminal loss of diameter in group A were significantly lower than group B (0.27 mm +/- 0.17 mm vs 1.12 mm +/- 0.79 mm, P = 0.009) or group C (1.20 mm +/- 0.31 mm, P = 0.013), restenosis rates in diameter in group A were significantly less than group B (8.90% +/- 4.47% vs 36.36% +/- 24.34%, P = 0.009) or group C (35.48 +/- 6.09, P = 0.017), luminal loss in CSA in group A were lower than group B (1.14 mm(2) +/- 0.9 mm(2) vs 3.96 mm(2) +/- 2.62 mm(2), P = 0.009) or group C (4.66 mm(2) +/- 1.66 mm(2), P = 0.006), and restenosis rates in CSA in group A were less than group B (15.43% +/- 7.89% vs 48.14% +/- 30.43%, P = 0.017) or group C (55.20% +/- 11.24%, P = 0.009). Almost all surfaces of 13 BMS stent struts were covered by significant neointimal coverage, surfaces of 10 DES struts were less significantly neointimal coverage, and some surfaces of DES struts were uncovered with neointima even at 29 months post stenting. CONCLUSION: OCT imaging can clearly visualize stent struts and neointimal formation of strut surfaces post DES or BMS stenting, and this new imaging modality will play important role in evaluating the efficacy of drug-eluting stent.

[Coronary artery atherosclerotic plaque and stent visualizations by optical coherence tomography].

OBJECTIVE: To evaluate coronary artery atherosclerotic plaque characteristics and changes post coronary stenting by optical coherence tomography (OCT). METHODS: OCT images were obtained in 22 diseased coronary vessels after coronary angiography or percutaneous coronary interventions (PCI) in 20 patients and in 23 stents [7 sirolimus-eluting stents (SES) follow up at 4-29 months post stenting and 8 bare mental stents (BMS) at 4-35 months post stenting, 8 stents immediately after PCI]. RESULTS: All 22 vessels and 23 stents OCT images were successfully acquired. Two thromboses, 8 fibrous, 9 lipid-rich and 3 calcium plaques as well as 3 plaque ruptures were visualized by OCT. No significant neointimal proliferation and restenosis were found in SES stents and some struts were not covered with neointima even at 29 months post stenting. Significant neointimal proliferation on surfaces of stent struts were visualized in all 8 BMS stents and restenosis was detected in 3 BMS stents. OCT images obtained immediately after PCI showed that 3 stents were well positioned, tissue prolapse between coronary stent struts occurred in 4 stents and stent dissociation with vessel wall could be seen in 1 stent. CONCLUSIONS: OCT imaging can clearly visualize different types of atherosclerotic plaques. By providing detailed information on plaque characteristics, this technique might help cardiologists in choosing suitable stents and guiding preventive therapy for patients with coronary heart disease.