Correlation between dual-axis rotational coronary angiography and intravascular ultrasound in a coronary lesion assessment.

The purpose of this study was to evaluate the accuracy of dual-axis rotational coronary angiography (DARCA) for coronary lesion assessment by directly comparing with intravascular ultrasound (IVUS). From October 2014 to December 2015, 40 patients (58 lesions) who had undergone both DARCA and IVUS were included in the image analysis. The minimum lumen diameter (MLD), lesion length, reference vessel diameter (RVD) and percent diameter stenosis at the same lesion, were identified and assessed. Significant correlation with IVUS was found for DARCA in either lesion length (r = 0.90, P < 0.001) or RVD (r = 0.81, P < 0.001) comparison. DARCA had fair correlation with IVUS for both MLD (r = 0.65, P < 0.001) and diameter stenosis (r = 0.48, P < 0.001). From the Bland-Altman plots, there was a good agreement between DARCA and IVUS regarding MLD (mean difference: -0.23 mm, 95 % limits of agreement: -0.96 to 0.50 mm) and RVD (mean difference: -0.15 mm, 95 % limits of agreement: -0.85 to 0.55 mm), while lesser agreement was found on lesion length (mean difference: -3.39 mm, 95 % limits of agreement: -12.63 to 5.85 mm) and diameter stenosis (mean difference: 4.82 %, 95 % limits of agreement: -17.05 to 26.68 %). There is an adequate correlation and agreement between DARCA and IVUS in coronary lesion assessment.

Down-regulation of SIRT3 promotes ovarian carcinoma metastasis.

Distant metastasis and local recurrence are still the major causes for failure of treatment in patients with ovarian carcinoma (OC), making it urgent to further elicit the molecular mechanisms of OC metastasis. Sirtuin-3 (SIRT3), a member of the NAD(+)-dependent Class III histone deacetylases, may function as different role depending on the cell-type and tumor-type. However, the function and mechanism of SIRT3 has been not explored in OC metastasis. Here, we found that SIRT3 was significantly down-regulated in the metastatic tissues and highly metastatic cell line of ovarian cancer. In addition, knockdown of SIRT3 enhanced the migration and invasion in vitro and the liver metastasis in vivo of ovarian cancer cell. By contrast, ectopic overexpression of SIRT3 dramatically suppressed cancer cell metastatic capability. Mechanistically, SIRT3 inhibits epithelial-to-mesenchymal transition (EMT) by down-regulating Twist in ovarian cancer cells. Furthermore, an interaction between SIRT3 and Twist was detected. In conclusion, our results demonstrated that SIRT3 plays a crucial suppressive role in the metastasis of ovarian cancer by down-regulating Twist, and that this novel SIRT3/Twist axis may be valuable to develop new strategies for treating OC patients with metastasis.

Administration of a loading dose of atorvastatin before percutaneous coronary intervention prevents inflammation and reduces myocardial injury in STEMI patients: a randomized clinical study.

BACKGROUND: Administration of a loading dose of atorvastatin 80 mg/d has been shown to be beneficial in patients with stable coronary artery disease and acute coronary syndromes. However, little is known about the impact and mechanism behind the beneficial effects of loading-dose atorvastatin treatment before percutaneous coronary intervention (PCI), especially for those patients experiencing cardiovascular inflammation in ST-segment elevation myocardial infarction (STEMI). OBJECTIVE: The goal of this randomized clinical study was to investigate whether, before emergency PCI, administration of loading-dose atorvastatin therapy in STEMI patients inhibits inflammation and improves cardiac function during 24 weeks of follow-up. METHODS: A total of 102 STEMI patients were enrolled into 3 groups: group A (n = 32) received 80 mg of atorvastatin before emergency PCI, post-PCI follow-up atorvastatin 40 mg for 4 weeks, and atorvastatin 20 mg for 20 weeks; group B (n = 32) received no pre-PCI loading dose of atorvastatin but did receive atorvastatin 40 mg for 4 weeks and then atorvastatin 20 mg for 20 weeks; and group C (n = 38) received only post-PCI atorvastatin 20 mg for 24 weeks. RESULTS: No differences were found in baseline demographic and angiographic characteristics among the 3 groups. Patients in group A had the lowest plasma levels of high-sensitivity C-reactive protein (hs-CRP), B-type natriuretic peptide (BNP), and matrix metalloproteinase type 9 (MMP-9) (P < 0.05). Patients in group A also showed improvement in heart performance, with significant increases in their left ventricular ejection fraction. To a lesser extent, group B displayed reductions in the plasma levels of hs-CRP, BNP, and MMP-9 at later time points (P < 0.05). Compared with those in group C, patients in group B also exhibited significant improvement in left ventricular ejection fraction (P < 0.05). CONCLUSIONS: Loading-dose atorvastatin therapy before emergency PCI reduced the inflammatory response and myocardial dysfunction in these STEMI patients by lowering hs-CRP, BNP, and MMP-9. Pre-PCI loading-dose atorvastatin treatment may help prevent inflammatory response and improve cardiac function in patients with acute coronary syndromes undergoing emergency PCI. ClinicalTrials.gov identifier: NCT01334671.

Long-term effects of biodegradable versus durable polymer-coated sirolimus-eluting stents on coronary arterial wall morphology assessed by virtual histology intravascular ultrasound.

BACKGROUND: The durable presence of polymer coating on drug-eluting stent (DES) surface may be one of the principal reasons for stent thrombosis. The long-term coronary arterial response to biodegradable polymer-coated sirolimus-eluting stent (BSES) in vivo remained unclear. METHODS: Forty-one patients were enrolled in this study and virtual histology intravascular ultrasound (VH-IVUS) was performed to assess the native artery vascular responses to BSES compared with durable polymer-coated SES (DSES) during long-term follow-up (median: 8 months). The incidence of necrotic core abutting to the lumen was evaluated at follow-up. RESULTS: With similar in-stent late luminal loss (0.15 mm (0.06-0.30 mm) vs. 0.19 mm (0.03-0.30 mm), P = 0.772), the overall incidence of necrotic core abutting to the lumen was significantly less in BSES group than in DSES group (44% vs. 63%, P < 0.05) (proximal 18%, stented site 14% and distal 12% in BSES group, proximal 19%, stented site 28% and distal 16% in DSES group). The DSES-treated segments had a significant higher incidence of necrotic core abutting to the lumen through the stent struts (73% vs. 36%, P < 0.01). In addition, more multiple necrotic core abutting to the lumen was observed in DSES group (overall: 63% vs. 36%, P < 0.05). Furthermore, when the stented segments with necrotic core abutting to the lumen had been taken into account only, DSES-treated lesions tended to contain more multiple necrotic core abutting to the lumen through the stent struts than BSES-treated lesions (74% vs. 33%), although there was no statistically significant difference between them (P = 0.06). CONCLUSIONS: By VH-IVUS analysis at follow-up, a greater frequency of stable lesion morphometry was shown in lesions treated with BSESs compared with lesions treated with DSESs. The major reason was BSES produced less toxicity to the arterial wall and facilitated neointimal healing as a result of polymer coating on DES surface biodegraded as time went by.

Coronary plaque characterization of nonculprit or nontarget lesions assessed by analysis of in vivo intracoronary ultrasound radio-frequency data.

BACKGROUND: Unheralded sudden death and acute myocardial infarction are common manifestations of coronary atherosclerosis. Such events are related to thrombotic occlusion at the site of non-flow limiting atherosclerotic plaques in epicardial coronary arteries. This study aimed to assess plaque characterization of nonculprit lesions in patients with acute coronary syndrome (ACS) compared with those with stable angina pectoris (SAP) determined by analysis of intravascular ultrasound (IVUS) radiofrequency (RF) data. METHODS: In 81 patients, nonculprit vessels with < 50% diameter stenosis and nontarget segment of culprit vessels with < 50% diameter stenosis were studied with IVUS. Tissue maps were reconstructed from RF data using IVUS-Virtual Histology software. RESULTS: Mean lipid core percentage was significantly higher in patients with ACS than in those with SAP ((25.78 +/- 6.30)% vs (9.11 +/- 4.90)%, P < 0.001). In addition, patients with SAP showed more fibrotic vessels ((59.66 +/- 16.87)% vs (49.07 +/- 10.20)%, P < 0.001). There was no significant difference in either mean calcium ((4.37 +/- 2.40)% vs (5.12 +/- 3.00)%, P = 0.225) or fibrolipid ((24.94 +/- 9.40)% vs (25.82 +/- 13.60)%, P = 0.731) percentages in nonculprit vessels, but the mean calcium percentage was significantly higher in nontarget lesions of culprit vessels ((5.51 +/- 3.29)% vs (3.57 +/- 2.10)%, P = 0.003). In addition, there was a positive correlation between lipid core and remodeling index (RI) (r = 0.847, P < 0.001) and a negative correlation between fibrous tissue and RI (r = -0.946, P < 0.001). CONCLUSIONS: In this study, in both nonculprit vessels and nontarget lesion of culprit vessels, plaque characterization of nonculprit lesions determined by spectral analysis of IVUS RF data was significantly different in patients with ACS. The percentage of lipid core was significantly higher in patients with ACS than in those with SAP. Conversely, SAP patients showed more fibrotic content. In vivo plaque composition and morphological changes were related to remodeling of the coronary artery tree.