| 1. |
- Girasis, Chrysafios, et al.
(författare)
-
SYNTAX score and Clinical SYNTAX score as predictors of very long-term clinical outcomes in patients undergoing percutaneous coronary interventions : a substudy of SIRolimus-eluting stent compared with pacliTAXel-eluting stent for coronary revascularization (SIRTAX) trial
- 2011
-
Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 32:24, s. 3115-3127
-
Tidskriftsartikel (refereegranskat)abstract
- AIMS:To investigate the ability of SYNTAX score and Clinical SYNTAX score (CSS) to predict very long-term outcomes in an all-comers population receiving drug-eluting stents.METHODS AND RESULTS:The SYNTAX score was retrospectively calculated in 848 patients enrolled in the SIRolimus-eluting stent compared with pacliTAXel-Eluting Stent for coronary revascularization (SIRTAX) trial. The CSS was calculated using age, and baseline left ventricular ejection fraction and creatinine clearance. A stratified post hoc comparison was performed for all-cause mortality, cardiac death, myocardial infarction (MI), ischaemia-driven target lesion revascularization (TLR), definite stent thrombosis, and major adverse cardiac events (MACE) at 1- and 5-year follow-up. Tertiles for SYNTAX score and CSS were defined as SSLOW ≤7, 7< SSMID ≤14, SSHIGH >14 and CSSLOW ≤8.0, 8.0 MID ≤17.0 and CSSHIGH >17.0, respectively. Major adverse cardiac events rates were significantly higher in SSHIGH compared with SSLOW at 1- and 5-year follow-up, which was also seen at 5 years for all-cause mortality, cardiac death, MI, and TLR. Stratifying outcomes across CSS tertiles confirmed and augmented these results. Within CSSHIGH, 5-year MACE increased with use of paclitaxel- compared with sirolimus-eluting stents (34.7 vs. 21.3%, P= 0.008). SYNTAX score and CSS were independent predictors of 5-year MACE; CSS was an independent predictor for 5-year mortality. Areas-under-the-curve for SYNTAX score and CSS for 5-year MACE were 0.61 (0.56–0.65) and 0.62 (0.57–0.67), for 5-year all-cause mortality 0.58 (0.51–0.65) and 0.66 (0.59–0.73) and for 5-year cardiac death 0.63 (0.54–0.72) and 0.72 (0.63–0.81), respectively.CONCLUSION:SYNTAX score and to a greater extent CSS were able to stratify risk for very long-term adverse clinical outcomes in an all-comers population receiving drug-eluting stents. Predictive accuracy for 5-year all-cause mortality was improved using CSS. Trial Registration Number: NCT00297661.
|
|
| 2. |
|
|
| 3. |
- Stein, Sokrates, et al.
(författare)
-
ApoE-/- PGC-1α-/- mice display reduced IL-18 levels and do not develop enhanced atherosclerosis.
- 2010
-
Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 5:10
-
Tidskriftsartikel (refereegranskat)abstract
- Atherosclerosis is a chronic inflammatory disease that evolves from the interaction of activated endothelial cells, macrophages, lymphocytes and modified lipoproteins (LDLs). In the last years many molecules with crucial metabolic functions have been shown to prevent important steps in the progression of atherogenesis, including peroxisome proliferator activated receptors (PPARs) and the class III histone deacetylase (HDAC) SIRT1. The PPARγ coactivator 1 alpha (Ppargc1a or PGC-1α) was identified as an important transcriptional cofactor of PPARγ and is activated by SIRT1. The aim of this study was to analyze total PGC-1α deficiency in an atherosclerotic mouse model.
|
|
| 4. |
- Stein, Stein, et al.
(författare)
-
SIRT1 decreases Lox-1-mediated foam cell formation in atherogenesis.
- 2010
-
Ingår i: European heart journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 31:18, s. 2301-2309
-
Tidskriftsartikel (refereegranskat)abstract
- Aims Endothelial activation, macrophage infiltration, and foam cell formation are pivotal steps in atherogenesis. Our aim in this study was to analyse the role of SIRT1, a class III deacetylase with important metabolic functions, in plaque macrophages and atherogenesis. Methods and results Using partial SIRT1 deletion in atherosclerotic mice, we demonstrate that SIRT1 protects against atherosclerosis by reducing macrophage foam cell formation. Peritoneal macrophages from heterozygous SIRT1 mice accumulate more oxidized low-density lipoprotein (oxLDL), thereby promoting foam cell formation. Bone marrow-restricted SIRT1 deletion confirmed that SIRT1 function in macrophages is sufficient to decrease atherogenesis. Moreover, we show that SIRT1 reduces the uptake of oxLDL by diminishing the expression of lectin-like oxLDL receptor-1 (Lox-1) via suppression of the NF-κB signalling pathway. Conclusion Our findings demonstrate protective effects of SIRT1 in atherogenesis and suggest pharmacological SIRT1 activation as a novel anti-atherosclerotic strategy by reducing macrophage foam cell formation.
|
|
