ABSTRACT
BACKGROUND: The safety and effectiveness of emergency percutaneous coronary intervention (PCI) in elderly patients with acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) are currently unknown. AIM: To compare the outcome of elderly patients with AMI complicated by CS who were treated with primary PCI or thrombolysis. METHODS: Between 2001 and 2006 at Xijing Hospital we evaluated the outcome of 94 patients l75 years old with AMI complicated by CS, of whom 33 underwent emergency PCI (PCI group), whereas the other 61 received initially conventional medication (CM group). RESULTS: Baseline characteristics, infarct location, rate of intra-aortic balloon pump support and time from AMI onset to therapy were similar between the two groups. The success rate of revascularisation in the PCI group was 90.9% and the success rate of thrombolysis in the CM group was 60.7% (p=0.004). The PCI group had a lower in-hospital mortality than the CM group (42.4 vs. 65.6%, p=0.026). Kaplan-Meier curves showed a significant difference in survival (48.48 vs. 21.31%, p=0.006), favouring early PCI. Multiple logistic regression identified time from AMI onset to therapy as an independent predictor of in-hospital death (p=0.036). Cox regression analysis indicated early PCI as an independent factor to improve mid-term survival (p=0.015). CONCLUSIONS: Emergency PCI improves 1-year survival compared with initial conventional medication for elderly patients with AMI complicated by CS.
Subject(s)
Myocardial Infarction/mortality , Myocardial Infarction/therapy , Shock, Cardiogenic/etiology , Aged , Emergencies , Female , Hospital Mortality , Humans , Intra-Aortic Balloon Pumping , Male , Myocardial Infarction/complications , Myocardial Revascularization , Prospective Studies , Survival Rate , Thrombolytic Therapy , Treatment OutcomeABSTRACT
OBJECTIVE: High glucose-induced apoptosis in vascular endothelial cells contributes to the acceleration of atherosclerosis associated with diabetes. We hypothesized that alpha-linolenic acid (ALA) might attenuate high glucose-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were cultured at 5.5 and 33 mmol/L for 72 h. ALA with different concentrations was added with defatted bovine serum albumin as a carrier for 18 h before incubation with high glucose. RESULTS: Exposure of HUVECs to high glucose media for 72 h significantly increased the number of apoptotic cells compared with normal glucose control, as evaluated by flow cytometry and terminal deoxyuridine triphosphate nick end labeling assay. Pretreatment with low concentrations of ALA (10, 50, and 100 micromol/L) significantly attenuated high glucose-induced apoptosis of HUVECs, but increasing ALA to 200 micromol/L exerted the opposite effect. Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose. Pretreatment with phosphatidylinositol 3' -kinase kinase inhibitor LY294002 and eNOS inhibitor N(G)-nitro-arginine methyl ester eliminated ALA' antiapoptotic effect. CONCLUSION: ALA exerts an antiapoptotic effect by the phosphatidylinositol 3'-kinase/Akt/eNOS pathway in HUVECs exposed to high glucose and thus may represent a candidate therapeutic agent for diabetic cardiovascular complications.
Subject(s)
Apoptosis/drug effects , Endothelial Cells/physiology , Glucose/adverse effects , alpha-Linolenic Acid/pharmacology , Cells, Cultured , Dose-Response Relationship, Drug , Endothelial Cells/cytology , Endothelial Cells/drug effects , Endothelial Cells/enzymology , Flow Cytometry , Humans , In Situ Nick-End Labeling , Nitric Oxide Synthase Type III/metabolism , Oncogene Protein v-akt/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Phosphorylation , Umbilical Veins/cytologyABSTRACT
Different subsets of T lymphocytes have different functions in atherosclerosis advancement. T helper 1 cells and T regulatory 1 cells have been demonstrated to play opposite roles in rupture of atherosclerotic lesion. However, the role of novel subset of T regulatory cells, known as CD4+CD25+Foxp3+ T cells, remains largely unknown in coronary artery disease (CAD). In this study, we investigated the peripheral CD4+CD25+Foxp3+ T cells of patients with CAD and controls. The patients submitted were divided into three groups: stable angina pectoris (SA) group, unstable angina pectoris (UA) group and acute myocardial infarction (AMI) group. We analyzed the frequencies of peripheral CD4+CD25+Foxp3+ T cells and T helper 1/T helper 2 cells, expression of Foxp3 in CD4+CD25+ T subsets and cytokines pattern in patients and controls. We found that the reduction of CD4+CD25+Foxp3+ T lymphocytes was consistent with the expansion of Th1 cells in patients with unstable CAD. The reversed development between CD4+CD25+ Tregs and Th1 cells might contribute to plaque destabilization.
