BackgroundPrimary percutaneous coronary intervention (PPCI) is the preferred reperfusion strategy in patients with ST-elevation myocardial infarction (STEMI), but its benefit over prehospital fibrinolysis (FL) is not clear.MethodsWe performed a systematic review and meta-analysis of randomized controlled trials in which outcomes of patients with STEMI managed with FL early in the prehospital setting versus PPCI were compared.ResultsCompared with PPCI, FL was consistently associated with similar rates of short-term (30–90 days) death (relative risk [RR] 0.94, 95 % CI 0.67–1.31) and cardiovascular death (RR 0.95, 95 % CI 0.64–1.4), a decreased risk of cardiogenic shock (RR 0.67, 95 % CI 0.48–0.95), and an increased risk of any stroke (RR 3.57, 95 % CI 1.39–9.17) and hemorrhagic stroke (RR 4.37, 95 % CI 1.25–15.26). FL was also associated with similar rates of 1-year mortality (RR 1.01, 95 % CI 0.75–1.34) and major bleeding (RR 1.31, 95 % CI 0.96–1.78) in comparison with PPCI, but with a notable level (I 2 index 30.5 % and 59.8 %) of heterogeneity among studies.ConclusionsOur study suggests that, compared with PPCI, FL performed in the early prehospital setting is associated with similar mortality rates, lower rates of cardiogenic shock, and higher rates of stroke in patients with STEMI. Although the number of studies comparing the two strategies is relatively low, our results support prehospital FL and transfer to hub percutaneous coronary intervention (PCI) centers as a valid alternative to PPCI, allowing potential limitation of resources allocated to developing proximity 24/7 PCI facilities.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1530-z) contains supplementary material, which is available to authorized users.
Rationale: Necrotic core formation during the development of atherosclerosis is associated with a chronic inflammatory response and promotes accelerated plaque development and instability. However, the molecular links between necrosis and the development of atherosclerosis are not completely understood. Clec9a (C-type lectin receptor) or DNGR-1 (dendritic cell NK lectin group receptor-1) is preferentially expressed by the CD8α + subset of dendritic cells (CD8α + DCs) and is involved in sensing necrotic cells. We hypothesized that sensing of necrotic cells by DNGR-1 plays a determinant role in the inflammatory response of atherosclerosis. Objective: We sought to address the impact of total, bone marrow–restricted, or CD8α + DC–restricted deletion of DNGR-1 on atherosclerosis development. Methods and Results: We show that total absence of DNGR-1 in Apoe (apolipoprotein e)–deficient mice ( Apoe −/− ) and bone marrow–restricted deletion of DNGR-1 in Ldlr (low-density lipoprotein receptor)–deficient mice ( Ldlr −/− ) significantly reduce inflammatory cell content within arterial plaques and limit atherosclerosis development in a context of moderate hypercholesterolemia. This is associated with a significant increase of the expression of interleukin-10 (IL-10). The atheroprotective effect of DNGR-1 deletion is completely abrogated in the absence of bone marrow–derived IL-10. Furthermore, a specific deletion of DNGR-1 in CD8α + DCs significantly increases IL-10 expression, reduces macrophage and T-cell contents within the lesions, and limits the development of atherosclerosis. Conclusions: Our results unravel a new role of DNGR-1 in regulating vascular inflammation and atherosclerosis and potentially identify a new target for disease modulation.
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