[8] Furthermore, there is an independent, graded increased risk of death and cardiovascular (CV) events associated with reduced eGFR,[6] BMS907351 and this relationship is also seen in survivors of acute MI (AMI) and NSTE-ACS.[9-11] Medical management of ACS, which include STEMI and NSTE-ACS, and chronic stable CAD has been extensively studied in the general population leading to evidence-based national clinical practice guidelines.[7-9] There are RCTs that have firmly established roles for reperfusion and primary PCI, antiplatelet and anticoagulant therapies, beta-blocker therapy, and ACEi or ARB therapy for ACS in the

general population. In the majority of these trials patients with moderate-to-severe renal impairment have been excluded, leading to unanswered concerns about efficacy and safety, and consequently significant underuse

of these therapeutic options in CKD patients.[9-11] The aim of this guideline is to examine the benefits and harms of medical management, specifically reperfusion therapy, antiplatelet and anticoagulant therapies, beta-blocker therapy, and ACEi/ARB therapy (but excluding lipid-lowering therapy), of ACS and chronic stable CAD in patients with CKD, including the dialysis and transplant populations. The benefits examined are: The risk of MI and CV death in patients presenting https://www.selleckchem.com/products/BIBW2992.html with ACS, including the risk of coronary

restenosis in patients with an ACS undergoing a PCI and receiving associated antiplatelet and/or anticoagulant therapy. The risk of MI and CV death in patients with chronic stable CAD. The harms examined relate to serious adverse Adenosine events reported in the literature in relation to the aforementioned medical therapies. There is little high quality evidence regarding the management of ACS or chronic stable CAD in patients with CKD. The RCT data examining the therapeutic options for the medical management of ACS or chronic stable CAD are all taken from post-hoc analyses of RCTs from the general population where patients with CKD were identified based on serum creatinine and/or eGFR, and outcomes analysed. These limitations also apply to assessing harms of ACS therapies. Specifically with regards to harm of anticoagulant therapies, data have been extrapolated from trials using anticoagulants for non-cardiac indications. Prospective and retrospective registry data or observational cohorts provide a significant proportion of the evidence for ACS therapies. The management of ACS in the general population has been published in the extensive guidelines available.[7-9] These guidelines support the use of PCI in favour of thrombolysis without specifically including or excluding CKD patients.