Impact of Chronic Kidney Disease on Long-Term Outcomes in Type 2 Diabetic Patients With Coronary Artery Disease on Surgical, Angioplasty, or Medical Treatment.

BACKGROUND: Coronary artery disease (CAD) among patients with diabetes and chronic kidney disease (CKD) is not well studied, and the best treatment for this condition is not established. Our aim was to compare three therapeutic strategies for CAD in diabetic patients stratified by renal function. METHODS: Patients with multivessel CAD that underwent coronary artery bypass graft (CABG), angioplasty (percutaneous coronary intervention [PCI]), or medical therapy alone (MT) were included. Data were analyzed according to glomerular filtration rate in three strata: normal (>90 mL/min), mild CKD (60 to 89 mL/min), and moderate CKD (30 to 59 mL/min). End points comprised overall rate of mortality, acute myocardial infarction, and need for additional revascularization. RESULTS: Among patients with normal renal function (n = 270), 122 underwent CABG, 72 PCI, and 76 MT; among patients with mild CKD (n = 367), 167 underwent CABG, 92 PCI, and 108 MT; and among patients with moderate CKD (n = 126), 46 underwent CABG, 40 PCI, and 40 MT. Event-free survival was 80.4%, 75.7%, 67.5% for strata 1, 2, and 3, respectively (p = 0.037). Survival rates among patients with no, mild, and moderate CKD are 91.1%, 89.6%, and 76.2%, respectively (p = 0.001) (hazard ratio 0.69; 95% confidence interval 0.51 to 0.95; p = 0.024 for stratum 1 versus 3). We found no differences for overall number of deaths or acute myocardial infarctions irrespective of strata. The need of new revascularization was different in all strata, favoring CABG (p < 0.001, p < 0.001, and p = 0.029 for no, mild, and moderate CKD, respectively). CONCLUSIONS: Mortality rates were higher in patients with mild and moderate CKD. Higher event-free survival was observed in the CABG group among patients with no and mild CKD. Besides, CABG was associated with less need for new revascularization compared with PCI and MT in all renal function strata. This trial was registered at http://www.controlled-trials.com as ISRCTN66068876.

Impact of hypoglycemic agents on myocardial ischemic preconditioning.

Murry et al in 1986 discovered the intrinsic mechanism of profound protection called ischemic preconditioning. The complex cellular signaling cascades underlying this phenomenon remain controversial and are only partially understood. However, evidence suggests that adenosine, released during the initial ischemic insult, activates a variety of G protein-coupled agonists, such as opioids, bradykinin, and catecholamines, resulting in the activation of protein kinases, especially protein kinase C (PKC). This leads to the translocation of PKC from the cytoplasm to the sarcolemma, where it stimulates the opening of the ATP-sensitive K(+) channel, which confers resistance to ischemia. It is known that a range of different hypoglycemic agents that activate the same signaling cascades at various cellular levels can interfere with protection from ischemic preconditioning. This review examines the effects of several hypoglycemic agents on myocardial ischemic preconditioning in animal studies and clinical trials.