losartan-potassium and Coronary-Stenosis

Experimental data have shown that Erythropoietin (EPO) stimulates angiogenesis and neovascularization which may result in improved collateral development. The aim of this study was to investigate the association between serum EPO levels and the extent of coronary collaterals. Patient characteristics possibly related with coronary collaterals were also sought.. A total of 256 patients with high grade coronary stenosis or occlusion were evaluated for the extent of coronary collaterals using Rentrop classification. Patients with grade 0 or 1 collaterals were grouped as poor collaterals, while grade 2 or 3 collaterals were grouped as good collaterals.. Mean age of the study population was 63 years, 77% were males. Subjects with good collaterals were significantly more likely to have anemia (p=0.038) and stable angina pectoris as clinical presentation (p=0.40). Serum EPO levels were not different among good and poor collateral groups (10.4±9.4 mU/mL vs. 9.7±11 mU/mL, p=0.397). The prevalence of all other cardiovascular risk factors, medications, and angiographic characteristics were similar between the two groups. After adjusting for age, gender, and clinical presentation with stable angina pectoris, presence of anemia persisted to be a significant correlate of the good collateral formation (OR: 1.95; 95%; CI: 1.07-3.54, p=0.029).. There has been conflicting results from trials studying the effects of serum EPO on coronary collateral development. The present study, with the largest patient population studying this topic, suggests that presence of anemia, but not serum EPO level, is associated with good collateral development.

Topics: Biomarkers; Collateral Circulation; Coronary Angiography; Coronary Stenosis; Coronary Vessels; Cross-Sectional Studies; Erythropoietin; Female; Humans; Male; Middle Aged

Recombinant human erythropoietin (rhEPO) has been proposed to possess important tissue protective, apart from haematopoietic, effects. Cardioprotective effects have thus been reported in rodents exposed to myocardial ischaemia. Pathways common to the mediation of ischaemic preconditioning may be involved. Before clinical testing such possible cardioprotective effects needs assessment in an experimental large animal model with closer similarity to human ischaemic pathophysiology.. A control group and two rhEPO groups were studied. EPO1 pigs were given EPO corresponding to the early window and EPO2 pigs to the early and late window of ischaemic preconditioning in a closed chest, catheter-based, porcine coronary occlusion model (45 min of occlusion of the left anterior descending artery). Infarct size as a proportion of the ischaemic area (IS/AAR) was measured in vivo by myocardial perfusion imaging (MPI) and postmortem by a histochemical procedure (at 150 min of reperfusion).. IS/AAR did not differ significantly between control (C), EPO1 and EPO2 groups, neither measured by MPI (mean+/-SD for C: 0.87+/-0.13; EPO1: 0.92+/-0.08; EPO2: 0.87+/-0.11), nor histochemically (mean+/-SD for C: 0.64+/-0.20; EPO1: 0.75+/-0.17; EPO2: 0.80+/-0.07). In the EPO2 group mean arterial pulmonary pressure and dP/dtmax were increased compared with control group.. Despite promising results from studies in rodents, rhEPO did not reduce infarct size measured after 2.5 h of reperfusion in our porcine model.

Topics: Animals; Blood Pressure; Cardiac Output; Cardiotonic Agents; Coronary Stenosis; Disease Models, Animal; Erythropoietin; Myocardial Infarction; Myocardial Ischemia; Recombinant Proteins; Swine; Tomography, Emission-Computed, Single-Photon