The use of a target hemoglobin level of 13.5 g per deciliter (as compared with 11.3 g per deciliter) was associated with increased risk and no incremental improvement in the quality of life. (ClinicalTrials.gov number, NCT00211120 [ClinicalTrials.gov].).

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PPRECIATION OF THE CRUcial role of risk factors in the development of coronary heart disease (CHD) is one of the most significant advances in the understanding of this important disease. Extensive epidemiological research has established cigarette smoking, 1 diabetes, 2 hyperlipidemia, 3 and hypertension 4 as independent risk factors for CHD. In addition, treatment of these risk factors has been convincingly shown to reduce the risk of future cardiac events. 1,5 Because of the strength of evidence supporting their role in the pathogenesis of CHD, these 4 risk factors have often been labeled as "conventional" risk factors. Although the importance of conventional risk factors is well established, it is commonly suggested that more than 50% of patients with CHD lack any of the conventional risk factors. 6-13 This implies that other factors play a significant role in the development of this disease and, furthermore, that there is a substantial void in current understanding of the pathogenesis of CHD. This perceived void has led to considerable research on nontraditional risk factors and genetic causes of heart disease. Yet, data to support this "50%" belief are limited, and some have suggested that conventional risk factors play a much more significant role. 14,15 Determining the validity of this idea is important for scientific accuracy and to guide the practice of clinical medicine, public health policies, and prioritization of research efforts. In addition, patients and physicians can better understand the impact of preventing or modifying these specific risk factors on the risk of future CHD. We therefore sought to determine the prevalence of the 4 conventional risk

Trials of anemia correction in chronic kidney disease have found either no benefit or detrimental outcomes of higher targets. We did a secondary analysis of patients with chronic kidney disease enrolled in the Correction of Hemoglobin in the Outcomes in Renal Insufficiency trial to measure the potential for competing benefit and harm from achieved hemoglobin and epoetin dose trials. In the 4 month analysis, significantly more patients in the high-hemoglobin compared to the low-hemoglobin arm were unable to achieve target hemoglobin and required high-dose epoetin-α. In unadjusted analyses, the inability to achieve a target hemoglobin and high-dose epoetin-α were each significantly associated with increased risk of a primary endpoint (death, myocardial infarction, congestive heart failure or stroke). In adjusted models, high-dose epoetin-α was associated with a significant increased hazard of a primary endpoint but the risk associated with randomization to the high hemoglobin arm did not suggest a possible mediating effect of higher target via dose. Similar results were seen in the 9 month analysis. Our study demonstrates that patients achieving their target had better outcomes than those who did not; and among subjects who achieved their randomized target, no increased risk associated with the higher hemoglobin goal was detected. Prospective studies are needed to confirm this relationship and determine safe dosing algorithms for patients unable to achieve target hemoglobin.

This study shows that minor elevations of CK-MB after successful coronary interventions identify a population with a worse long-term prognosis compared with patients with no enzyme elevations and appear to have an adverse effect on long-term prognosis. Future studies of percutaneous coronary revascularization should include routine measurements of biochemical cardiac markers as important predictors of long-term prognosis.

Although we found a highly significant excess in mortality consistent across 4 trials with 3 different oral glycoprotein IIb/IIIa inhibitor agents, this was associated with a reduction in the need for urgent revascularization and no increase in myocardial infarction. These findings suggest the potential for a direct toxic effect with these agents and argue against a prothrombotic mechanism. Further investigation to elucidate the cause of this increased fatality risk is warranted.

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