Hemoglobin and Change in Hemoglobin Status Predict Mortality, Cardiovascular Events, and Bleeding in Stable Coronary Artery Disease - 27/09/17
, Nicola Greenlaw, MS b, Roberto Ferrari, MD c, Ian Ford, PhD b, Jean-Claude Tardif, MD d, Michal Tendera, MD e, Christopher M. Reid, MD f, Nicolas Danchin, MD g, Janina Stepinska, MD h, Ph. Gabriel Steg, MD i, j, Kim M. Fox, MD jfor the
ProspeCtive observational LongitudinAl RegIstry oF patients with stable coronary arterY disease (CLARIFY) Investigators∗
Abstract |
Background |
Anemia is a predictor of adverse outcomes in acute myocardial infarction. We studied the relationship of hemoglobin, or its change over time, and outcomes in patients with stable coronary artery disease.
Methods |
The ProspeCtive observational LongitudinAl RegIstry oF patients with stable coronary arterY disease is a prospective, cohort study of outpatients with stable coronary artery disease (32,901 in 45 countries 2009-2010): 21,829 with baseline hemoglobin levels. They were divided into hemoglobin quintiles and anemia status (anemic or normal at baseline/follow-up: normal/normal; anemic/normal; normal/anemic; anemic/anemic. All-cause mortality, cardiovascular events, and major bleeding at 4-year follow-up were assessed.
Results |
Low baseline hemoglobin was an independent predictor of all-cause, cardiovascular, and noncardiovascular mortality, the composite of cardiovascular death/myocardial infarction or stroke and major bleeds (all P <.001; unadjusted models). Anemia at follow-up was independently associated with all-cause mortality (hazard ratio [HR], 1.90; 95% confidence interval [CI], 1.55-2.33 for anemic/anemic; 1.87; 1.54-2.28 for normal/anemic; both P <.001), noncardiovascular mortality (P <.001), and cardiovascular mortality (P = .001). Patients whose baseline anemia normalized (anemic/normal) were not at increased risk of death (HR, 1.02; 95% CI, 0.77-1.35), although the risk of major bleeding was greater (HR, 2.06; 95% CI, 1.23-3.44; P = .013) than in those with normal hemoglobin throughout. Sensitivity analyses excluding patients with heart failure and chronic kidney disease at baseline yielded qualitatively similar results.
Conclusions |
In this large population with stable coronary artery disease, low hemoglobin was an independent predictor of mortality, cardiovascular events, and major bleeds. Persisting or new-onset anemia is a powerful predictor of cardiovascular and noncardiovascular mortality.
Le texte complet de cet article est disponible en PDF.Keywords : Anemia, Coronary artery disease, Hemoglobin
Plan
| Funding: This work was supported by research grants from Servier, France. The study was designed and conducted by the investigators. All data were collected and analyzed by NG and IF at the independent academic statistics center at the Robertson Centre for Biostatistics at the University of Glasgow, United Kingdom, and interpreted by the investigators. The sponsor had no role in the design and management of the study, in the analysis and interpretation of the data, and in the decision to submit the manuscript for publication, but did assist with the setup, data collection, and management of the study in each country. The sponsor funded editorial support for editing and revision of the manuscript and received the manuscript for review before submission. The ProspeCtive observational LongitudinAl RegIstry oF patients with stable coronary arterY disease registry enforces a no ghostwriting policy. |
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| Conflict of Interest: PRK reports personal fees from Servier, during the conduct of the study, and personal fees and other from Servier, Alere, Amgen, BMS, Janssen, Novartis, Pfizer, Pharmacosmos, Vifor and research grants from Servier, Alere and Pharmacosmos outside the submitted work. NG reports grants from Servier during the conduct of the study. RF reports grants and personal fees from Servier and Novartis, personal fees from Merck Serono, grants and personal fees from Boehringer Ingelheim, grants from Irbtech, and personal fees from Amgen, outside the submitted work. IF reports grants and personal fees from Servier, during the conduct of the study, and grants and personal fees from Amgen, outside the submitted work. J-CT reports grants from Servier, during the conduct of the study, grants and other from Servier, grants from Roche, grants and other from Pfizer, grants from AstraZeneca and Merck, grants and other from Sanofi, grants from Eli-Lilly, grants and other from Thrasos, grants from Valeant, and other from Takeda, outside the submitted work. MT reports personal fees from Servier during the conduct of the study, personal fees from Bayer, Celyad, Janssen-Cilag, Novartis, Servier, and Stealth Biotherapeutics, and grants from Polish National Center for Research and Development outside the submitted work. ND reports grants, personal fees, and nonfinancial support from Amgen, grants, personal fees, and nonfinancial support from AstraZeneca, grants and personal fees from Bayer and Daiichi Sankyo, grants, personal fees, and nonfinancial support from Eli Lilly, personal fees from GSK, grants and personal fees from MSD, personal fees from Novartis, Novo-Nordisk, Pfizer, and Roche, grants, personal fees, and nonfinancial support from Sanofi, personal fees and nonfinancial support from Servier, and personal fees from BMS and Boehringer Ingelheim, during the conduct of the study. JS reports grants from Novartis, grants, personal fees, and nonfinancial support from Servier, personal fees from Abbott, AstraZeneca, and Bayer, personal fees and nonfinancial support from Boehringer Ingelheim, and personal fees from Elli Lilly, Sanofi, and Amgen, outside the submitted work. PGS reports grants and personal fees from Servier, during the conduct of the study, personal fees from Amarin, AstraZeneca, Bayer, Boehringer-Ingelheim, Bristol-Myers-Squibb, Daiichi-Sankyo, GlaxoSmithKline, Lilly, Merck-Sharpe-Dohme, Novartis, Pfizer, and Roche, grants and personal fees from Sanofi and Servier, personal fees from Janssen, personal fees and nonfinancial support from The Medicines Company, and personal fees from Regado and Regeneron, outside the submitted work. KMF reports personal fees from Servier, nonfinancial support from Servier, during the conduct of the study, personal fees and nonfinancial support from Servier, personal fees from AstraZeneca and TaurX, nonfinancial support from Armgo, personal fees and nonfinancial support from Broadview Ventures, personal fees from CellAegis, outside the submitted work; and Director of Heart Research Ltd and Vesalius Trials Ltd; minimal stockholder of Armgo and CellAegis. |
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| Authorship: All authors had access to the data and played a role in writing this manuscript. |
Vol 130 - N° 6
P. 720-730 - juin 2017 Retour au numéro
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