Malin Hultcrantz1, Anton Modlitba2, Senthil K Vasan3, Arvid Sjölander2, Klaus Rostgaard4, Ola Landgren5, Henrik Hjalgrim6, Henrik Ullum7, Christian Erikstrup8, Sigurdur Y Kristinsson9, Gustaf Edgren10. 1. Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Myeloma Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. Electronic address: malin.hultcrantz@ki.se. 2. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. 3. Oxford Center for Diabetes, Endocrinology, and Metabolism, University of Oxford, Oxford, United Kingdom. 4. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. 5. Myeloma Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 6. Department of Hematology, Copenhagen University Hospital, Copenhagen, Denmark. 7. Department of Clinical Immunology, the Blood Bank, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark. 8. Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark. 9. Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Faculty of Medicine, University of Iceland and Department of Hematology, Landspitali National University Hospital, Reykjavik, Iceland. 10. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Cardiology, Södersjukhuset, Stockholm, Sweden.
Abstract
INTRODUCTION: There are conflicting results whether elevated hematocrit is associated with an increased risk of thromboembolic events in individuals without polycythemia vera. To assess the risk of vascular events in relation to hemoglobin concentration, we conducted a large population-based cohort study based on Scandinavian health registers. MATERIALS AND METHODS: We included 1,538,019 Swedish and Danish blood donors between 1987 and 2012. Hazard ratios (HRs) of arterial and venous thrombosis were estimated using Cox regression. Additionally, we fitted person-stratified models where each donor was compared only to him-/herself. RESULTS: The risk of myocardial infarction and ischemic stroke increased with higher hemoglobin concentration in both men and women. The HRs for myocardial infarction and ischemic stroke in men with hemoglobin concentration ≥ 17.5 g/dL were 3.52 (95% confidence interval [CI], 2.85-4.36) and 2.36 (95% CI, 1.63-3.43), respectively, compared to the reference group. The corresponding HRs for women with hemoglobin concentration ≥ 16.0 g/dL were 3.22 (2.12-4.89) and 2.35 (1.37-4.02) for myocardial infarction and ischemic stroke, respectively. The risk of venous thrombosis was highest in men with subnormal hemoglobin concentration (<13.0 g/dL), HR 1.69 (95% CI, 1.40-2.04). In the person-stratified model, the association between elevated hemoglobin concentration and risk of myocardial infarction was attenuated but remained significant. CONCLUSIONS: In this large cohort of Scandinavian blood donors, elevated hemoglobin concentration was associated with an increased risk of vascular events, primarily arterial events. Even though associations were weakened when each person served as their own control, a high hemoglobin concentration may serve as a cardiovascular risk marker.
INTRODUCTION: There are conflicting results whether elevated hematocrit is associated with an increased risk of thromboembolic events in individuals without polycythemia vera. To assess the risk of vascular events in relation to hemoglobin concentration, we conducted a large population-based cohort study based on Scandinavian health registers. MATERIALS AND METHODS: We included 1,538,019 Swedish and Danish blood donors between 1987 and 2012. Hazard ratios (HRs) of arterial and venous thrombosis were estimated using Cox regression. Additionally, we fitted person-stratified models where each donor was compared only to him-/herself. RESULTS: The risk of myocardial infarction and ischemic stroke increased with higher hemoglobin concentration in both men and women. The HRs for myocardial infarction and ischemic stroke in men with hemoglobin concentration ≥ 17.5 g/dL were 3.52 (95% confidence interval [CI], 2.85-4.36) and 2.36 (95% CI, 1.63-3.43), respectively, compared to the reference group. The corresponding HRs for women with hemoglobin concentration ≥ 16.0 g/dL were 3.22 (2.12-4.89) and 2.35 (1.37-4.02) for myocardial infarction and ischemic stroke, respectively. The risk of venous thrombosis was highest in men with subnormal hemoglobin concentration (<13.0 g/dL), HR 1.69 (95% CI, 1.40-2.04). In the person-stratified model, the association between elevated hemoglobin concentration and risk of myocardial infarction was attenuated but remained significant. CONCLUSIONS: In this large cohort of Scandinavian blood donors, elevated hemoglobin concentration was associated with an increased risk of vascular events, primarily arterial events. Even though associations were weakened when each person served as their own control, a high hemoglobin concentration may serve as a cardiovascular risk marker.
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