Hélène Greigert1, Marianne Zeller2, Alain Putot3, Eric Steinmetz4, Béatrice Terriat5, Maud Maza2, Nicolas Falvo6, Géraldine Muller7, Louis Arnould8, Catherine Creuzot-Garcher8, André Ramon9, Laurent Martin10, Georges Tarris10, Tibor Ponnelle11, Sylvain Audia12, Bernard Bonnotte12, Yves Cottin13, Maxime Samson14. 1. Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Department of Vascular Medicine, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France. 2. PEC2, EA 7460 Dijon, France. 3. PEC2, EA 7460 Dijon, France; Department of Geriatric Internal Medicine, Dijon University Hospital, Dijon, France. 4. Department of Cardiovascular and Thoracic Surgery, Dijon University Hospital, Dijon, France. 5. Department of Vascular Medicine, Dijon University Hospital, Dijon, France. 6. Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France. 7. Department of Internal Medicine and Systemic Diseases, Dijon University Hospital, Dijon, France. 8. Department of Ophthalmology, Dijon University Hospital, Dijon, France. 9. Department of Rheumatology, Dijon University Hospital, Dijon, France. 10. Department of Pathology, Dijon University Hospital, Dijon, France. 11. Cypath pathology center, Dijon, France. 12. Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France. 13. Cardiology Department, Dijon University Hospital, Dijon, France. 14. Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France. Electronic address: maxime.samson@u-bourgogne.fr.
Abstract
BACKGROUND: Cardiovascular risk is increased in giant cell arteritis (GCA). We aimed to characterize myocardial infarction (MI) in a GCA cohort, and to compare the GCA and non-GCA population affected by MI. METHODS: In patients with a biopsy-proven diagnosis of GCA between 1 January 2001 and 31 December 2016 in Côte D'Or (France), we identified patients with MI by crossing data from the territorial myocardial infarction registry (Observatoire des Infarctus de Côte d'Or) database. Five controls (non-GCA + MI) were paired with one case (GCA + MI) after matching for age, sex, cardiovascular risk factors and prior cardiovascular disease. MI were characterized as type 1 MI (T1MI), resulting from thrombus formation due to atherothrombotic disease, or type 2 MI (T2MI), due to a myocardial supply/demand mismatch. GCA-related MI was defined as MI occurring within 3 months of a GCA flare (before or after). RESULTS: Among 251 biopsy-proven GCA patients, 13 MI cases were identified and paired with 65 controls. MI was GCA-related in 6/13 cases, accounting for 2.4% (6/251) of our cohort. T2MI was more frequently GCA-related than GCA-unrelated (80% vs. 16.7%, p = 0.080), and GCA diagnosis was the only identified triggering factor in 75% of GCA-related T2MI. GCA-unrelated MI were more frequently T1MI and occurred in patients who had received a higher cumulative dose of prednisone (p = 0.032). GCA was not associated with poorer one-year survival. CONCLUSIONS: GCA-related MI are mainly T2MI probably caused by systemic inflammation rather than coronaritis. GCA-unrelated MI are predominantly T1MI associated with atherothrombotic coronary artery disease.
BACKGROUND: Cardiovascular risk is increased in giant cell arteritis (GCA). We aimed to characterize myocardial infarction (MI) in a GCA cohort, and to compare the GCA and non-GCA population affected by MI. METHODS: In patients with a biopsy-proven diagnosis of GCA between 1 January 2001 and 31 December 2016 in Côte D'Or (France), we identified patients with MI by crossing data from the territorial myocardial infarction registry (Observatoire des Infarctus de Côte d'Or) database. Five controls (non-GCA + MI) were paired with one case (GCA + MI) after matching for age, sex, cardiovascular risk factors and prior cardiovascular disease. MI were characterized as type 1 MI (T1MI), resulting from thrombus formation due to atherothrombotic disease, or type 2 MI (T2MI), due to a myocardial supply/demand mismatch. GCA-related MI was defined as MI occurring within 3 months of a GCA flare (before or after). RESULTS: Among 251 biopsy-proven GCA patients, 13 MI cases were identified and paired with 65 controls. MI was GCA-related in 6/13 cases, accounting for 2.4% (6/251) of our cohort. T2MI was more frequently GCA-related than GCA-unrelated (80% vs. 16.7%, p = 0.080), and GCA diagnosis was the only identified triggering factor in 75% of GCA-related T2MI. GCA-unrelated MI were more frequently T1MI and occurred in patients who had received a higher cumulative dose of prednisone (p = 0.032). GCA was not associated with poorer one-year survival. CONCLUSIONS: GCA-related MI are mainly T2MI probably caused by systemic inflammation rather than coronaritis. GCA-unrelated MI are predominantly T1MI associated with atherothrombotic coronary artery disease.
Authors: Hélène Greigert; André Ramon; Georges Tarris; Laurent Martin; Bernard Bonnotte; Maxime Samson Journal: J Clin Med Date: 2022-01-05 Impact factor: 4.241