Gunnar Tomasson, MD; Christine Peloquin, MPH; Aladdin Mohammad, MD, PhD; Thorvardur J. Love, MD, PhD; Yuqing Zhang, DSc; Hyon K. Choi, MD, DrPH; Peter A. Merkel, MD, MPH
Grant Support: This work was supported in part by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (P60 AR047785) and the Boston University School of Medicine.
Potential Conflicts of Interest: None disclosed. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M12-3046.
Reproducible Research Statement:Study protocol and data set: Not available. Statistical code: Available from Dr. Tomasson (e-mail, firstname.lastname@example.org).
Requests for Single Reprints: Gunnar Tomasson, MD, Department of Public Health Sciences, University of Iceland, Stapi Hringbraut, 101 Reykjavik, Iceland; e-mail, email@example.com.
Current Author Addresses: Dr. Tomasson: Department of Public Health Sciences, University of Iceland, Stapi Hringbraut, 101 Reykjavik, Iceland.
Ms. Peloquin and Drs. Zhang and Choi: Boston University, 650 Albany Street, Suite 200, Boston, MA 02118.
Dr. Mohammad: Department of Rheumatology, Skåne University Hospital, Lund SE-221 85, Sweden.
Dr. Love: Faculty of Medicine, University of Iceland, Vatnsmyrarvegur 16, 101 Reykjavik, Iceland.
Dr. Merkel: University of Pennsylvania, 8th Floor Penn Tower, 3400 Spruce Street, Philadelphia, PA 19104.
Author Contributions: Conception and design: G. Tomasson, T.J. Love, Y. Zhang, H.K. Choi, P.A. Merkel.
Analysis and interpretation of the data: G. Tomasson, A. Mohammad, Y. Zhang, H.K. Choi, P.A. Merkel.
Drafting of the article: G. Tomasson, Y. Zhang, H.K. Choi, P.A. Merkel.
Critical revision of the article for important intellectual content: G. Tomasson, T.J. Love, Y. Zhang, H.K. Choi, P.A. Merkel.
Final approval of the article: G. Tomasson, A. Mohammad, T.J. Love, Y. Zhang, H.K. Choi, P.A. Merkel.
Statistical expertise: G. Tomasson, Y. Zhang, H.K. Choi.
Obtaining of funding: H.K. Choi.
Administrative, technical, or logistic support: G. Tomasson, H.K. Choi, P.A. Merkel.
Collection and assembly of data: C. Peloquin, H.K. Choi.
Tomasson G., Peloquin C., Mohammad A., Love T., Zhang Y., Choi H., Merkel P.; Risk for Cardiovascular Disease Early and Late After a Diagnosis of Giant-Cell Arteritis: A Cohort Study. Ann Intern Med. 2014;160:73-80. doi: 10.7326/M12-3046
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Published: Ann Intern Med. 2014;160(2):73-80.
Involvement of large arteries is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascular events is not well-understood.
To evaluate the risks for incident myocardial infarction (MI), cerebrovascular accident (CVA), and peripheral vascular disease (PVD) in individuals with incident GCA in a general population context.
Observational cohort study.
U.K. primary care database.
3408 patients with incident GCA and 17 027 age- and sex-matched reference participants without baseline cardiovascular disease (MI, CVA, or PVD).
Diagnoses of GCA, outcomes, and cardiovascular risk factors were identified from electronic medical records. One combined and 3 separate cohort analyses were conducted for the outcomes of MI, CVA, and PVD. The association of GCA with study outcomes is expressed with hazard ratios (HRs) with 95% CIs after adjustment for potential cardiovascular risk factors.
Among 3408 patients with GCA (73% female; mean age, 73 years), the incidence rates of MI, CVA, and PVD were 10.0, 8.0, and 4.2 events per 1000 person-years, respectively, versus 4.9, 6.3, and 2.0 events per 1000 person-years, respectively, among reference participants. The HRs were 1.70 (95% CI, 1.51 to 1.91) for the combined outcome, 2.06 (CI, 1.72 to 2.46) for MI, 1.28 (CI, 1.06 to 1.54) for CVA, and 2.13 (CI, 1.61 to 2.81) for PVD. The HRs were more pronounced in the first month after GCA diagnosis (combined HR, 4.92 [CI, 2.59 to 9.34]; HR for MI, 11.89 [CI, 2.40 to 59.00]; HR for CVA, 3.93 [CI, 1.76 to 8.79]; HR for PVD, 3.86 [CI, 0.78 to 19.17]).
Information on temporal arterial biopsies was not available, and there was a substantial amount of missing data on cardiovascular risk factors.
Giant-cell arteritis is associated with increased risks for MI, CVA, and PVD.
National Institute of Arthritis and Musculoskeletal and Skin Diseases.
Claude Bachmeyer, Milène Buffo, Bérénice Soyez.
Department of Internal Medicine, Tenon Hospital (AP-HP), Paris, France
January 30, 2014
Risk of Cardiovascular Disease Early After a Diagnosis of Giant-Cell Arteritis
We read with great interest the article by Tomasson et al. (1) indicating a high risk for cardiovascular disease early after diagnosis of giant-cell arteritis (GCA). However the authors acknowledge that major data are missing on cardiovascular risk factors. Indeed these cardiovascular events including myocardial infarction, cerebrovascular accident, and peripheral vascular disease could be related to GCA and to the delay of treatment, but also to corticotherapy with well-known adverse effects such as diabetes mellitus, dyslipidemia, hypertension, in elderly patients with frequent preexisting cardiovascular risk factors.
In our department, patients diagnosed with GCA and with high-risk cardiovascular factors are initially given treatment with aspirin and statins as adjunctive therapy to glucocorticoids. Indeed the efficacy of both drugs is well-known in patients with atherosclerosis risk factors and co-administration of aspirin and statins shows additional effects in reducing cardiovascular mortality in the general population (2). These drugs could reduce the inflammatory components of atherosclerosis by interfering with a variety of immune-inflammatory pathways that are also involved in the pathogenesis of GCA, preventing thrombosis in a vessel related to inflammation, myointimal thickening, and stenosis, leading to ischemic complications (3). No definitive evidence of the efficacy of these drugs has been demonstrated to date in GCA, as noted by others (3). Only two retrospective studies suggest a protective role of aspirin. The first study showed that 3/36 (8%) of patients treated with aspirin before glucorticosteroid treatment was started developed cranial ischemic complications, compared with 40/130 (29%) of the non-aspirin-treated patients (p=0.01). After diagnosis of GCA was established, cranial ischemic complications were observed in 2/73patients (3%) of the aspirin-treated patients, compared with 12/93 (13%) of the patients treated with prednisone only (p=0.02) (4). In the other study including 143 patients, 11/68 (16.2%) patients under aspirin or anticoagulant therapy developed an ischemic accident compared with 36 of 75 patients (48.0%) not receiving such therapy (p<0.0005) (5).
We recommend antiplatelet therapy and statins at least in patients with GCA and ischemic cephalic complications or symptomatic arteritis of lower or upper limbs at the time of diagnosis during the first months of corticotherapy. However such a treatment should be discussed in each patient based on evaluation of individual risk of cardiovascular events and of hemorrhagic risk.
Therefore, can the authors indicate whether treatment with aspirin and statins was associated to corticotherapy and what was the delay between initial symptoms and treatment of GCA?
1. Tomasson G, Peloquin C, Mohammad A, Love TJ, Zhang Y; Choi HK, et al. Risk for cardiovascular disease early and late after a diagnosis of giant-cell arteritis: A cohort study. Ann Intern Med. 2014;160:73-80-80.
2. Hennekens CH, Schneider WR. The need for wider and appropriate utilization of aspirin and statins in the treatment and prevention of cardiovascular disease. Expert Rev Cardiovasc Ther. 2008;6:95-107.
3. Spiera RF, Spiera H. Therapy for giant cell arteritis: can we do better? Arthritis Rheum. 2006;54:3071-4.
4. Nesher G, Berkun Y, Mates M, Baras M, Rubinow A, Sonnenblick M. Low-dose aspirin and prevention of cranial ischemic complications in giant cell arteritis. Arthritis Rheum. 2004;50:1332-7.
5. Lee MS, Smith SD, Galor A, Hoffman GS. Antiplatelet and anticoagulant therapy in patients with giant cell arteritis. Arthritis Rheum. 2006;54:3306-9.
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