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      Myocarditis in systemic lupus erythematosus diagnosed by 18F-fluorodeoxyglucose positron emission tomography

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          Abstract

          Objectives

          Cardiovascular diseaseand heart failure (CHF) are leading causes of death in systemic lupus erythematosus (SLE). The underlying mechanisms for increased CHF in SLE are unclear but myocardial inflammation and lupus myocarditis (LM) may play a role. We propose that 18F-fluorodeoxyglucose–positron emission tomography ( 18F-FDG–PET)/CT can help diagnose LM.

          Methods

          This report describes eight patients with presumed LM; five patients were evaluated due to active cardiorespiratory symptoms and three patients were participating in a pilot study to determine the prevalence of subclinical myocarditis in SLE. Clinical characteristics, laboratory and cardiac testing including electrocardiography (ECG), transthoracic echocardiogram (TTE), coronary artery evaluation as well as 18F-FDG–PET/CT imaging are discussed.

          Results

          Four patients were African American and the others were Hispanic. Half presented with chest pain; 37% had dyspnoea and 25% were asymptomatic. The median SLE Disease Activity Index (SLEDAI-2K) was 5 (2–18) and SLICC Damage Index (SDI) 0.5 (0–5). The median troponin level was 0.08 ng/mL (0–0.9). The most common ECG findings were non-specific ST-T wave abnormalities (n=5). Fifty per cent of the patients had a decreased ejection fraction on TTE and all patients had diffuse myocardial FDG uptake on 18F-FDG–PET/CT consistent with myocardial inflammation.

          Conclusion

          This case series is the first to describe the use of 18F-FDG–PET/CT in the diagnosis of LM and discuss the clinical characteristics and cardiac findings of eight patients with LM supporting the role for cardiac 18F-FDG–PET/CT in its diagnosis.

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          Most cited references36

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          Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study.

          The authors ascertained cardiovascular events (myocardial infarction and angina pectoris) in 498 women with systemic lupus erythematosus seen at the University of Pittsburgh Medical Center from 1980 to 1993 (3,522 person-years). Subjects were stratified by age, and cardiovascular event incidence rates were determined. The authors compared these rates with cardiovascular event rates were determined. The authors compared these rates with cardiovascular event rates occurring over the same time period in 2,208 women of similar age participating in the Framingham Offspring Study (17,519 person-years). Age-specific rate ratios were computed to determine whether the cardiovascular events in the lupus cohort were greater than expected. The risk factors associated with cardiovascular events in women with lupus were determined. There were 33 first events (11 myocardial infarction, 10 angina pectoris, and 12 both angina pectoris and myocardial infarction) after the diagnosis of lupus: two thirds were under the age of 55 years at the time of event. Women with lupus in the 35- to 44-year age group were over 50 times more likely to have a myocardial infarction than were women of similar age in the Framingham Offspring Study (rate ratio = 52.43, 95% confidence interval 21.6-98.5). Older age at lupus diagnosis, longer lupus disease duration, longer duration of corticosteroid use, hypercholesterolemia, and postmenopausal status were more common in the women with lupus who had a cardiovascular event than in those who did not have an event. Premature cardiovascular disease is much more common in young premenopausal women with lupus than in a population sample. With the increased life expectancy of lupus patients due to improved therapy, cardiovascular disease has emerged as a significant threat to the health of these women. The impact of this problem has been underrecognized, with little focus placed on aggressive management of hypercholesterolemia and other possible risk factors.
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            Prevalence and correlates of accelerated atherosclerosis in systemic lupus erythematosus.

            Although systemic lupus erythematosus is associated with premature myocardial infarction, the prevalence of underlying atherosclerosis and its relation to traditional risk factors for cardiovascular disease and lupus-related factors have not been examined in a case-control study. In 197 patients with lupus and 197 matched controls, we performed carotid ultrasonography, echocardiography, and an assessment for risk factors for cardiovascular disease. The patients were also evaluated with respect to their clinical and serologic features, inflammatory mediators, and disease treatment. The risk factors for cardiovascular disease were similar among patients and controls. Atherosclerosis (carotid plaque) was more prevalent among patients than the controls (37.1 percent vs. 15.2 percent, P<0.001). In multivariate analysis, only older age, the presence of systemic lupus erythematosus (odds ratio, 4.8; 95 percent confidence interval, 2.6 to 8.7), and a higher serum cholesterol level were independently related to the presence of plaque. As compared with patients without plaque, patients with plaque were older, had a longer duration of disease and more disease-related damage, and were less likely to have multiple autoantibodies or to have been treated with prednisone, cyclophosphamide, or hydroxychloroquine. In multivariate analyses including patients with lupus, independent predictors of plaque were a longer duration of disease, a higher damage-index score, a lower incidence of the use of cyclophosphamide, and the absence of anti-Smith antibodies. Atherosclerosis occurs prematurely in patients with systemic lupus erythematosus and is independent of traditional risk factors for cardiovascular disease. The clinical profile of patients with lupus and atherosclerosis suggests a role for disease-related factors in atherogenesis and underscores the need for trials of more focused and effective antiinflammatory therapy. Copyright 2003 Massachusetts Medical Society
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              Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus.

              The frequency of coronary heart disease (CHD) and stroke are increased in systemic lupus erythematosus (SLE), but the extent of the increase is uncertain. We sought to determine to what extent the increase could not be explained by common risk factors. The participants at two SLE registries were assessed retrospectively for the baseline level of the Framingham study risk factors and for the presence of vascular outcomes: nonfatal myocardial infarction (MI), death due to CHD, overall CHD (nonfatal MI, death due to CHD, angina pectoris, and congestive heart failure due to CHD), and stroke. For each patient, the probability of the given outcome was estimated based on the individual's risk profile and the Framingham multiple logistic regression model, corrected for observed followup. Ninety-five percent confidence intervals (95% CIs) were estimated by bootstrap techniques. Of 296 SLE patients, 33 with a vascular event prior to baseline were excluded. Of the 263 remaining patients, 34 had CHD events (17 nonfatal MIs, 12 CHD deaths) and 16 had strokes over a mean followup period of 8.6 years. After controlling for common risk factors at baseline, the increase in relative risk for these outcomes was 10.1 for nonfatal MI (95% CI 5.8-15.6), 17.0 for death due to CHD (95% CI 8.1-29.7), 7.5 for overall CHD (95% CI 5.1-10.4), and 7.9 for stroke (95% CI 4.0-13.6). There is a substantial and statistically significant increase in CHD and stroke in SLE that cannot be fully explained by traditional Framingham risk factors alone.
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                Author and article information

                Journal
                Lupus Sci Med
                Lupus Sci Med
                lupusscimed
                lupus
                Lupus Science & Medicine
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2053-8790
                2018
                12 July 2018
                : 5
                : 1
                : e000265
                Affiliations
                [1 ] departmentDivision of Rheumatology , Columbia University College of Physicians and Surgeons, New York Presbyterian Hospital , New York City, New York, USA
                [2 ] departmentDivision of Cardiology , Columbia University College of Physicians and Surgeons, New York Presbyterian Hospital , New York City, New York, USA
                [3 ] departmentNuclear Cardiology Laboratory , Columbia University College of Physicians and Surgeons, New York Presbyterian Hospital , New York City, New York, USA
                Author notes
                [Correspondence to ] Dr Laura Geraldino-Pardilla; lbg2124@ 123456cumc.columbia.edu

                AA and LG-P are joint senior authors.

                Author information
                http://orcid.org/0000-0002-0979-4586
                Article
                lupus-2018-000265
                10.1136/lupus-2018-000265
                6069920
                30094040
                2a0b2523-d819-4473-aac3-e72964733918
                © Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

                History
                : 03 April 2018
                : 24 May 2018
                : 12 June 2018
                Categories
                Co-Morbidities
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