Possibilities of early detection of severe cardiovascular manifestations of SLE


Authors: D. Tegzová 1;  D. Ambrož 1;  P. Jansa 1;  T. Paleček 1;  L. Dušek 2
Authors‘ workplace: Revmatologický ústav Praha, 1II. interní klinika kardiologie a angiologie VFN 1. LF UK v Praze ;  Institut biostatistiky a analýz v Brně 2
Published in: Čes. Revmatol., 15, 2007, No. 3, p. 131-141.
Category: Original Papers

Overview

Objective:
the aim of the study was to determine particular cardiovascular manifestations in systemic lupus erythematosus (SLE), to describe their type and severity, find out a relationship with particular SLE characteristics and suggest possibilities for early detection of those complications.

Methods:
Twenty-nine patients with SLE and 15 healthy controls were investigated. Patients had extensive echocardiographic evaluation including exercise stress testing evaluation after 6 minutes of walk as well as Holter monitoring. Basic demographic data, type of immunosuppressive treatment and time-course of its administration, the dose of glucocorticoids, presence of autoantibodies (anti-dsDNA, anti-Ro, La, Sm, aCL), haemostatic parameters, lipid spectrum, presence of organ manifestations, pulmonary functions as well as activity of the disease according the SLEDAI score were evaluated. The association between particular cardiovascular pathologies and SLE parameters was studied.

Results:
Presence of cardiovascular manifestations in our group was relatively small. The difference between standard and exercise stress testing echocardiography was found. After the 6 minute-walk test, several heart pathologies appeared. No significant changes were found during echocardiographic examination. Higher levels of Tei index significantly differentiated between control individuals and patients with SLE. Moderate difference, however not statistically significant, was also observed between SLE patients with high and low disease activity. PG max on tricuspidal valve according to echocardiography and systolic excursion (TAPSE) were not different from those in healthy controls. Those values did not differ also between patients with different disease activity of SLE. Biochemistry and haemostatic parameters revealed statistically significant differences between healthy controls and SLE patients for D-dimers that are significantly increased in SLE patients and correlate with the disease activity. The value of DLCO, on the contrary, decreases with the disease activity of SLE patients. The significance of evaluating the ratio of FVC/DLCO index for the diagnosis of pulmonary hypertension was not confirmed. Significantly lower values of DLCO were associated with increased PG max in the exercise stress testing. DLCO was of greater importance than the FVC/DLCO index. Exercise stress testing echocardiography was beneficial for the diagnosis of early forms of pulmonary hypertension particularly in the evaluation of PG max on tricuspidal valve that increased after the exercise up-to the borderline levels of detectable pulmonary hypertension. Increase of Tei after the exercise stress testing did not correlate with the increase of PG max in patients with the risk of pulmonary hypertension. Pericardial effusion was diagnosed in 17.3 % of patients.

Conclusion:
Exercise stress testing echocardiography demonstrated benefit for the detection of potential onset of pulmonary hypertension. Patients with SLE and higher risk of cardiovascular manifestation should be regularly monitored by echocardiography. More specific examination for cardiovascular pathologies is exercise stress testing echocardiography. Another reasonable and beneficial examination is DLCO.

Key words:
SLE, cardiovascular manifestation, echocardiography, exercise stress testing echocardiography, pulmonary hypertension, SLE activity


Sources

1. Gordon C. Long-term complications of systemic lupus erythematosus. Rheumatology 2002, 41: 1095–1100.

2. Manger K, Manger B, Repp R, et al. Definition of risk factors for death, and stage renal disease, and thromboembolic events in a monocentric cohort of 338 patients with systemic lupus erythematosus. Ann Rheum Dis 2002; 61: 1065–1070.

3. Manzi S. Systemic lupus erythematosus: a model for atherogenesis? Rheumatology 2000; 39: 353–359.

4. Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham study. Am J Epidemiol 1997; 145: 408–415.

5. Nuttall SL, Heaton S, Piper MK, et al. Cardiovascular risk in systemic lupus erythematosus – evidence of increased oxidative stress and dyslipidaemia. Rheumatology 2003; 42: 758–762.

6. Raza K, Thambyrajah J, Townend JN, et al. Suppression of inflammation in primary systemic vasculitis restores vascular endothelial function: lessons for atherosclerotic disease? Circulation 2000; 102: 1470–1472.

7. Schattner A, Liang MH. The cardiovascular burden of lupus. Arch Intern Med 2003; 163(13): 1507–1510.

8. Selzer F, Sutton-Tyrrell K, Fitzgerald S, et al. Vascular stiffness in women with systemic lupus erythematosus. Hypertension 2001; 37: 1075–1082.

9. Svenungsson E, Sensen-Urstad K, Heimbuerger M, et al. Risk factors for cardiovascular disease in systemic lupus erythematosus. Circulation 2001; 104: 1887–1893.

10. Thiagarajan P. Atherosclerosis, autoimunity and systemic lupus erythematosus. Circulation 2001; 104: 1876–1877.

11. Asherson RA, Mackworth-Young CG, Boey ML, et al. Pulmonary hypertension in systemic lupus erythematosus. B M J 1983; 287: 1024–1025.

12. Petri 1992, Sturfet 1992, Quismorio 1993, Winslow 1995,Word Symposium -Primary Pulmonary Hypertension 1998, 2003)

13. Gaine SP. Pulmonary hypertension. JAMA 2000; 284:3160–3168

14. Yokoi T, Tomita Y, Fukaya M, et al. Pulmonary hypertension associated with systemic lupus erythematosus: predominantly thrombotic arteriopathy accompanied by plexiform lesions. Arch Pathol Lab Med 1998; 122(5): 467–70

15. Hoeper M, Galie N, Simonneau G, Rubin LJ. Pulmonary perspective: New treatments for pulmonary arterial hypertension. Am J Resp Crit Care Med 2002; 165: 1209–16

16. Galie N, Torbicki A. Pulmonary arterial hypertension: new ideas and perspectivers. Heart 2001; 85: 475–480.

17. Nowak J, Nilsson T, Sylvén C, et al. Potential of carotid ultrasonography in the diagnosis of coronary artery disease. Stroke 1998; 29: 439–446.

18. Urowitz MB, Gladman DD. How to improve morbidity and mortality in systemic lupus erythematosus. Rheumatology 2000; 39: 238–244.

19. Altman DG. Practical Statistics for Medical Research. London: Chapman and Hall, 619p, 1991.

20. Zar JH. Biostatistical Methods. 2nd ed. London: Prentice Hall, 556p, 1984.

Labels
Dermatology & STDs Paediatric rheumatology Rheumatology
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