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In recent years there has been increasing interest in the influence of inflammatory rheumatic diseases on the cardiovascular system.1 There is growing evidence that inflammation plays a major part in the initiation and progression of atherosclerosis.2
Polymyalgia rheumatica (PMR) affects primarily the elderly and exhibits evidence of a systemic inflammatory response.3 Because PMR is known to respond well clinically to corticosteroids, we wanted to examine whether this treatment might also have an effect on arterial stiffness in these patients. The aim of this study, therefore, was to investigate the influence of therapy with steroids on the augmentation index (AIx), a marker of arterial stiffness, as measured with non-invasive pulse wave analysis (PWA) in newly diagnosed patients with PMR before and 4 weeks after initiation of treatment with corticosteroids (25 mg prednisolone daily).
Arterial stiffness is a marker of vascular dysfunction. An association has been shown between increased arterial stiffness and a number of traditional vascular risk factors.4 Augmentation of pulse pressure has been shown to be a strong, independent risk marker for premature coronary artery disease: it is associated with cardiovascular risk and predicts adverse cardiovascular events in patients with established coronary artery disease.5 AIx can be assessed non-invasively by applanation tonometry of the radial artery.6 The subendocardial viability ratio (SEVR), also determined in this study, is a measure of myocardial perfusion relative to cardiac workload.6 It provides a useful measure of the relationship between subepicardial/subendocardial blood flow and cardiac workload and, thus, reflects the supply/demand relationship of the myocardium.
Included in the analysis were 13 patients (nine male; mean age 66.5 (SD 9.8) years). Pulse wave analysis was performed using applanation tonometry with a high-fidelity micro-manometer (SPC-301, Millar Instruments, Houston, TX, USA) and the Sphygmocor apparatus (Sphygmocor AtCor Medical, version 6.31, Sydney, Australia). To exclude the influence of heart rate on the AIx, the normalised index for 75 beats per minute is given.7 Thirty age- and sex-matched subjects (19 male; mean age 65.6 (8.2) years) served as a control group for comparison of AIx.
After treatment with corticosteroids, markers of systemic inflammation as well as pain improved statistically significantly. AIx improved significantly from 28.5 (9.1%) to 25.3 (9.9%) (p = 0.006). In addition, the SEVR also improved. Table 1 summarises all results. At baseline AIx tended to be higher in the PMR group compared with controls, but this difference did not reach statistical significance (28.5 (9.1%) vs 24.7 (6.4%); p = 0.19). After 4 weeks of treatment AIx was nearly equal in both groups (p = 0.83). We found no significant correlation between the improvement of any of the inflammatory markers and improvement of the AIx; this is probably because of the small sample size. Alternatively, this may be related to the fact that AIx tends to flatten after the age of 55 years. For the reduction of fibrinogen and increase of SEVR there was a tendency toward a linear relationship (r = −0.506).
Systemic inflammation has been associated with endothelial dysfunction,8 and increased arterial stiffness has been found to be present in different inflammatory rheumatic diseases (eg, rheumatoid arthritis9). There is growing evidence that suppression of systemic inflammation might improve vessel function.10 This could explain the reduction of arterial stiffness in patients with PMR, when systemic inflammation is ameliorated after treatment with corticosteroids.
Competing interests: none.
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