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European Heart Journal Advance Access originally published online on June 5, 2009
European Heart Journal 2009 30(15):1837-1843; doi:10.1093/eurheartj/ehp205
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org

Chronic inflammation and coronary microvascular dysfunction in patients without risk factors for coronary artery disease

Alejandro Recio-Mayoral1, Justin C. Mason1, Juan C. Kaski2, Michael B. Rubens3, Olivier A. Harari1 and Paolo G. Camici1,*

1 Medical Research Council Clinical Sciences Centre and National Heart and Lung Institute, Imperial College School of Medicine, Du Cane Road, London W12 0NN, UK
2 Division of Cardiac and Vascular Sciences, St George's Hospital Medical School, London, UK
3 Department of Radiology, Royal Brompton Hospital, London, UK

Received 9 February 2009; revised 6 April 2009; accepted 1 May 2009; online publish-ahead-of-print 5 June 2009.

* Corresponding author. Tel: +44 20 8383 3186, Fax: +44 20 8383 3742, Email: paolo.camici{at}csc.mrc.ac.uk

Aims: To demonstrate that exposure to chronic inflammation results in coronary microvascular dysfunction (CMD).

Methods and results: Using positron emission tomography, resting and hyperaemic (adenosine, 140 µg/kg/min) myocardial blood flow (MBF) was measured in 25 patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA). Coronary flow reserve (CFR) was calculated as adenosine/resting MBF. Patients had normal or minimally diseased (i.e. ≤20% luminal diameter) coronary arteries at angiography and no cardiovascular risk factors. Twenty five age- and gender-matched healthy volunteers served as controls. Resting MBF was similar in patients and controls (1.25 ± 0.27 vs. 1.15 ± 0.24 mL/min/g; P = 0.15) while patients had lower hyperaemic MBF (2.94 ± 0.83 vs. 4.11 ± 0.84 mL/min/g; P < 0.001) and CFR (2.44 ± 0.78 vs. 3.81 ± 1.07; P < 0.001). CFR was inversely related to disease duration (r = –0.65; P < 0.001) and SLE disease activity (r = –0.69; P = 0.01). Seven patients showed ischaemic electrocardiographic changes during adenosine. They had longer disease duration (21 ± 7 vs. 14 ± 5 years; P = 0.03) and lower CFR (1.76 ± 0.81 vs. 2.49 ± 0.54; P = 0.006) when compared with patients without changes.

Conclusion: A reduced CFR in the absence of significant coronary disease is suggestive of CMD. We speculate that this is the consequence of prolonged systemic inflammation, which may precede and contribute to premature coronary artery disease in these patients.

Key Words: Coronary circulation • Myocardial blood flow • Inflammation • Rheumatoid arthritis • Systemic lupus erythematosus • Positron emission tomography


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