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

Alejandro Recio-Mayoral, Justin C. Mason, Juan C. Kaski, Michael B. Rubens, Olivier A. Harari, Paolo G. Camici

Research output: Contribution to journalArticlepeer-review

Abstract

AimsTo demonstrate that exposure to chronic inflammation results in coronary microvascular dysfunction (CMD).Methods and resultsUsing positron emission tomography, resting and hyperaemic (adenosine, 140 g/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.

Original languageEnglish
Pages (from-to)1837-1843
Number of pages7
JournalEuropean Heart Journal
Volume30
Issue number15
DOIs
Publication statusPublished - Aug 2009

Keywords

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

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Chronic inflammation and coronary microvascular dysfunction in patients without risk factors for coronary artery disease'. Together they form a unique fingerprint.

Cite this