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

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.