Myocardial perfusion reserve is impaired in patients with chronic obstructive pulmonary disease: a comparison to current smokers

Recent studies have demonstrated that chronic obstructive pulmonary disease (COPD) is associated with cardiovascular disease (CVD). However, the association between COPD and coronary microcirculatory dysfunction is unknown. We sought to assess whether myocardial perfusion reserve (MPR) is impaired in patients with COPD, even in the absence of regional myocardial ischaemia or infarction, by using quantitative myocardial perfusion cardiovascular magnetic resonance (CMR).

We recruited 60 subjects with a normal CMR study: 20 individuals with mild-to-moderate COPD; 20 age-matched control smokers, and 20 age-matched control-never smokers. Individuals with established CVD and diabetes mellitus were excluded. Stress–rest myocardial blood flow (MBF) was quantified in 16 myocardial segments by using a Patlak plot method. There were no significant differences in the rest MBF among COPD patients, control smokers, and control-never smokers. However, the mean MPR was significantly lower in COPD patients than in control smokers and control-never smokers (1.76 ± 0.58, 2.57 ± 1.30, and 3.56 ± 1.27, respectively). Univariate associations with MPR were smoking (r = −0.44, P < 0.001), forced expiratory volume in 1 s (FEV1) (r = 0.30, P = 0.02), haematocrit (r = 0.25, P = 0.04), and C-reactive protein (CRP; r = −0.46, P < 0.001). On multivariable analysis, the levels of CRP, FEV1, and renal dysfunction were independent predictors of the impaired MPR. The presence of COPD was associated with a five-fold increased risk of MPR <1.5 (95% confidence interval, 1.4–19.0; P = 0.01).

The MPR, which was independently associated with systemic inflammation and airflow limitation, was impaired in patients with COPD. The presence of COPD was a powerful predictor of impaired MPR in patients without regional myocardial ischaemia or infarction.