Inflammation and coronary flow reserve in chronic stable coronary artery disease: Evidence for a long standing interplay

Abstract Funding Acknowledgements Type of funding sources: None. Background Low grade inflammation is involved in pathogenesis ischemia and outcome coronary artery disease (CAD). Dobutamine stress echo (DSE) flow reserve (CFR) are both related with incident CAD respective as well. Purpose To evaluate the potential relationship between inflammation, evaluated by high-sensitivity C-reactive protein surrogate, DSE outcome/left anterior descending (LAD) CFR stable chronic CAD. Methods We studied 132 consecutive pts (age 58±12years, 18 females, 33 diabetics) CAD, concomitant evaluation LAD CFR. A cut off 3 mg/dL was used to define high low CRP groups (CRPH/30pts, CRPL/92pts). distribution positive skewed (median 1.7mg/l) then normalized log transformation (CRP 0.72±0.9, logCRP 3.2±3.3). Sixty-three out had a follow up reevaluation at 98±74 months. Absolute % changes were estimated. Results CRPH CRPL similar baseline: (CRPH: 2.3±0.6, CRPL: 2.4±0.6mg/dl), creatinine (1.0±0.2 vs 1.1±0.4mg/dl), HbA1c (5.4±1.0 5.6±1.3%) LDL (109±46 102±35mg/dl). also hemodynamic burden incidence DSE. dCFR %dCFR lower (0.20±0.70 0.69±0.92, p = 0.02 0.13±0.33 0.46±0.67 0.01). Further clustering based on optimal treatment achieved baseline (guidelines defined resting heart rate LDL) did not change findings. inversely (figure 1: r=-0.21, 0.04) (r=-0.18 0.05). Moreover, during improvement (%dCFR) 2: r=0.30 0.03). In stepwise logistic regression analysis for prediction CFR>2, including categorical classification (>3), diabetes, (>80), Lpa(>50) rate, only CRP>3 finally selected (exp(B)=0.38, Conclusion Inflammation activity estimated irrespectively from outcome, well dynamically long term up. The independent LDL, Lpa levels diabetic substrate, thus implying strong pathophysiological interplay.