Why the study?
Does elevated C-reactive protein reduce coronary blood flow responses in patients with single-vessel coronary artery disease?
Does elevated C-reactive protein reduce coronary blood flow responses in patients with single-vessel coronary artery disease?
In patients with CAD, systemic inflammation as indicated by elevated CRP is independently associated with coronary microvascular dysfunction, which may precipitate myocardial ischemia.
Answers are grounded in this paper and cite their sources.
Elevated CRP may mark microvascular dysfunction in CAD; hypothesis-generating and should not yet change practice.
AIMS: It is still unknown whether elevated C-reactive protein levels are responsible for coronary microcirculatory dysfunction in patients with coronary artery disease (CAD). This study was aimed at evaluating the association between C-reactive protein levels and endothelium-dependent and endothelium-independent coronary blood flow (CBF) responses in non-culprit arteries of patients with CAD. METHODS AND RESULTS: We studied 28 patients (14 with normal and 14 with elevated C-reactive protein levels, >5 mg/L) with single-vessel disease and otherwise angiographically normal coronary arteries undergoing percutaneous transluminal coronary angioplasty (PTCA). CBF was measured in the non-PTCA vessel using an intracoronary Doppler guide wire and quantitative coronary angiography at baseline, after intracoronary infusion of substance P and of adenosine, and expressed as per cent change from baseline. The increases in CBF during infusion of substance P and of adenosine were lesser in patients with elevated than in those with normal C-reactive protein levels (34+/-22 vs. 61+/-34%, P=0.04 and 131+/-53 vs. 189+/-89%, P=0.03, respectively). Multivariable analysis identified elevated C-reactive protein level as the only independent predictor of reduced response to substance P (P=0.01) and adenosine (P=0.02). CONCLUSION: In patients with CAD, evidence of systemic inflammation is independently associated with endothelium-dependent and endothelium-independent coronary microvascular dysfunction, which, in turn, may be critical to precipitate myocardial ischaemia, in particular, in unstable patients.
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Tomai et al. (2005) studied this question.
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