Elevated C-reactive protein levels and coronary microvascular dysfunction in patients with coronary artery disease.
OBJECTIVE
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.


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).


CONCLUSIONS
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.
Tomai
Fabrizio
F
Division of Cardiology and Cardiac Surgery, Università di Roma Tor Vergata, European Hospital, via Portuense 700, 00149 Rome, Italy. f.tomai@tiscali.it
Ribichini
Flavio
F
Ghini
Anna S
AS
Ferrero
Valeria
V
Andò
Giuseppe
G
Vassanelli
Corrado
C
Romeo
Francesco
F
Crea
Filippo
F
Chiariello
Luigi
L
D000241:Adenosine / Q000494:pharmacology; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D023921:Coronary Stenosis / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008833:Microcirculation / Q000502:physiology; D017566:Microvascular Angina / Q000097:blood / Q000503:physiopathology; D008875:Middle Aged; D013373:Substance P / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D014665:Vasodilator Agents; D013373:Substance P; D002097:C-Reactive Protein; D000241:Adenosine