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Increased High Sensitive CRP Level and Its Significance in Pathogenesis of Slow Coronary Flow

Faculty of Medicine, Department of Cardiology, Kocatepe University, Afyon, irfanbarutcu{at}yahoo.com

Alpay Turan Sezgin, MD

Practice and Research Hospital, Department of Cardiology, Baskent University, Adana

Nurzen Sezgin, MD

Adana Hospital, Biochemical Department, Baskent University, Adana

Hakan Gullu, MD

Faculty of Medicine, Department of Cardiology, Inonu University, Malatya, Turkey

Ali Metin Esen, MD

Faculty of Medicine, Department of Cardiology, Kocatepe University, Afyon

Ergun Topal, MD

Faculty of Medicine, Department of Cardiology, Inonu University, Malatya, Turkey

Ramazan Ozdemir, MD

Faculty of Medicine, Department of Cardiology, Inonu University, Malatya, Turkey

Feridun Kosar, MD

Faculty of Medicine, Department of Cardiology, Inonu University, Malatya, Turkey

Sengul Cehreli, MD

Faculty of Medicine, Department of Cardiology, Inonu University, Malatya, Turkey

Previous studies have suggested that microvascular abnormalities cause slow coronary flow (SCF). The role of inflammation has not been investigated, to date. The purpose of this study was to determine the role of inflammation in pathogenesis of SCF. The study included 32 patients with angiographically proven SCF (mean age 49 ±9 years) (group I) and 30 subjects with normal coronary flow (mean age 48 ±8 years) (group II). Blood samples were collected for high sensitive CRP (hs-CRP) measurements. Thrombolysis in myocardial infarction frame count (TFC) was compared in both groups. Distribution of sex, age, body mass index (BMI), arterial blood pressure, and ejection fraction were similar in the 2 groups. TFC was significantly higher in group I than in group II for each artery including left anterior descending coronary artery (LAD), left circumflex artery (Cx), and right coronary artery (RCA) (38.9 ±6.6 vs 22.1 ±1.8 frames, p = 0.0001; 39.6 ±4.9 vs 22.3 ±1.8 frames, p = 0.001 ; 39.0 ±3.8 vs 22.0 ±1.8 frames, p = 0.001, respectively). In group I, serum hs-CRP concentration was significantly higher than that of group II (0.6 ±0.58 vs 0.24 ±0.1 mg/dL p = 0.03). Correlation analysis showed a positive correlation between hs-CRP level and TFC for each artery (for CTFC_LAD, r = 0.36 p = 0.004; for TFC_Cx, r = 0.42 p = 0.003; and for TFC_RCA, r = 0.42, p = 0.0001 respectively). Increased hs-CRP level suggests that inflammation may be associated with pathogenesis of SCF or at least in part contributes to its pathogenesis. Increased hs-CRP level may also be an early marker of impaired coronary blood flow.

This version was published on September 1, 2007

Angiology, Vol. 58, No. 4, 401-407 (2007)
DOI: 10.1177/0003319707304943


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