[Clinical and angiographic characteristics of patients with slow coronary flow].

ABSTRACT

OBJECTIVE: To analyze the clinical and angiographic characteristics of patients with slow coronary flow (SCF). METHODS: In this retrospective study, 140 patients with SCF and 140 control subjects without SCF were included. SCF were diagnosed by the combination of TIMI flow grade method and TIMI frame count method. All subjects had angiographically normal coronary arteries. The clinical and laboratory data were obtained from medical records at admission. RESULTS: Compared to control group, patients with SCF were younger [(57.8 +/- 10.7) years vs. (59.8 +/- 8.2) years], rate of smokers (59.3% vs. 46.4%) and diabetes mellitus (49.3% vs. 30.7%), fasting blood glucose (FBG) level [(7.8 +/- 2.8) mmol/L vs. (6.2 +/- 2.0) mmol/L, P < 0.05] and triglyceride (TG) level [(2.11 +/- 1.93) mmol/L vs. (1.67 +/- 1.01) mmol/L, P < 0.05] were higher, while high density lipoprotein cholesterol (HDL-C) level [(1.05 +/- 0.35) mmol/L vs. (1.42 +/- 0.74) mmol/L, P < 0.01] and apolipoprotein A1 (apoA1) level [(1.10 +/- 0.19) mmol/L vs. (1.31 +/- 0.31) mmol/L, P < 0.01] were lower. Among the 140 SCF patients, left anterior descending artery (LAD), left circumflex artery (LCX) and right coronary artery (RCA) were involved at the same time in 92 patients. Among the three vessels, RCA is the most frequent involved vessel (n = 119). After adjusting for other risk factors, current smoking (OR = 1.92, 95% CI 1.04 - 3.57, P < 0.05), DM history (OR = 2.44, 95% CI1.32-4.76, P < 0.01), FBG (OR = 2.13, 95% CI1.16-3.98, P < 0.05), TG (OR = 1.47, 95% CI1.03-2.13, P < 0.05), HDL-C (OR = 0.47, 95% CI0.24-0.85, P < 0.05) and apoA1 (OR = 0.55, 95% CI0.40 - 0.75, P < 0.01) were independent factors for SCF (all P < 0.05). CONCLUSIONS: Our results demonstrated that patients with SCF were prone to have a significant metabolic disorder compared to the control group. Patients with high levels of FBG, TG and low levels of HDL-C were more likely to suffer from SCF, which maybe explained by the development of coronary endothelium and microvascular dysfunction.