| Objective:Since the first description of this phenomenon in1972, coronary slow flow phenomenon (CSFP) has been an important entity attracted cardiologist's attention gradually with the extensive use of angiography. Some researches have confirmed that CSFP is an important clinical entity as it may be the cause of typical angina pectoris, acute coronary syndrome, acute myocardial infarction, malignant ventricular fibrillation, and even sudden death. However, its pathophysiological mechanism is less well understood, and the standard anti-angina therapeutics has limit effect on CSFP. So we performed this study in order to investigate the relationship between endothelial dysfunction and pathogeny of CSFP, and to observe the effect of nicorandil on CSFP, in order to provide evidence of pathophysiology mechanism and assistance for clinical treatment.Methods:The CSFP group population consisted of30patients with slow coronary flow who had angiographically normal coronary arteries with delayed opacification of the distal vasculature from March2010to July2011in The Third Hospital of Hebei Medical University, but coronary spasm, coronary artery ectasia, coronary artery thrombus, coronary dissection, coronary aneurysm, myocardial infarction, myocardosis and valvular heart disease were excluded.30patients with normal coronary flow and angiographically normal coronary arteries were enrolled as control group in this study. The CSFP group was divided into two subgroups randomizedly as CSFP nicorandil subgroup (n=15) and CSFP standard subgroup (n=15). All blood samples were centrifuged within2hours, and stored at-70℃. The levels of plasma ET-1and NO in both CSFP group and control group were measured. Then the CSFP nicorandil subgroup patients were administrated of standard anti-angina and oral nicorandil treatment, the CSFP standard subgroup was administrated of standard anti-angina treatment only. The blood samples of both subgroups were collected at the first month and the third month after treatment. The blood samples were centrifuged and stored at-70℃. The levels of plasma ET-1and NO in both CSFP nicorandil subgroup and CSFP standard subgroup were measured, and the events of angina pectoris were followed. Data Analysis were performed by SPSS16.P<0.05was considered statistically significant.Results:1Comparison of clinical characteristics between CSFP group and control group:there was no significantly difference between the two groups in gender, age, BMI, family history, fasting blood glucose, blood lipid, SBP, DBP, and heart rate. However, rate of smoking status and levels of uric acid were significantly higher in the CSFP group compared with the control group(P=0.025,P=0.000).2Comparison of the levels of plasma NO and ET-1between CSFP group and control group before treatment:Plasma NO was significantly lower in the CSFP group than that of the control group(P=0.001), and plasma ET-1was significantly higher in the CSFP group than that of the control group(P=0.009).3Comparison of the effect of the two methods of treatment3.1Comparison of the effect between the two subgroups:patients treated with nicorandil felt less chest uncomfort than those in the standard subgroup (P=0.01) after3months'treatment, no difference between the two subgroups at the first month after the treatment (P=0.143).3.2Comparison of the levels of plasma NO between CSFP nicorandil subgroup and CSFP standard subgroup:there was no significantly difference between the two subgroups in plasma NO before treatment (P=0.961). One month after treatment, there were no significantly difference in plasma NO between the two subgroups pre-treatment and after-treatmernt (P=0.375P=0.125). Whereas after3months'treatment, the level of plasma NO in the CSFP nicorandil subgroup was significantly higher compared with that of pre-treatment (p=0.000), which was also higher than that of CSFP standard subgroup after3months' treatment (p=0.043). However, after3months' treatment, the plasma level of NO in the CSFP standard subgroup had no significantly difference compared with that of pre-treatment (p=0.160).3.3Comparison of the levels of plasma ET-1between CSFP nicorandil subgroup and CSFP standard subgroup: there was no significantly difference in plasma ET-1between the two subgroups pre-treatment and after-treatmernt (p=0.990). One month after treatment, there were no significantly difference in plasma ET-1between the two subgroups pre-treatment and after-treatmernt (p=0.191, p=0.053). Whereas after3months' treatment, the level of plasma ET-1in the CSFP nicorandil subgroup was significantly lower compared with that of pre-treatment (p=0.001), which was also lower than that of CSFP standard subgroup after3months' treatment(p=0.045). However, after3months' treatment, the plasma level of ET-1in the CSFP standard subgroup had no significantly difference compared with that of pre-treatment(p=0.062).Conclusion:1CSFP patients have a high uric acid level and smoking percent, which indicates that high uric acid level and smoking perhaps play an important role in the pathogenesis of CSFP.2CSFP patients have a lower level of NO and higher level of ET-1. which indicates that impaired endothelial function may lead to CSFP.3Standard anti-angina therapy has limited benefit in the management of the patients with CSFP and the improvement of endothelial function. However, nicorandil as an adjunct may further improvement chest uncomfort and ameliorate endothelial function. |
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