| Coronary slow flow phenomenon(CSFP), characterized by deceased distal progression of dye to coronary arteries in the absence of obstructive coronary disease, is a distinct finding, but coronary spasm, coronary artery ectasia, myocardial dysfunction, valvular heart disease and certain connective disease is exclusived. This unique angiographic finding had been reported years, but, up to now, the clinical signification, underlying pathophysiological mechanism as well as therapeutics is less well understood, the researches about this are limitation. The endothelium function and myocardial microvascular infusion should be investigated deeply because endothelium dysfunction and increased myocardial microvascular resistance are thought to play the important roles in this situation. So we performed this study in order to investigate the pathophysiology and its underlying mechanisms of CSFP, so as to provide assistance for clinical analysis, disease risk stratification, prognosis assessment, and treatement.Objective 1. To probe the mechanism of CSFP by observing the changes of plasma nitric oxide(NO), endothelin-1(ET-1) and hydrogen sulfide(H2S) and inspect the endothelium function of CSFP patients. 2.To investigate the myocardial microvascular function of CSFP patients through myocardial contrast echocardiography(MCE). Methods 1. Patients who were hospitalized with the compain of chest pain, therefore underwent coronary angiography(CAG) and MCE examation were enrolled in this study. 2. The patients were divided into 2 groups according to their coronary angiography results, i.e. 30 patients in CSFP group, 30 patients in normal coronary flow(NCF) group. 3. Coronary flow patterns of the cases were determined by corrected thrombolysis in myocardial infarction (TIMI) frame count(CTFC). 4. The change plasma NO, ET-1 and H2S were measured. 4. To evaluate the myocardial flow infusion, the two groups underwent MCE examatiom. Segments of satisfied imaging was analyzed to abtain the refilling curve and the values of A(amplitude of enhancement of intensity),β(rate of intensive rise) and A·β(myocardial blood flow volume ). Results 1. Patients with CSFP revealed both higher frame counts in native coronary arteries and higher mean frame counts than NCF(40.67±22.79 vs 24.78±2.17, P<0.0001). 2. Plasma NO and H2S level(umol/L) was significantly lower in patients with CSFP than in the NCF (35.21±4.61 vs 57.97±3.62 P<0.0001, 38.7±5.90 vs 64.24±3.87 P<0.0001, respectively), and plasma ET-1 level (ng/L)was significantly higher in patients with CSFP than in the NCF (61.25±5.51 vs 35.98±3.00, P<0.0001). In CSFP patients group, plasma NO and H2S level were significantly lower in patients who were classified in 1, 2, or 3 vessel CSFP patients : For NO, 39.86±1.20, 37.44±1.85, 30.62±2.44 respectively; For H2S, 46.72±2.45, 37.58±1.81, 33.83±1.88 respectively(ANOVA, P<0.001 and P<0.001, respectively). The highest ET-1 level was detected in patients with CSFP in all of 3 coronary arteries. There were no significant difference for plasma NO, H2S and ET-1 levels among patients with CSFP in LAD, LCX and RCA(P>0.05). 3. The plasma NO and H2S level had negative correlation with CTFC(r=-0.68,P<0.001; r=-0.75,P<0.001), The plasma ET-1 level had positive correlation with CTFC(r=-0.71,P<0.001) . 4. In patients with CSFP the A,βand product of A·βwere lower than that of NCF(4.57±2.99 vs 7.75±2.99, 0.56±0.27 vs 0.69±0.39, 3.52±1.46 vs 2.31±1.03 P<0.05, respectively). Conclusion 1. Impaired endothelial function might lead to decreasing endogenous NO and H2S level and increasing endogenous ET-1 level in patients with CSFP. These finding suggest that the present of endothelial dysfunction may contribute to the etipathogenesis of the CSFP. 2. Patients with CSFP show myocardial flow infusion lower than NCF patients, that implied endothelial dysfunction associated with myocardial microvascular disorder in CSFP. |
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