Chufan Luo

Fujian Medical University, Min-hou, Fujian, China

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Publications (11)37.23 Total impact

  • International journal of cardiology. 08/2014;
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    ABSTRACT: Although increased coronary microvascular resistance (CMR), resulting in coronary microvascular dysfunction, is speculated to be responsible for myocardial ischemia in patients with cardiac syndrome X (CSX), it has never been directly demonstrated, and the correlation between CMR and severity of myocardial ischemia has not been elucidated in this setting. This study aimed to ascertain the increased CMR directly and to explore the relationship between CMR and severity of ischemia in patients with CSX. We studied 18 patients with CSX and 18 age- and sex-matched control subjects. Thermodilution-derived coronary flow reserve and index of microvascular resistance were measured using a pressure-temperature sensor-tipped coronary wire. Exercise treadmill test was performed by the Bruce protocol for calculating Duke treadmill score. Coronary flow reserve was significantly lower (2.37±0.81 versus 3.68±0.72; P<0.001) and index of microvascular resistance was higher (33.1±7.9 versus 18.8±5.6 U; P<0.001) in patients with CSX compared with those in control subjects. The Duke treadmill score was correlated positively to coronary flow reserve (r=0.539; P=0.021) and negatively to index of microvascular resistance (r=-0.742; P<0.001) in patients with CSX. Using an intracoronary thermodilution method, we for the first time directly demonstrated an increased microvascular resistance in patients with CSX. Furthermore, severity of ischemia was found to be intimately associated with CMR in this setting.
    Circulation Cardiovascular Interventions 01/2014; · 6.54 Impact Factor
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    ABSTRACT: OBJECTIVES: C-reactive protein (CRP), an inflammation marker, is a strong independent risk factor for cardiovascular disease. Vessels are able to express CRP; however, the molecular mechanism behind this expression is not clear. METHODS: Reverse transcription PCR and ELISA were used to detect messenger RNA and proteins of CRP and nuclear factor κB (NF-κB) activity in vessel rings stretched with different mechanical strains. RESULTS: Interleukin (IL)-6 treatment did not induce CRP expression in vessels in the absence of mechanical strain. In contrast, IL-6 augmented CRP expression in vessel rings stretched with mechanical strains of 3 and 5 g (CRP mRNA, IL-6: 11.367±1.68 and 12.78±0.76 vs vehicle: 7.27±0.88 and 8.3±0.91 folds, respectively; CRP, IL-6: 12.79±1.62 and 14.05±2.1 vs vehicle: 7.72±1.04 and 8.16±1.52 folds, respectively; p<0.05 vs 0 g group and vehicle control group; n=5), and this effect was completely blocked by treatment with gadolinium III chloride hexahydrate (GdCl(3)). Moreover, IL-6 treatment increased NF-κB activity in vessels stretched with a mechanical strain of 3 g, and this effect was blocked by stretch-activated channel inhibitors (streptomycin or GdCl(3)) and the NF-κB peptide inhibitor SN50, but not by the inactive SN50 analogue SN50M. We also performed similar experiments on human internal mammary arteries and obtained similar results. CONCLUSIONS: These results indicate that the inflammatory cytokine IL-6 alone does not induce CRP synthesis in vessels in the absence of mechanical strain; however, IL-6 augments mechanical strain-induced CRP synthesis in vessels via the stretch-activated channel-NF-κB pathway.
    Heart (British Cardiac Society) 12/2012; · 5.01 Impact Factor
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    ABSTRACT: INTRODUCTION: Atrial fibrillation (AF) is associated with impaired coronary flow by means of Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC). Mean platelet volume (MPV) is elevated in patients with AF. In the present study we aimed to investigate the relationship between MPV and TFC in patients with AF in the absence of obstructive coronary artery disease (CAD). METHODS: This observational study enrolled 185 AF patients and 189 control subjects, all with angiographically documented normal coronary arteries. MPV was measured at baseline and mean TFC was assessed after diagnostic coronary angiography. RESULTS: The MPV was 9.95±1.32 in the AF group and 9.02±1.16 in the control group (p<0.001). In AF patients, MPV was significantly correlated with mean TFC (r=0.419, p<0.001), AF duration (r=0.407, p<0.001), AF classification (r=0.378, p<0.001), systemic hypertension (r=0.165, p=0.024), diabetes mellitus (r=0.233, p=0.001), left ventricular ejection fraction (r=-0.347, p<0.001), and baseline use of diuretics (r=0.177, p=0.016). In linear regression analysis, mean TFC, left ventricular ejection fraction and diabetes mellitus were found to be independently associated with MPV (p<0.001, p=0.028 and p=0.045 respectively). CONCLUSION: Mean platelet volume seems to be independently associated with coronary blood flow in patients with atrial fibrillation in the absence of obstructive coronary artery disease.
    Heart Lung &amp Circulation 09/2012; · 1.25 Impact Factor
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    ABSTRACT: Background: Although enhanced external counterpulsation (EECP) showed short-term effects in improving coronary flow in patients with coronary slow flow (CSF), whether such improvement is durable remains uncertain, and the relationships between such improvement and changes in endothelial function as well as inflammatory markers have not been elucidated. Objectives: The aim of the present study was to investigate the effects of EECP on transthoracic coronary flow, flow-mediated dilatation (FMD), and high-sensitivity C-reactive protein (hsCRP) in patients with CSF. Methods: Forty-five patients with documented CSF underwent transthoracic Doppler echocardiography (TTDE) for the assessment of coronary diastolic peak flow velocity (DPFV) and coronary flow reserve (CFR), and measurements of FMD and hsCRP; they were then nonrandomly assigned to two groups. Subjects in the control group (n = 24) received only medical therapy, and those in the EECP group (n = 21) were additionally treated with the 36 one-hour sessions of EECP. After 8 weeks of medical/EECP therapy, TTDE, FMD, and hsCRP examinations were repeated, and TTDE was additionally repeated after the 6-month clinical follow-up. Results: In the EECP group, resting DPFV, hyperemic DPFV, and CFR were significantly increased shortly after therapy (p < 0.001) and the improvement was maintained up to the 6-month follow-up, whereas in the control group those variables were not statistically increased. Meanwhile, hsCRP significantly decreased and FMD increased after therapy in the EECP group (p < 0.001). In all subjects, CFR improvement was negatively correlated with hsCRP change and positively correlated with FMD increase (p < 0.001). Conclusions: EECP may have a durable effect in improving coronary flow in patients with CSF. Such improvement is related to the favorable effects of EECP on vascular inflammation and endothelial function.
    Cardiology 08/2012; 122(4):260-8. · 1.52 Impact Factor
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    ABSTRACT: Lipid disorder causes vascular endothelial cell damage and contributes to the early development of dyslipidaemia-induced atherosclerosis. In vivo and in vitro, it has been found that increasing shear stress can improve endothelial function. Clinically, enhanced external counterpulsation (EECP) plays important roles in the treatment of coronary artery disease by promoting arterial shear stress. The present study aims to evaluate the effect of EECP on vascular endothelial function in porcine hypercholesterolaemic model. Twenty-six hypercholesterolaemic pigs were equally divided into EECP group (HC-EECP group) and control group (HC group). Shear stress of a right forearm superficial artery was measured during EECP in comparison with the basal physiological status in the HC-EECP group. Endothelial-dependent flow-mediated vasodilation (FMD) was applied to assess endothelial function. Serum high-sensitivity C-reactive protein (hs-CRP) levels were measured at indicated time points. Endothelial shear stress was increased significantly during EECP treatment (P<0.001). Compared to HC group, hs-CRP decreased significantly by EECP at 18- and 36-h, respectively (P<0.05). FMD was improved significantly by EECP compared to that of HC group at 18 h (11.09 ± 5.63%) and at 36 h (11.42 ± 2.75%) post-EECP, P<0.05. Meanwhile, in animals of HC group, FMD was decreased from baseline 7.76 ± 3.70% to 6.75 ± 3.57% at 18 h and 5.07 ± 1.97% at 36 h, P<0.05. Long-term EECP can improve endothelial function partially by an increased endothelial shear stress in hypercholesterolaemic porcine model. This implies that long-term EECP can be used as a complementary therapeutic strategy to prevent atherosclerosis in hypercholesterolaemic patients.
    Clinical Physiology and Functional Imaging 07/2012; 32(4):262-7. · 1.33 Impact Factor
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    ABSTRACT: BACKGROUND: Atrial fibrillation (AF) is associated with impaired coronary flow and diminished myocardial perfusion. In the present study we aimed to evaluate coronary blood flow by means of Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) in patients with AF in the absence of obstructive coronary artery disease (CAD). METHODS: This prospective study initially enrolled 166 patients with AF and 332 age- and gender-matched control subjects without AF. After diagnostic coronary angiography, TFC was assessed in the participants without obstructive CAD, with 146 in the AF group and 150 in the control group. RESULTS: The TFC for three major coronary arteries and the mean TFC were found to be significantly higher in AF patients compared to control subjects (34.1±10.4 vs. 25.0±10.4, 31.8±9.7 vs. 23.7±9.1, and 32.3±9.5 vs. 24.1±8.4 for each artery and 32.8±9.2 vs. 24.3±8.9 for mean TFC, p<0.001 for all comparisons). The mean TFC was 28.8±7.9 in patients with paroxysmal AF, 33.7±8.7 in those with persistent AF, and 39.0±8.8 in those with long-standing or permanent AF (p<0.01 for all comparisons). After multivariate analysis, we found that the presence of AF remains to be independently associated with mean TFC. In AF group, baseline heart rate, left ventricular ejection fraction, AF duration and left atrium diameter were found to be independently associated with mean TFC. CONCLUSIONS: Patients with atrial fibrillation in the absence of obstructive coronary artery disease have significantly higher TIMI frame counts for all three coronary vessels, indicating impaired coronary blood flow, compared to the control subjects without atrial fibrillation.
    International journal of cardiology 04/2012; · 6.18 Impact Factor
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    ABSTRACT: Although earlier studies demonstrated endothelial dysfunction and systemic inflammation in patients with microvascular angina (MVA), the correlations between flow-mediated dilation (FMD), high-sensitivity C-reactive protein (hsCRP) levels and Duke treadmill score (DTS), a comprehensive index representing the severity of ischemia, have not been elucidated in this setting. To explore the possible relationships among brachial FMD, serum hsCRP levels and DTS in MVA patients. A total of 89 subjects with chest pain and a normal coronary angiogram were studied. The exercise treadmill test (ETT) was performed using the Bruce protocol for calculating the DTS. Brachial FMD and serum hsCRP levels were measured. The mean (± SD) brachial FMD was 5.45±2.24% in the group with positive ETT and 8.19±2.78% in the group with a negative ETT (P<0.001). Mean serum hsCRP levels were significantly higher in the group with positive ETT than in the group with negative ETT (4.93±1.63 mg/L versus 3.41±1.65 mg/L; P<0.001). Brachial FMD and serum hsCRP levels showed significant differences among the three groups according to DTS risk stratification. The DTS was positively correlated with FMD (r=0.532; P<0.001) and negatively correlated with hsCRP level (r= 0.461; P<0.001). Brachial FMD and serum hsCRP levels may be associated with DTS in patients with MVA.
    Experimental and clinical cardiology 01/2012; 17(4):197-201. · 1.10 Impact Factor
  • International journal of cardiology 11/2011; 154(1):84-5. · 6.18 Impact Factor
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    ABSTRACT: We try to clear the relationship between high-sensitive C-reactive protein (hsCRP) release and abdominal aortic aneurysm formation. A rabbit abdominal aortic aneurysm model was created by elastase perfusion. At days 10, 20, and 30 after elastase perfusion, mean serum hsCRP levels detected by ELISA increased over 200% over their basal level (n = 11, P < 0.05). Serum hsCRP levels were significantly higher in the aneurysm groups than in the sham controls by day 5 (n = 11, P < 0.05) and were positively correlated with percentage vessel diameter changes in the aneurysm group by day 10 (r = 0.8012, n = 33, P < 0.05). In the aneurysm group, increased serum CRP was derived from the liver in early stages, yet from dilated vessels in the later stages, as shown by immunostaining, western blot, and reverse transcriptase-PCR. Similar increased hsCRP levels were also observed in dissected rabbit aortic ring explants from the aneurysm model. Pretreatment with the stretch-activated channel blockers gadolinium or streptomycin, as well as nuclear factor-kappaB inhibitor SN50, blocked hsCRP production in the dilated aortic rings. Stretch-activated channel blockers also inhibited the activation of nuclear factor-kappaB. During abdominal aortic aneurysm formation, increased serum hsCRP levels derive from aneurysmal arteries with degenerating elastic lamina. This process is mediated by mechanical stretch-activated channel-dependent nuclear factor-kappaB translocation to the nucleus.
    Journal of Hypertension 06/2009; 27(9):1829-37. · 4.22 Impact Factor
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    ABSTRACT: C-reactive protein (CRP) is a powerful independent risk factor for cardiovascular diseases. Elevated mechanical strain on vessels induces the local expression of proinflammatory cytokines. We hypothesized that mechanical strain on vessels may induce local CRP expression. Human saphenous vein and internal mammary artery (IMA) rings were stretched in vitro with a mechanical strength of 1, 3, or 5 g. Reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay results showed that mechanical stretching significantly induced CRP mRNA and protein expression in the saphenous vein and IMA rings in a strength-dependent manner reaching a maximum at a mechanical strength of 3 g, but CRP expression returned at strengths of >5 g. In vessels, mechanical strain-induced CRP expression was blocked by two stretch-activated ion channel (SAC) blockers: GdCl(3) and streptomycin. Mechanical strain also increased activation of nuclear factor kappaB (NF-kappaB), which was detected with a nonradioactive NF-kappaB p50/p65 EZ-TFA transcription factor assay. Mechanical strain-induced NF-kappaB activation was blocked by SAC blockers and the NF-kappaB inhibitor (SN50, H-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-Val-Gln-Arg-Lys-Arg-Gln-Lys-Leu-Met-Pro-OH). SN50 also blocked mechanical strain-induced CRP expression in vessels. In conclusion, mechanical strain induces CRP expression in IMAs and saphenous veins by activating the SAC-induced NF-kappaB pathway.
    Journal of Pharmacology and Experimental Therapeutics 04/2009; 330(1):206-11. · 3.89 Impact Factor