[Effects of rho-kinase inhibitor on cardiac hypertrophy of left ventricle in spontaneously hypertensive rats].

OBJECTIVE: To explore the effects of Rho-kinase inhibitor on cardiac hypertrophy of left ventricle in spontaneously hypertensive rats (SHR). METHODS: SHRs (n = 30) were randomly divided into 5 groups (n = 6 each): SHR control group, 5 mg/kg fasudil group (SHRL), 10 mg/kg fasudil group (SHRM), 20 mg/kg fasudil group (SHRH) and nifedipine group (XBDP, 10 mg/kg). Six male Wistar-Kyoto rats were selected as normal control group (WKY group). Systolic blood pressure (SBP) was measured before and after treatment every 2 weeks. The hypertrophic parameters of left ventricular weight index (LVWI) and cardiomyocyte transverse diameter (TDM) were measured. In addition, the expression levels of Rho kinase mRNA and protein in cardiomyocytes were observed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. RESULTS: The levels of LVWI and TDM in WKY group were significantly lower than those in SHR control group [(2.98 ± 0.05) vs (3.16 ± 0.08) mg/g, (18.18 ± 0.75) vs (21.32 ± 1.25) µm, P < 0.01]. After 8 weeks, the levels of LVWI and TDM in three fasudil groups were markedly lower than those in SHR control group [SHRL group: (3.12 ± 0.05) mg/g, SHRM group: (3.10 ± 0.07) mg/g, SHRH group: (3.08 ± 0.09) mg/g vs SHR control group: (3.16 ± 0.08) mg/g, SHRL group: (20.11 ± 1.15) µm, SHRM group: (19.63 ± 1.62) µm, SHRH group: (18.91 ± 1.05) µm vs SHR control group: (21.32 ± 1.25) µm, P < 0.05 or P < 0.01]. But the levels of LVWI and TDM were not different between SHR control and XBDP groups [(3.14 ± 0.08) mg/g,(21.42 ± 1.23) µm, P > 0.05]. Compared with SHR control group, the expression of Rho kinase mRNA and protein in cardiomyocytes significantly decreased in three fasudil groups [SHRL group mRNA: (0.45 ± 0.08), SHRM group mRNA: (0.37 ± 0.07), SHRH group mRNA: (0.32 ± 0.07) vs SHR control group mRNA: (0.63 ± 0.07), SHRL group protein: 0.78 ± 0.11), SHRM group protein: (0.73 ± 0.10), SHRH group protein: (0.68 ± 0.10) vs SHR control group protein: (0.90 ± 0.1), P < 0.05 or P < 0.01], but showed no obvious change in XBDP group [mRNA: (0.56 ± 0.07), protein: (0.85 ± 0.10), P > 0.05]. CONCLUSIONS: Rho kinase inhibitor may significantly down-regulate the expression of Rho kinase in cardiomyocytes of SHR. The mechanism is probably due to the favorable effects of Rho kinase inhibitor in the prevention of cardiac hypertrophy of left ventricle.

[Clinical value of dual-source CT in evaluating coronary artery disease].

OBJECTIVE: To analyze the clinical value of dual-source CT (DSCT) in the diagnosis of coronary artery disease. METHODS: Fifty-five patients with suspected coronary heart disease underwent both DSCT coronary angiography (DSCTCA) and selective coronary angiography (CAG) examination, and the diagnostic sensitivity, specificity and accuracy of the DSCTCA was evaluated. RESULTS: The sensitivity, specificity, positive and negative predictive value, and accuracy of DSCT in the diagnosis of coronary heart disease were 97.7%, 72.6%, 93.5%, 88.9% and 92.7% by the number of patients, respectively; by calculating the coronary arteries, the sensitivity, specificity, positive and negative predictive value, accuracy were 94.9%, 95.8%, 92.5%, 97.1%, 95.5%, respectively. According to the lesion segment, these values were 88.2%, 96.9%, 90.5%, 96.1%, 94.7%, respectively. DSCTCA showed no significant difference from CAG for a diagnostic purpose, nor did their vessel sensitivity, specificity, positive and negative predictive value, and accuracy in different coronaries differ significantly. CONCLUSION: DSCT has a diagnostic accuracy of coronary heart disease close to that CAG and can on some occasion serve as an alternative to CAG in the screening of coronary artery disease.

[Correlation of adiponectin, monocyte chemoattractant protein-1, and endothelial function to vascular remodeling in coronary in-stent restenosis].

OBJECTIVE: To investigate the correlation between vascular remodeling index (RI) and serum adiponectin, plasma monocyte chemoattractant protein-1 (MCP-1), endothelial function and evaluate the mechanism of coronary in-stent restenosis. METHODS: RI 6 months after percutaneous coronary intervention (PCI), serum adiponectin, plasma MCP-1 and flow-mediated dilation (FMD) before and 3 days,6 months after PCI were measured in 30 patients with and 30 without coronary in-stent restenosis. RESULTS: Compared with patients without restenosis and those with restenosis before PCI, the patients with coronary in-stent restenosis showed significantly increased plasma MCP-1 3 days and 6 months after PCI (P<0.05) and reduced RI 6 months after PCI, serum adiponectin and FMD 3 days and 6 months after PCI (P<0.05). RI was positively correlated to serum adiponectin and FMD and inversely to MCP-1. CONCLUSION: The occurrence of coronary in-stent restenosis is the result of the interrelations between multiple factors.