ABSTRACT
PURPOSE: An attempt was made to characterize the orbital shear stress by comparing the effects of orbital shear stress on vascular endothelial cells (ECs) with the results of animal experiments. MATERIALS AND METHODS: In the laboratory study, cultured ECs of well were distinguished by center and periphery then exposed to orbital shear stress using an orbital shaker. In the animal study, arteriovenous (AV) fistulas were made at the right femoral arteries of Sprague-Dawley rats to increase the effect of the laminar flow. The condition of the stenosis was given on the left femoral arteries. The protein expression of inducible nitric oxide synthase (iNOS) and Akt phosphorylation were observed and compared. RESULTS: Under orbital shear stress, ECs showed an increase in iNOS protein expression and phosphorylation of Akt but most of the protein expressions derived from the periphery. When compared to the animal study, the increased expression of iNOS protein and phosphorylation of Akt were observed in the sample of AV fistula conditions and the iNOS protein expression was decreased in the stenosis conditions. CONCLUSION: Orbital shear stress did not show the characteristics of a pure turbulent shear force. By comparing the observation with the morphological changes of vascular ECs and site-specific protein expression on the results of animal experiments, uniform directional lamina shear stress forces were expressed at the periphery.
Subject(s)
Animals , Rats , Animal Experimentation , Constriction, Pathologic , Endothelial Cells , Femoral Artery , Fistula , Nitric Oxide Synthase , Nitric Oxide Synthase Type II , Orbit , Phosphorylation , Rats, Sprague-DawleyABSTRACT
Background The benefit of statin use after acute ST-segment elevation myocardial infarction (STEMI) has been well established, however, the influence of the timing of statin administration has not been elucidated. The objective of this study focused on early clinical outcomes after percutaneous coronary intervention (PCI). Methods This analysis of the Korea Working Group on Myocardial Infarction registry (KorMI) study included 3,584 STEMI patients (mean age, 63 ±13 years;male, 2,684, 74.9%) undergoing PCI from January 2008 to June 2009. Rates of major adverse cardiac events (MACE:all-cause death, recurrent MI, and target lesion revascularization) were compared among patients grouped according to statin therapy timing:I, both during and after hospitalization (n=2,653, 74%);II, only during hospita-lization (n=309, 8.6%);III, only after discharge (n=157, 4.4%);and IV, no statin therapy (n=465, 13%). Mean follow-up duration was 234 ± 113 days. Results Multivariate factors of statin use during hospitalization included prior statin use, multiple diseased vessels, final thrombolysis in myocardial infarction flow grade III, and low-density lipoprotein cholesterol level. At 6-month follow-up, groups III and IV had the highest MACE rates (2.3%, 3.9%, 5.1%, and 4.9%for groups I-IV, respectively, P=0.004). After adjusting for confounders, groups II-IV had a higher MACE risk than group I [hazard ratio (HR):3.20, 95%confidence interval (95%CI):1.31-7.86, P=0.011;HR:3.84, 95%CI:1.47-10.02, P=0.006;and HR:3.17, 95%CI:1.59-6.40, P=0.001;respectively]. Conclusions This study, based on the national registry database, shows early and continuous statin therapy improvs early outcomes of STEMI patients after PCI in real-world clinical prac-tice.
ABSTRACT
BACKGROUND: The accumulation of lipoprotein and monocyte in the intima of the arterial wall is the most important step of the development of coronary artery disease (CAD). Lipoprotein lipase (LPL) plays an anti-atherogenic role by lipolysis of triglyceride-rich lipoproteins, but, it may also act as a receptor of some lipoproteins and monocyte at the arterial wall and act as a atherogenic molecule. Previous studies showed somewhat contradictory results about the association of CAD and LPL polymorphisms and mutations. Racial and dietary difference may contribute to these contradictory results. In this study, we tried to find out the association of CAD and the genetic variation of the LPL (PvuII RFLP in intron 6, HindIII RFLP in intron 8 and Ser 447 Ter mutation in exon 9) in Korean population. METHOD AND RESULT: CAD patients (n=146), confirmed by coronary angiography and healthy Korean adult volunteers (n=110) were genotyped for PvuII/HindIII RFLP and Ser447Ter mutation of the LPL gene by PCR-digestion method. Between two groups, the genotype frequency of these genetic variations was not different. But, the genetic variations showed different effect on lipid profile and body mass index (BMI) in the CAD group and in the control group. In the CAD group, P1 allele carriers showed higher total cholesterol (P1P1+P1P2:P2P2=216+-51 mg/dl:198+/-38 mg/dl, p=0.039) and higher LDL cholesterol level (P1P1+P1P2:P2P2=143+/-46 mg/dl:126+/-36 mg/dl, p=0.047), and H1 allele carriers had lower Body mass index than non-carriers (23.8+/-2.3 kg/m2 :24.8+/-2.9 kg/m2 , p=0.047). In the control group, the Ser447Ter mutation carriers had higher HDL cholesterol level than non-carriers (59+/-10mg/dl versus 53+/-11mg/dl, p=0.049) and patients with P1 allele showed lower body mass index (P1P1+P1P2: P2P2=23.1+/-2.6 kg/m 2 :24.5+/-2.6 kg/m2 , p=0.006). CONCLUSION: In Korean, PvuII/HindIII RFLP and Ser447Ter mutation was not associated with CAD, and they showed different effect on the lipid profile and on the body mass index according to the study group. These results suggests that the phenotypic characteristics of the LPL gene of the Korean people are different from those of occidental people.