This study has shown that omega3FA reduce blood pressure, heart rate and triglycerides in patients with CKD. CoQ had no independent effect on blood pressure but increased heart rate. These results show that omega3FA lower blood pressure and may reduce cardiovascular risk in nondiabetic patients with moderate-to-severe CKD.

Objectives The objective is to identify the factors that affect the optimal linear endovenous energy density (LEED) to ablate incompetent truncal veins. Methods We performed a literature review of clinical studies, which reported truncal vein ablation rates and LEED. A PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) flow diagram documents the search strategy. We analysed 13 clinical papers which fulfilled the criteria to be able to compare results of great saphenous vein occlusion as defined by venous duplex ultrasound, with the LEED used in the treatment. Results Evidence suggests that the optimal LEED for endovenous laser ablation of the great saphenous vein is >80 J/cm and <100 J/cm in terms of optimal closure rates with minimal side-effects and complications. Longer wavelengths targeting water might have a lower optimal LEED. A LEED <60 J/cm has reduced efficacy regardless of wavelength. The optimal LEED may vary with vein diameter and may be reduced by using specially shaped fibre tips. Laser delivery technique and type as well as the duration time of energy delivery appear to play a role in determining LEED. Conclusion The optimal LEED to ablate an incompetent great saphenous vein appears to be >80 J/cm and <95 J/cm based on current evidence for shorter wavelength lasers. There is evidence that longer wavelength lasers may be effective at LEEDs of <85 J/cm.

Alcohol-induced hypertension is well recognized with clear evidence for a direct pressor effect of chronic alcohol consumption provided by a number of intervention studies in humans. In experimental animals, the effect of alcohol on blood pressure is less consistent; however, in Sprague-Dawley rats, alcohol feeding consistently induces a hypertensive response. The mechanism of alcohol-induced hypertension is not clearly understood. Ethanol is known to induce certain cytochrome P450 (CYP) enzymes, particularly the 2E1 isoform, which has been shown to metabolise arachidonic acid (AA) to the 19-hydroxy metabolite (19-HETE), which could have pro-hypertensive activity; CYP4A, by comparison, is the principal AA omega-hydroxylase in the liver. Polyphenolic compounds, such as flavonoids, have been shown to inhibit some CYPs. 2. In this study, we determined the effect of alcohol administration on blood pressure and CYP-dependent AA metabolism in the rat and its possible modulation by red wine polyphenols. 3. Thirty male Sprague-Dawley rats were randomly allocated to three groups, which received water, low-dose ethanol (5% v/v) or red wine (diluted to contain 5% ethanol) for a period of 9 weeks. Bodyweight and blood pressure were measured weekly and 24h urine collected at baseline and every 2 weeks. Animals were killed at 9 weeks and blood and tissue samples were collected. The blood pressure of rats fed with alcohol increased significantly over the period of the study compared with controls (P<0.001). The blood pressure of animals fed 5% alcohol in the form of red wine was not significantly different from controls over the study period. The urinary excretion of 20-HETE did not differ significantly among the treatment groups over the study period and there was no effect of any treatment on the metabolism of AA by renal microsomes. Red wine, but not administration of the relatively low dose of alcohol alone, increased the expression of CYP2E1 protein in the liver and kidney and CYP4A in the kidney. Both red wine and alcohol decreased CYP4A protein levels in the liver compared with controls. 4. Our results suggest that constituents of red wine, possibly polyphenols, can attenuate the alcohol-induced rise in blood pressure in the Sprague-Dawley rat, although this effect does not appear to be mediated by the inhibition of CYP-derived AA metabolism.

No abstract