Effect of Sclerovit on endothelial dysfunction, hemorheological parameters, platelet aggregation, plasma concentration of homocysteine and progression of atherosclerosis in patients with vascular diseases.

In our prospective study the effect of Sclerovit (0.8 mg folic acid, 20 mug vitamin B12,5 mg vitamin B6,100 mg vitamin E) on inflammatory markers, hemorheological parameters, platelet aggregation, von Willebrand factor activity as a marker of endothelium dysfunction, plasma lipids, plasma levels of folic acid, vitamin B12 and homocysteine (hcy), flow mediated vasodilatation (FMD) and thickness of carotis intima-media after 1 and 6 months of treatment in patients with vascular diseases (10 patients took 1 capsule, 10 patients 2 capsules of Sclerovit and 10 patients placebo) was determined.Plasma level of vitamin B12, folic acid and elongation index of red blood cells (RBC) increased significantly (p<0.05-0.001), hcy and triglyceride concentrations decreased significantly (p<0.05-0.001) in patients taking Sclerovit. HDL-cholesterol, RBC count, hematocrit, plasma and whole blood viscosity increased significantly (p<0.05-0.001) both in patients taking placebo or vitamins. Fibrinogen and CRP showed a significant (p<0.05-0.01) increase in patients on placebo, but did not change in patients on Sclerovit therapy. FMD showed a significant (p<0.05) amelioration in patients on 1 capsule of Sclerovit.Beside the favorable effects of Sclerovit on some of the measured parameters, the observed deterioration in hemorheological parameters can correlate with the contradictory results of large prospective studies with vitamins.

The role of homocysteine-lowering B-vitamins in the primary prevention of cardiovascular disease.

Cardiovascular disease (CVD) is the leading cause of mortality in the Western world. The effort of research should aim at the primary prevention of CVD. Alongside statin therapy, which is maintained to be an effective method of CVD prevention, there are alternative methods such as vitamin B substitution therapy with folic acid (FA), and vitamins B12 and B6 . B-vitamins may inhibit atherogenesis by decreasing the plasma level of homocysteine (Hcy)-a suspected etiological factor for atherosclerosis-and by other mechanisms, primarily through their antioxidant properties. Although Hcy-lowering vitamin trials have failed to demonstrate beneficial effects of B-vitamins in the prevention of CVD, a meta-analysis and stratification of a number of large vitamin trials have suggested their effectiveness in cardiovascular prevention (CVP) in some aspects. Furthermore, interpretation of the results from these large vitamin trials has been troubled by statin/aspirin therapy, which was applied along with the vitamin substitution, and FA fortification, both of which obscured the separate effects of vitamins in CVP. Recent research results have accentuated a new approach to vitamin therapy for CVP. Studies undertaken with the aim of primary prevention have shown that vitamin B substitution may be effective in the primary prevention of CVD and may also be an option in the secondary prevention of disease if statin therapy is accompanied by serious adverse effects. Further investigations are needed to determine the validity of vitamin substitution therapy before its introduction in the protocol of CVD prevention.

Why do homocysteine-lowering B vitamin and antioxidant E vitamin supplementations appear to be ineffective in the prevention of cardiovascular diseases?

Homocysteine has been established as a serious, independent risk factor for atherosclerosis. An elevated plasma homocysteine concentration is accompanied by increased cardiovascular risk; therefore, it can be assumed that lowering the plasma homocysteine level results in a decreased risk. Vitamin B complex (folic acid, and vitamins B6 and B12) substitution therapy decreases the plasma homocysteine level, inhibits oxidative stress, and ameliorates some biochemical and clinical parameters that indicate the progression of atherosclerosis. Vitamin E administration may also reduce atherogenesis through its antioxidant effect. The effectiveness of B and E vitamin substitution in decreasing cardiovascular risk has been suggested by cohort as well as prospective and retrospective studies undertaken during the last two decades. On the other hand, recent large, randomized clinical trials did not substantiate a beneficial effect of homocysteine-lowering B vitamin supplementation or vitamin E antioxidant therapies in reducing cardiovascular risk in humans. We analyzed eight B vitamin and four E vitamin trials from a critical point of view, and in this article we reviewed and commented on their results and focused on the contradictions found in them. We showed that the possible factors implicated in the failure of vitamin therapies included inappropriate designs. The protocols neglected an essential fact: that the impact of some confounding factors, such as concomitant use of statins, acetylsalicylic acid, folic acid, and other drugs, might have led to bias and an inappropriate interpretation of the data. The cardiovascular protective and preventive effects of statins and aspirin might have reduced or abolished the possibility of observing a difference in the number of events between the vitamin and placebo groups for the clinical endpoints. We concluded that the vitamin preventive effect on cardiovascular disease may not be rejected in reference to the negative trial evidence.