Oxidative stress greatly influences the pathogenesis of various cardiovascular disorders. Coronary interventions, including balloon angioplasty and coronary stent implantation, are associated with ...increased vascular levels of reactive oxygen species in conjunction with altered endothelial cell and smooth muscle cell function. These alterations potentially lead to restenosis, thrombosis, or endothelial dysfunction in the treated artery. Therefore, the understanding of the pathophysiological role of reactive oxygen species (ROS) generated during or after coronary interventions, or both, is essential to improve the success rate of these procedures. Superoxide O2·− anions, whether derived from uncoupled endothelial nitric oxide synthase, nicotinamide adenine dinucleotide phosphate oxidase, xanthine oxidase, or mitochondria, are among the most harmful ROS. O2·− can scavenge nitric oxide, modify proteins and nucleotides, and induce proinflammatory signaling, which may lead to greater ROS production. Current innovations in stent technologies, including biodegradable stents, nitric oxide donor-coated stents, and a new generation of drug-eluting stents, therefore address persistent oxidative stress and reduced nitric oxide bioavailability after percutaneous coronary interventions. This review discusses the molecular mechanisms of ROS generation after coronary interventions, the related pathological events—including restenosis, endothelial dysfunction, and stent thrombosis—and possible therapeutic ways forward.
The aim of this study was to test the influence of high-dose folic acid (10 mg/d) on endothelial function in patients referred for coronary intervention after an acute myocardial infarction (AMI) and ...determine its relation to homocysteine levels. Flow-mediated dilation (FMD) of the brachial artery was performed in 40 patients after AMI (16 with normal homocysteine levels and 24 patients with elevated levels >11 μmol/L). Subjects were randomized to receive first folic acid (10 mg/day; group A) or placebo (group B) for 6 weeks in a double-blind crossover trial with a 2-week washout. Plasma folate, total homocysteine and its subtypes (oxidized, reduced, and protein-bound), FMD, and nitroglycerin-mediated dilation were assessed at baseline and at 6 and 14 weeks. In group A, folic acid improved FMD from 3.98 ± 0.35% to 6.44 ± 0.56% (p <0.001). This effect persisted after the crossover with placebo (5.42 ± 0.59, p = 0.13). In group B, placebo did not increase FMD (4.01 ± 0.34% vs 4.46 ± 0.38, p = 0.38); however, a significant increase was observed in the second active treatment period (6.49 ± 0.56%, p = 0.005). In both groups, improved FMD neither correlated with basal levels of homocysteine and its subtypes nor with changes induced during the folate treatment. Nitroglycerin-mediated dilation did not change significantly in either group. Folic acid increased FMD in both normo- and hyperhomocysteinanemic groups (p = 0.006 and p <0.001). In conclusion, 6-week treatment with high-dose folic acid improves endothelial function in post-AMI patients, independent from homocysteine status. Folic acid can be recommended to improve postinfarction endothelial dysfunction in patients with normo- and hyperhomocysteinemia.
Folic Acid as a Cardiovascular Drug: Dose Matters Kietadisorn, Rinrada, DVM, MSc; Schmidt, Harald H., MD, PhD; Moens, An L., MD, PhD
The American journal of cardiology,
12/2010, Letnik:
106, Številka:
11
Journal Article
...we revealed that CD40L-expressing CD4+ T lymphocytes stimulate the human anti-caps-PS antibody response in an indirect way through interaction with CD40-expressing CD14+ monocytes. ...the data ...described in this report implicate a role for endogenous CD40-CD40L interactions in the human antibody response to TI-2 antigens in general and to intact heat-inactivated S pneumoniae in particular.
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