Antioxidant Vitamins Reduce Oxidative Stress and Ventricular Remodeling in Patients with Acute Myocardial Infarction

Abstract

We analyzed soluble vascular adhesion molecules (sVCAM-l), reactive oxygen metabolites (ROMs) level, total antioxidant status (TAS) and telediastolic left ventricular volume (TLVV) in patients with myocardial infarction undergoing reperfusion therapy and treated with antioxidant vitamins (AT) or placebo (P) before and for 1 month after reperfusion. After reperfusion, sVCAM-l serum concentration, reactive oxygen metabolites level, and TLVV were significantly higher in patients treated with placebo than in those treated with antioxidant vitamins, while TAS was significantly higher in patients treated with antioxidant supplementation. We observed that 48 hours after reperfusion sVCAM-l (P) vs sVCAM -l(AT) was 2.03±O.5 vs 1.63±O.7 ug/ml with p<O.Ol; ROMs (P) vs ROMs (AT) were 335.60±35.80 vs 307.50±47.10 V.CARR with p<O.05; TAS (P) vs TAS (AT) was 526.47±44.24 vs 737.65±51.15 umol/l with p<O.Ol; 1 week after reperfusion TLVV (P) vs TLVV (AT) was 125.12±29.80vs 119.40±29.40 ml with p<O.05; 1 month after reperfusion TLVV (P) vs TLVV (AV) was 132.00±33.50 vs 123.40±21.60 ml with p<O.05. In the first period after infarction, vitamin treatment improves the antioxidant system and reduces oxidative stress, inflammatory process and left ventricular remodeling.In acute myocardial infarction (AMI), the ischemic events are triggered by disruption of atheromatous plaque, with thrombus formation (1). The plaque derives from cholesterol deposition and intima infiltration from monocytes and neutrophils (PMN). The PMN generate free radicals that damage the endothelial cells and increase proinflammatory cytokines and tumour necrosis factor-alpha level (2-5). These molecules activate PMN, that play an important role in this process, by release of proteolytic enzyme and generation of oxygen free radicals, that can cause injury to membranes and mitochondria (6-10).ROS derived by PMN activation (11) may have an important role in the pathophysiology of AMI because it can induce functional and structural damage of cardiac myocytes (12-14) due to the damage of cellular membranes, proteins, mitochondria, DNA, lipoproteins, and lipid peroxydation (15-18). Moreover, reperfusion therapy after AMI can induce a response similar to the acute inflammation, with endothelial cell injury and inflammatory cell infiltration that produce further ROS (6,(19)(20)(21)(22).AMI frequently produces left ventricular (LV) dilatation and hypertrophy of the noninfarcted

Oxidative Stress in Young Subjects With Acute Myocardial Infarction: Evaluation at the Initial Stage and After 12 Months

“…It is not possible to exclude that all these aspects may be related to the high prevalence of inflammatory gene polymorphism demonstrated in these young subjects with AMI. [35][36][37][38][39] The persistence of an impaired oxidative stress 12 months after AMI requires 2 different considerations: first, the use of antioxidant therapy after AMI may be advisable [40][41][42][43] ; moreover, the altered oxidative status observed much later after AMI may be present also before AMI. Regarding this latter aspect, our project of reevaluating the same AMI subjects 2 years or even later after AMI may give further information.…”

Oxidative Stress-Related Biomarkers in Essential Hypertension and Ischemia-Reperfusion Myocardial Damage

“…Nonenzymatic antioxidants include a variety of mostly exogenous biological molecules, such as ascorbic acid (vitamin C), α -tocopherol (vitamin E), reduced glutathione (GSH), carotenoids, flavonoids, polyphenols, and other exogenous antioxidants [29]. …”

Metabolic stress, reactive oxygen species, and arrhythmia

“…The dismutation of superoxide by superoxide dismutase results in the generation of H 2 O 2 , which catalase further metabolizes to water and oxygen. In the nonenzymatic pathways, there are a variety of redox-defense system including antioxidant scavengers, such as vitamins E and C [41], the ratio of reduced glutathione (GSH) to oxidized glutathione disulfide (GSSH), the ratio of oxidized and reduced forms nicotinamide adenine dinucleotide, NADH/NAD + , and the thioredoxin [14, 42]…”