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BackgroundMany patients with coronary artery disease (CAD) have overlapping gastroenterological causes of recurrent chest pain, mainly due to gastroesophageal reflux (GER) and aspirin-induced gastrointestinal tract damage. These symptoms can be alleviated by proton pump inhibitors (PPIs). The study addressed whether omeprazole treatment also affects general health-related quality of life (HRQL) in patients with CAD.Study48 patients with more than 50% narrowing of the coronary arteries on angiography without clinically overt gastrointestinal symptoms were studied. In a double-blind, placebo-controlled, cross-over study design, patients were randomized to take omeprazole 20 mg bid or a placebo for two weeks, and then crossed over to the other study arm. The SF-36 questionnaire was completed before treatment and again after two weeks of therapy.ResultsPatients treated with omeprazole in comparison to the subjects taking the placebo had significantly greater values for the SF-36 survey (which relates to both physical and mental health), as well as for bodily pain, general health perception, and physical health. In comparison to the baseline values, therapy with omeprazole led to a significant increase in the three summarized health components: total SF-36; physical and mental health; and in the following detailed health concept scores: physical functioning, limitations due to physical health problems, bodily pain and emotional well-being.ConclusionsA double dose of omeprazole improved the general HRQL in patients with CAD without severe gastrointestinal symptoms more effectively than the placebo.

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IntroductionThe proton pump inhibitor empirical trial, besides the analysis of symptoms, is the main method in the diagnosis of gastro-oesophageal reflux disease-related chest pain. β-Endorphin acts as an endogenous analgesia system. The aim of the study was verify whether β-endorphin plasma level is affected by omeprazole administration and influences the severity of anginal symptoms and outcome of the “omeprazole test” in patients with coronary artery disease (CAD) and chest pain of suspected non-cardiac origin.Material and methodsOmeprazole was administered to 48 patients with CAD in a randomized, placebo-controlled, crossover study design. At the beginning of the study, and again after the 14-day omeprazole and placebo treatment, the β-endorphin plasma concentration was determined.ResultsThe level of plasma β-endorphin after the administration of omeprazole was significantly greater than at the start of the study and following the placebo. Responders to omeprazole had an average lower β-endorphin plasma concentration than subjects who failed to respond to this therapy. Subjects with symptoms in class III (according to the Canadian Cardiovascular Society classification) after omeprazole administration had a greater β-endorphin plasma level than subjects in class II for anginal symptom severity.ConclusionsFourteen-day therapy with a double omeprazole dose significantly increases the β-endorphin plasma concentration in patients with CAD. Circulating β-endorphin does not seem to be involved in the mechanism for the “omeprazole test” outcome, although an individually different effect on pain threshold cannot be excluded.

IntroductionEndothelial dysfunction is recognized as the earliest disorder in the development of atherosclerosis, in the pathogenesis of which oxidative stress plays a crucial role. The aim of this study was to determine the relationships between non-invasive parameters of vascular dysfunction and oxidative stress.Material and methodsForty-eight individuals without clinical manifestation of atherosclerosis were studied. The plasma concentrations of the following were determined in all 48 subjects: retinol, ascorbic acid, α-tocopherol and uric acid, as well as the products of oxidative DNA damage repair: 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG) in blood leukocytes and urine, and 8-oxo-7,8-dihydroguanine (8-oxoGua) in urine. The following parameters of vascular dysfunction were also examined: flow- (FMD) and nitroglycerin- (NMD) mediated dilatation of the brachial artery, pulse pressure (PP), distensibility coefficient (DC), pulsation (PI) and resistance (RI) index, carotid intima-media thickness (cIMT), and ankle-brachial index (ABI).ResultsIndividuals with an FMD value of ≥ 8.8% had significantly higher blood concentrations of antioxidative vitamins and lower concentrations of 8-oxodG in their urine and blood leukocytes than their counterparts. Blood concentration of alpha-tocopherol or ascorbic acid positively correlated with FMD, PI, RI, DC and ABI and negatively with PP and cIMT. The reverse was the case for 8-oxodG in urine and leukocytes. In multiple regression analysis, markers of oxidative DNA damage positively determined the variance in PP and ABI.ConclusionsIn persons without clinical manifestation of atherosclerosis, oxidative stress was an independent factor associated with vascular wall dysfunction, and a better predictor than smoking and blood concentrations of glucose, lipids and creatinine.

Introduction. Oxidative stress plays an important role in atherosclerosis, but numerous clinical trials have not confirmed a favourable effect of antioxidant supplementation. We aimed to determine the oxidative stress parameters in patients without clinical manifestation of vascular disease. Material and methods. Forty-eight patients were divided into two groups in relation to the presence or absence of clinically silent signs of atherosclerosis (ankle-brachial index < 0.9, intima-media thickness ≥ 0.9 mm, the presence of carotid atherosclerotic plaques, silent ischaemia in a treadmill stress test or focal myocardial contractility found in echocardiography). Plasma concentrations of: retinol, ascorbic acid, alpha-tocopherol and uric acid, as well as the products of oxidative DNA damage repair: 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in blood leucocytes and urine, and 8-oxo-7,8-dihydroguanine (8-oxo-Gua) in urine. Results. Patients with signs of subclinical atherosclerosis had lower blood concentration of alpha-tocopherol, and a non-significantly greater urine concentration of 8-oxoGua. Women had significantly greater blood concentration of ascorbic acid and alpha-tocopherol, as well as lower level of retinol and uric acid. They also had greater leucocyte concentration of 8-oxodG. Plasma concentration of alpha-tocopherol 30.34 μM distinguished patients with and without signs of subclinical atherosclerosis. Conclusions. Oxidative stress has clinical importance in the early stages of atherosclerosis and may be helpful in predicting its subclinical stage. Women had higher level of antioxidant defence, which explains their natural protection against early atherosclerosis development. Further studies are needed to determine the usefulness of tocopherol determination as a biomarker for atherosclerosis risk evaluation.

125 patients in the early stages of Parkinson's syndrome were randomized and subjected to prearranged treatment adaptation period. Subsequently they were treated with either a mean dosage of 444 mg levodopa and benserazide (47 patients) or a combination of a mean of 298 mg levodopa and benserazide plus 17 mg bromocriptine (32 patients). Follow-up was done up to three years. Combined treatment permitted reduction of the levodopa dosage by 39%. As assessed by improvement of symptoms of Parkinson's syndrome in patients with a minimum treatment period of 1 or 3 years combined treatment was shown to be superior to monotherapy.

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