Aim: To study whether an oat bran enriched diet has a specific effect in lowering total and low-density lipoprotein cholesterols, in addition to caloric and fat restriction. Methods: We performed a randomized, controlled, parallel-group, single-centre study in which 1,994 patients from the Wehrawald Hospital (Todtmoos, Germany) were screened and 235 met the criteria male gender, hypercholesterolemia, and overweight. All patients in the Wehrawald Hospital took part in a 4-week standardized inpatient lifestyle health program consisting of dietary intervention, increased physical activity, and health education. Caloric restriction, fat modification, and oat bran supplementation were part of the nutritional regimen within the lifestyle health program. Ninety-nine patients were randomized to a fat-modified diet with caloric restriction and a daily intake of 35–50 g oat bran and 136 patients to a fat-modified, oat bran-free diet with caloric restriction. Fifty-three male overweight but normocholesterolemic subjects were selected as controls. Results: The most significant decreases in total cholesterol (–67.7 ± 37.2 mg/dl; p < 0.01), low-density lipoprotein cholesterol (–56.3 ± 35.1 mg/dl; p < 0.01), and apolipoprotein B (–42.4 ± 34.1 mg/dl; p < 0.01) were found with the combination of the fat-modified and oat bran enriched food. Conclusions: Added to a fat-modified diet, oat bran within a practical range of intake significantly reduces total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B. These beneficial effects occurred independent of covariables such as physical activity or caloric and fat restriction in the diet.

Metaanalyses have indicated that ACE inhibitors are more effective than other first-line therapies in reducing left ventricular hypertrophy (LVH). The average treatment period, however, was only approximately 6 months. The aim of the present study, therefore, was to clarify the time course and degree of reversal, and primarily to find out in how many patients a complete normalization of LVH can be achieved. Secondly, we sought to determine whether atrial enlargement can be reduced. Previously untreated hypertensive patients (mean age 46.3 +/- 9 years, eight women, 15 men) with echocardiographically confirmed LVH (left ventricular mass index ([LVMI] > 125 g/m2 for men; > 110 g/m2 for women) were prospectively treated over a 3-year treatment period with quinapril. Nine patients received 10 mg quinapril, 12 received 20 mg of quinapril daily, and five patients additionally received 25 mg hydrochlorothiazide. The time course of changes in LVMI, relative wall thickness, left atrial size, fractional shortening, and diastolic function was evaluated and ambulatory blood pressure monitoring (ABPM) and an exercise test were performed every 6 months. After a mean treatment period of only 7.5 months, there was a significant (P < .001), 17.5% decrease in LVMI with a further continuous and significant (P < .001) decrease of 38.6% after 38.3 +/- 3 months of therapy. In 90.5% of the patients a complete reversal of LVH was achieved. Fractional shortening increased significantly, the maximum being 14.6% after 38.3 +/- 3 months. The peak early/atrial velocity (E/A) ratio increased significantly (P < .01) after just 7.5 +/- 3.1 months with no further changes during follow-up. There seemed to be a parallel change with the decrease in left atrial dimension, where the most important decrease occurred after only 7.5 +/- 3.1 months (P < .01), with a further continuous reduction. Our study clearly shows that maximum reversal of LVH is a time-consuming process and that an essential goal of antihypertensive therapy should be not only a reduction in LVH but also a normalization in LV mass, left atrial size, and in diastolic dysfunction.

1. The effects on glucose and lipid metabolism and on plasma catecholamines at rest and during exercise, of 4 weeks treatment with non-selective beta-blockade (pindolol, 15 mg daily) and with cardio-selective blockade (metoprolol, 200 mg, and acebutolol, 500 mg, respectively) were compared in different groups of hypertensive men (mean age 37 years) by single blind cross-over technique. All patients continued the treatment with either metoprolol or acebutolol for another 12--14 months. 2. All antagonists reduced blood pressures and exercise heart rates in a virtually identical manner. Whereas lipolysis was similarly inhibited by both selective beta 1-antagonists and non-selective beta 1-beta 2-blockers, glycogenolysis in the muscle was inhibited only by non-selective beta-receptor blockade. 3. The inhibition of glycogen breakdown resulted in exercise hypoglycaemia and in increases of plasma adrenaline and ACTH, which probably reflect counter-regulatory mechanisms. No major metabolic changes occurred after 12--14 months compared with 4 weeks of treatment.

No abstract

No abstract