Background. In myocardial infarction patients, heart rate-adjusted QT interval (QT), an electrocardiographic indicator of sympathetic balance, is prognostic for survival.

The objective of the study was to assess the blood pressure response to changes in sodium and potassium intake and examine effect modification by age, gender, blood pressure, body weight and habitual sodium and potassium intake. Randomised trials of sodium reduction or potassium supplementation and blood pressure were identified through reference lists of systematic reviews and an additional MEDLINE search (January 1995-March 2001. A total of 40 sodium trials and 27 potassium trials in adults with a minimum duration of 2 weeks were selected for analysis. Data on changes in electrolyte intake and blood pressure during intervention were collected, as well as data on mean age, gender, body weight, initial electrolyte intake and initial blood pressure of the trial populations. Blood pressure effects of changes in electrolyte intake were assessed by weighted metaregression analysis, overall and in strata of trial population characteristics. Analyses were repeated with adjustment for potential confounders.Sodium reduction (median: À77 mmol/24 h) was associated with a change of À2.54 mmHg (95% CI: À3.16, À1.92) in systolic blood pressure and À1.96 mmHg (À2.41, À1.51) in diastolic blood pressure. Corresponding values for increased potassium intake (median: 44 mmol/24 h) were À2.42 mmHg (À3.75, À1.08) and À1.57 mmHg (-2.65, -0.50). Blood pressure response was larger in hypertensives than normotensives, both for sodium (systolic: À5.24 vs À1.26 mmHg, Po0.001; diastolic: À3.69 vs À1.14 mmHg, Po0.001) and potassium (systolic: À3.51 vs À0.97 mmHg, P ¼ 0.089; diastolic: À2.51 vs À0.34 mmHg, P ¼ 0.074). In conclusion, reduced intake of sodium and increased intake of potassium could make an important contribution to the prevention of hypertension, especially in populations with elevated blood pressure.

Background and Purpose Several studies have reported elevated circulating homocyst(e)ine levels in subjects with cerebral atherosclerosis. We assessed prospectively whether high plasma levels of homocyst(e)ine affect risk of ischemic stroke and evaluated whether high blood pressure modifies any such effect.Methods The study sample was drawn from the Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in 22 071 US male physicians. A total of 14 916 subjects 40 to 84 years old with no prior history of stroke, transient ischemic attack, or myocardial infarction provided blood samples at baseline and were followed for 5 years, with 99.7% morbidity and 100% mortality follow-up. Using a nested case-control design, we assayed homocyst(e)ine in samples from 109 subjects who subsequently developed ischemic stroke and 427 control subjects.Results The mean plasma concentration of homocyst(e)ine was slightly higher in subjects with stroke (ll.l±4.0 [±SD] nmol/mL) than in control subjects (10.6±3.4 nmol/mL), but the difference was not statistically significant (P=.12). The crude odds ratio of ischemic stroke for subjects in the upper

Several lines of evidence suggest that oxidatively modified low density lipoprotein (LDL) is atherogenic and that antioxidants may protect LDL against oxidation. In addition, cigarette smoking is known to induce oxidant stress. We have examined the effect of ingestion of the antioxidants D,L-ar-tocopherol (vitamin E) and 0-carotene and of smoking on the resistance of LDL against copper-mediated oxidation. Six healthy nonsmoking volunteers ingested 1,000 IU/day D,L-a-tocopherol acetate for 7 days. After vitamin E ingestion concentrations of or-tocopherol in plasma and LDL increased 3.0-and 2.4-fold, respectively. Simultaneously, the oxidation resistance of LDL was elevated significantly (+41%), and the rate of oxidation was decreased significantly (-19%). The increase in o-tocopherol content of LDL and the increase in resistance time were highly correlated (r,=0.89, p=0.014). Eight weeks after termination of the vitamin E intake, o-tocopherol concentrations in plasma and LDL and oxidation resistance of LDL had returned to baseline values. In smokers (n=46), plasma levels of vitamin C (-26%) and concentrations of 0-carotene (-44%, -43%) and total carotenoids (-23%, -29%) in plasma and LDL, respectively, were significantly lower compared with nonsmokers (n=23). No differences were found in o-tocopherol content of LDL and the susceptibility of LDL to lipid peroxidation in both groups. Supplementation of a group of smokers in a 14-week randomized, double-blind, placebo-controlled intervention trial witĥ -carotene resulted in a 16.6-and 5.0-fold increase of LDL /^-carotene and total carotenoid content, respectively. Similar increases were found in plasma without changes in other vitamins. Comparison of the changes in the length of the resistance time between the /J-carotene group (R=23) and the placebo group (n=23) showed no significant differences. We conclude that Ingestion of vitamin E strongly protects LDL against oxidative modification, whereas ^-carotene is not effective, and that smoking does not alter the oxidation resistance of LDL. (Arteriosclerosis and Thrombosis 1992;12:554-562) KEY WORDS • low density lipoprotein oxidation • vitamin E • /3-carotene • cigarette smoking E levated plasma levels of low density lipoprotein (LDL) are associated with an accelerated development of atherosclerotic lesions, which is one of the main causes of coronary artery disease.

Calcium plays a role in blood pressure (BP) regulation, but the importance of supplemental calcium intake for the prevention of hypertension is still debated. We conducted a meta-analysis of randomized controlled trials to determine the effect of calcium supplementation on BP. A systematic search for randomized trials of calcium supplementation and BP in non-pregnant subjects was performed in Medline from 1966 to June 2003. Seventy-one trials were identified, 40 of which met the criteria for meta-analysis (total of 2492 subjects). Two persons independently extracted data from original publications on changes in calcium intake and BP. In addition, data were collected on subjects' characteristics, that is, age, gender, initial BP and initial calcium intake. A random effects model was used to obtain the effect of calcium supplementation on BP, overall and in predefined population subgroups. Calcium supplementation (mean daily dose: 1200 mg) reduced systolic BP by À1.86 mm Hg (95% confidence interval: À2.91 to À0.81) and diastolic BP by À0.99 mm Hg (À1.61 to À0.37). In people with a relatively low calcium intake (p800 mg per day) somewhat larger BP estimates were obtained, that is, À2.63 (À4.03 to À1.24) for systolic BP and À1.30 (À2.13 to À0.47) for diastolic BP. Our study suggests that an adequate intake of calcium should be recommended for the prevention of hypertension. More research on BP in people with calcium-deficient diets is warranted.