Jenifer d'El-Rei

Oral magnesium supplementation improves endothelial function and attenuates subclinical atherosclerosis in thiazide-treated hypertensive women

Background: Epidemiological studies demonstrate an inverse association between serum magnesium and incidence of cardiovascular disease. Diuretics commonly cause hypomagneseamia. Method: We evaluated effects of magnesium supplementation on blood pressure (BP) and vascular function in thiazide-treated hypertensive women in a randomized, double-blind, clinical trial. Hypertensive women (40–65 years) on hydrochlorothiazide and mean 24-h BP at least 130/80 mmHg were divided into placebo and supplementation (magnesium chelate 600 mg/day) groups. Patients were evaluated for nutritional and biochemical parameters, office and ambulatory blood pressure monitoring, brachial flow-mediated dilatation (FMD), peripheral arterial tonometry, assessment of carotid intima–media thickness, central hemodynamic parameters and pulse wave velocity at inclusion and after 6-month follow-up. Results: The magnesium group had a significant reduction in SBP (144 ± 17 vs. 134 ± 14 mmHg, P = 0.036) and DBP (88 ± 9 vs. 81 ± 8 mmHg, P = 0.005) at 6 months, without effect on plasma glucose, lipids, or arterial stiffness parameters. The placebo group showed a significant increase in carotid intima-media thickness (0.78 ± 0.13 vs. 0.89 ± 0.14 mm, P = 0.033) without change in the magnesium group (0.79 ± 0.16 vs. 0.79 ± 0.19 mm, P = 0.716) after 6 months. The magnesium group demonstrated a significant increase in variation of FMD vs. the placebo group (+3.7 ± 2.1 vs. 2.4 ± 1.2%, P = 0.015). There was a significant correlation between the intracellular magnesium variation and FMD (r = 0.44, P = 0.011). Conclusion: Magnesium supplementation was associated with better BP control, improved endothelial function and amelioration of subclinical atherosclerosis in these thiazide-treated hypertensive women.

Characterisation of hypertensive patients with improved endothelial function after dark chocolate consumption.

Recent findings indicate an inverse relationship between cardiovascular disease and consumption of flavonoids. We aimed to identify clinical and vascular parameters of treated hypertensive who present beneficial effects of dark chocolate for one-week period on vascular function. Twenty-one hypertensive subjects, aged 40–65 years, were included in a prospective study with measurement of blood pressure (BP), brachial flow-mediated dilatation (FMD), peripheral arterial tonometry, and central hemodynamic parameters. These tests were repeated after seven days of eating dark chocolate 75 g/day. Patients were divided according to the response in FMD: responders (n = 12) and nonresponders (n = 9). The responder group presented lower age (54 ± 7 versus 61 ± 6 years, P = 0.037), Framingham risk score (FRS) (2.5 ± 1.8 versus 8.1 ± 5.1%, P = 0.017), values of peripheral (55 ± 9 versus 63 ± 5 mmHg, P = 0.041), and central pulse pressure (PP) (44 ± 10 versus 54 ± 6 mmHg, P = 0.021). FMD response showed negative correlation with FRS (r = −0.60, P = 0.014), baseline FMD (r = −0.54, P = 0.011), baseline reactive hyperemia index (RHI; r = −0.56, P = 0.008), and central PP (r = −0.43, P = 0.05). However, after linear regression analysis, only FRS and baseline RHI were associated with FMD response. In conclusion, one-week dark chocolate intake significantly improved endothelial function and reduced BP in younger hypertensive with impaired endothelial function in spite of lower cardiovascular risk.

Cardiometabolic disorders in hypertensive women with abdominal obesity

Weight gain and increased waist circumference are important prognostic indicators of systemic arterial hypertension (SAH) and abdominal obesity (AO) is a relevant indicator of increased cardiovascular risk (CVR).1,2 Recent studies suggest that AO is more strongly associated with blood pressure (BP) than general adiposity3 and its association with SAH is recognized.4 In fact, there seems to be a direct influence of body mass index (BMI) and waist circumference on BP levels since adolescence.5 Additionally, it is well documented that weight loss causes reduced BP.6,7 Besides this direct influence on BP, AO is recognized as one of the main characteristics of metabolic syndrome (MS) and probably one of the most important CVR factors of the syndrome.8