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Type 2 diabetes mellitus (T2DM) is associated with premature atherosclerosis and arterial stiffening due to the accumulation of advanced glycation end-products in vessel walls. Green tea polyphenols are considered cardio-protective substances. In this randomised double-blind placebo-controlled trial (NCT02627898), we evaluated the effect of Green tea extract on arterial stiffness parameters, lipids, body composition and sRAGE levels. Twenty normotensive patients with T2DM treated with the standard therapy and statins, mean age 53.2 ± 9.4 years and mean BMI 30.1 ± 4.5 kg/m2, were randomised to receive a daily dose of 400 mg of green tea extract (polyphenols ≥90%, EGCG ≥45%) or placebo for 12 weeks. Compared to placebo, administration of green tea extract decreased central augmentation index (-3.05 ± 10.8% vs. 6.7 ± 0.1%, p = .04). These findings suggest that green tea extract could be used as an adjunct to the standard therapy to improve arterial stiffness in T2DM. [ABSTRACT FROM AUTHOR]

Background: Nowadays does not exist enough studies related with cutoff points of arterial stiffness and obstruction in Mexican population compared with patients with T2DM [1]; also, is important to have a landmark on these clinical assessments to identify arterial stiffness and obstruction timely to provide also an early treatment [2-3]. Aim: To identify cutoff points, differences and correlations of arterial stiffness and obstruction between healthy/T2DM population. Methods: In a cross-sectional study, a total of 296 western Mexican individuals (163 healthy, 133 with T2DM according with ADA 2022 [4])were enrolled, aged 40-65 years (mean 52.7 ± 6.6). Variables like sex, BMI, baPWV and ankle-brachial index (ABI) were measured. T-student was used for equality of means and Pearson's test for correlation. Results: When comparing groups (healthy/T2DM), there was not a significative difference on age (52.07 ± 6.30, 53.59 ± 0.09, p:0.052) and ABI (1.12 ± 0.07, 1.13 ± 0.13, p:0.55); we found a significative difference on BMI (25.96 ± 3.29, 29.41 ± 5.08, p: < 0.01), beats/min (62.17 ± 10.63, 70.5 ± 13.3, p: < 0.01) and baPWV (1310.31 ± 186.75, 1595.33 ± 321.99, p: < 0.01); additionally there were a significative correlation between age & baPWV (r = 0.358, p: < 0.01) and baPWV & ABI (r = 0.188, p: < 0.01). Conclusion: We found a greater arterial stiffness in T2DM patients, BMI and beats/min; also, a correlation between age, ABI with arterial stiffness; and there were not differences between healthy/T2DM on ABI, and provide cutoff points for further studies. [ABSTRACT FROM AUTHOR]

The article discusses the study that assesses myocardial oxygen supply/demand ratio in healthy people during acute exposure at high altitude, and evaluates the effect of acetazolamide. The study found a decrease in oxygen supply/demand ratio at high altitude under the placebo and acetazolamide, with values remaining higher on acetazolamide. The study suggests that administration of acetazolamide may antagonize reduced subendocardial oxygen supply resulting from exposure to hypobaric hypoxia.

Aims We assessed the haemodynamic changes induced by exposure to high altitude hypoxia and the effects on them of acetazolamide, a drug prescribed to prevent and treat mountain sickness. Methods and results In 42 subjects (21 males, age 36.8 ± 8.9 years) randomized to double blind acetazolamide 250 mg b.i.d. or placebo, pulse wave velocity and pulse wave parameters were assessed (PulsePen) at baseline; after 2-day treatment at sea level; within 6 h and on 3rd day of exposure to high altitude. Exposure to high altitude significantly increased diastolic (P < 0.005) and mean blood pressure (BP) (P < 0.05, after prolonged exposure) in placebo but not in the acetazolamide group. Therefore, subjects on acetazolamide showed significantly lower values of diastolic (P < 0.005) and mean BP (P < 0.05) at altitude. Furthermore, they also showed significantly lower values of systolic BP (P < 0.05). Pulse wave velocity did not change at high altitude, while the augmentation index, normalized for a theoretical heart rate of 75 b.p.m., significantly increased (P < 0.05) under placebo, but not under acetazolamide. In a multivariate model, unadjusted augmentation index at high altitude was not affected by BP changes, while significant determinants were heart rate and gender. Conclusion Acute exposure to high altitude induced a rise in brachial BP and changes in pulse waveform-derived parameters, independent from changes in mean BP and partly counteracted by treatment with acetazolamide. The impact of acetazolamide on the haemodynamic alterations induced by hypobaric hypoxia may be considered among the beneficial effects of this drug in subjects prone to mountain sickness. [ABSTRACT FROM PUBLISHER]