Hypertension最新文献

Background: Hypertensive disorders of pregnancy are associated with high maternal and fetal morbidity and mortality. There are limited global data on the characteristics of women during and after pregnancy hypertension.

Methods: May Measurement Month is a global campaign to raise awareness of the importance of blood pressure. Adults (≥18 years) recruited through opportunistic sampling during May 2019 had blood pressure measured and comorbidities and lifestyle data collected. This secondary analysis included 16 519 pregnant women and 529 172 nonpregnant women (16 457 with previous raised blood pressure in pregnancy) from 64 countries.

Results: Almost half of the pregnant women (56.7%) reported not having had their blood pressure measured in the past year, and 14.3% (95% CI, 12.1-16.6) had hypertension (blood pressure ≥140/90 mm Hg or taking antihypertensive medication). Diabetes was self-reported in 7.6% (5.9-9.3) of pregnant women with hypertension and 2.8% (1.9-3.6) of pregnant women without hypertension. In nonpregnant women with and without a history of pregnancy hypertension, age-standardized proportions with current hypertension were 53.2% (50.8-55.7) versus 33.3% (29.3-37.3); with diabetes were 14.4% (11.8-17.0) versus 8.5% (6.3-10.9); and with body mass index ≥30 kg/m² were 28.4% (23.5-33.3) versus 16.6% (13.0-20.2).

Conclusions: Hypertension in pregnancy was common in this global sample but many cases had not previously been identified. There was a clustering of cardiovascular risk factors in both pregnant women with current hypertension and previously raised blood pressure in pregnancy. This work highlights the importance of screening pregnant women for hypertension, which remains a challenge in large parts of the world.

Background: High heritability of salt sensitivity suggests an essential role for genetics in the relationship between sodium intake and blood pressure (BP). The role of glycosaminoglycan genes, which are crucial for salinity tolerance, remains to be elucidated.

Methods: Interactions between 54 126 variants in 130 glycosaminoglycan genes and daily sodium excretion on BP were explored in 20 420 EPIC-Norfolk (European Prospective Investigation Into Cancer in Norfolk) subjects. The UK Biobank (n=414 132) and the multiethnic HELIUS study (Healthy Life in an Urban Setting; n=2239) were used for validation. Afterward, the urinary glycosaminoglycan composition was studied in HELIUS participants (n=57) stratified by genotype and upon dietary sodium loading in a time-controlled crossover intervention study (n=12).

Results: rs2892799 in NDST3 (heparan sulfate N-deacetylase/N-sulfotransferase 3) showed the strongest interaction with sodium on mean arterial pressure (false discovery rate 0.03), with higher mean arterial pressure for the C allele in high sodium conditions. Also, rs9654628 in HS3ST5 (heparan sulfate-glucosamine 3-sulfotransferase 5) showed an interaction with sodium on systolic BP (false discovery rate 0.03). These interactions were multiethnically validated. Stratifying for the rs2892799 genotype showed higher urinary expression of N-sulfated heparan sulfate epitope D0S0 for the T allele. Conversely, upon dietary sodium loading, urinary D0S0 expression was higher in participants with stable BP after sodium loading, and sodium-induced effects on this epitope were opposite in individuals with and without BP response to sodium.

Conclusions: The C allele of rs2892799 in NDST3 exhibits higher BP in high sodium conditions when compared with low sodium conditions, whereas no differences were detected for the T allele. Concomitantly, both alleles demonstrate distinct expressions of D0S0, which, in turn, correlates with sodium-mediated BP elevation. These findings underscore the potential significance of genetic glycosaminoglycan variation in human BP regulation.

Background: Resistant hypertension is characterized by elevated blood pressure (BP) despite using 3 antihypertensive agents. Ambulatory BP monitoring (ABPM) detects the presence of white-coat resistant hypertension (24-hour BP <130/80 mm Hg). The aim of the study was to evaluate risks of death in resistant hypertension compared with controlled hypertension, as well as in ABPM-confirmed (24-hour BP ≥130 or 80 mm Hg), versus white-coat resistant hypertension.

Methods: We selected 8146 patients with controlled hypertension (office BP <140/90 mm Hg while being treated with ≤3 antihypertensive drugs) and 8577 with resistant hypertension (BP ≥140 or ≥90 mm Hg while being treated with ≥3 drugs). All-cause and cardiovascular mortalities (median follow-up, 9.7 years) were compared between groups, as well as between patients with white-coat (3289) and ABPM-confirmed (5288) resistant hypertension. Hazard ratios (HRs) from Cox models after adjustment for clinical confounders were used for comparisons.

Results: Compared with controlled hypertension, resistant hypertension was associated with an increased risk in all-cause (HR, 1.21 [95% CI, 1.12-1.30]) and cardiovascular mortalities (HR, 1.33 [95% CI, 1.17-1.51]) in confounder-adjusted models. Compared with white-coat, ABPM-confirmed resistant hypertension was associated with an increased risk of all-cause (HR, 1.45 [95% CI, 1.32-1.60]) and cardiovascular (HR, 1.68 [95% CI, 1.43-1.98]) mortalities. When ABPM-confirmed and white-coat resistant hypertension were separately compared with controlled hypertension, only the former was associated with an increased risk of death and cardiovascular death (HR, 1.36 [95% CI, 1.26-1.48] and 1.56 [95% CI, 1.36-1.79]), respectively.

Conclusions: ABPM-confirmed resistant hypertension is associated with an increased risk of death and cardiovascular death with respect to both controlled hypertension and white-coat resistant hypertension.

Pulmonary hypertension (PH) is a rare and severe condition characterized by increased pressure in the pulmonary circulation, often resulting in right ventricular failure and death. The autonomic nervous system (ANS) plays a crucial role in the cardiovascular and pulmonary controls. Dysfunction of ANS has been implicated in the pathogenesis of cardiopulmonary diseases. Conversely, dysfunctions in ANS can arise from these diseases, impacting cardiac and pulmonary autonomic functions and contributing to disease progression. The complex interaction between ANS dysfunction and PH plays a crucial role in the disease progression, making it essential to explore interventions that modulate ANS, such as physical exercise, to improve the treatment and prognosis of patients with PH. This review addresses autonomic dysfunctions found in PH and their implications for the cardiopulmonary system. Furthermore, we discuss how physical exercise, a significant modulator of ANS, may contribute to the prognosis of PH. Drawing from evidence of aerobic and resistance exercise training in patients and experimental models of PH, potential cardiovascular benefits of exercise are presented. Finally, we highlight emerging therapeutic targets and perspectives to better cope with the complex condition. A comprehensive understanding of the interaction between ANS and PH, coupled with targeted physical exercise interventions, may pave the way for innovative therapeutic strategies and significantly improve the treatment and prognosis of vulnerable patients.

Background: Both blood pressure-lowering medication and sodium reduction are effective in hypertension control, but whether blood pressure-lowering medication modifies the effect of sodium reduction is unclear. This study aims to evaluate the dose-response effect of sodium intake reduction on blood pressure in treated hypertensive individuals and the impact of different classes of blood pressure-lowering drugs.

Methods: We searched multiple databases and reference lists up to July 9, 2024. Randomized controlled trials with a duration of ≥2 weeks comparing the effect of different levels of sodium intake (measured by 24-hour urinary sodium excretion) on blood pressure in hypertensive individuals treated with constant blood pressure-lowering medications were included. Instrumental variable meta-analyses based on random effects models were conducted to evaluate the dose effect of sodium reduction on blood pressure. Subgroup analyses were performed based on the class of blood pressure-lowering drugs.

Results: We included 35 studies (median duration of 28 days) with a total of 2885 participants. For every 100 mmol reduction in 24-hour urinary sodium excretion, systolic blood pressure decreased by 6.81 mm Hg (95% CI, 4.96-8.66), diastolic blood pressure decreased by 3.85 mm Hg (95% CI, 2.26-5.43), and mean arterial pressure decreased by 4.83 mm Hg (95% CI, 3.22-6.44). The dose-response effects varied across classes of blood pressure-lowering medications, with greater effects observed in the β-blockers, renin-angiotensin-aldosterone system inhibitors, and dual therapy groups. No significant subgroup differences were observed based on age, baseline 24-hour urinary sodium excretion, blood pressure levels, or study duration.

Conclusions: Pooled evidence suggests a dose-response relationship between sodium reduction and blood pressure in treated individuals with hypertension, influenced by the class of blood pressure-lowering medications.