Hypertension最新文献

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.

The purpose of this article is to summarize disparities in blood pressure (BP) by race in the United States, discuss evidence-based strategies to increase equity in BP, review recent American Heart Association BP equity initiatives, and highlight missed opportunities for achieving equity in hypertension. Over 122 million American adults have hypertension, with the highest prevalence among Black Americans. Racial disparities in hypertension and BP control in the United States are estimated to be the single largest contributor to the excess risk for cardiovascular disease among Black versus White adults. Worsening disparities in cardiovascular disease and life expectancy during the COVID-19 pandemic warrant an evaluation of the strategies and opportunities to increase equity in BP in the United States. Racial disparities in hypertension are largely driven by systemic inequities that limit access to quality education, economic opportunities, neighborhoods, and health care. To address these root causes, recent studies have evaluated evidence-based strategies, including community health workers, digital health interventions, team-based care, and mobile health care to enhance access to health education, screenings, and BP care in Black communities. In 2021, the American Heart Association made a $100 million pledge and 10 commitments to support health equity. This commitment included implementing multifaceted interventions with a focus on hypertension as a seminal risk factor contributing to disparities in cardiovascular disease mortality and morbidity. The American Heart Association is one organizational example of advocacy for equity in BP. Achieving equity nationwide will require sustained collaboration among individual stakeholders and public, private, and community organizations to address barriers across multiple socioecological levels.

Background: A subset of patients with postural tachycardia syndrome (POTS) are thought to have a primary hyperadrenergic cause. We assessed clinical biomarkers to identify those that would benefit from sympatholytic therapy.

Methods: We measured sympathetic function (supine muscle sympathetic nerve activity, upright plasma norepinephrine, and blood pressure responses to the Valsalva maneuver) in 28 patients with POTS (phenotyping cohort) to identify clinical biomarkers that are associated with responsiveness to the central sympatholytic guanfacine in a separate uncontrolled treatment cohort of 38 patients that had received guanfacine clinically for suspected hyperadrenergic POTS (HyperPOTS).

Results: In the phenotyping cohort, an increase in diastolic blood pressure (DBP) >17 mm Hg during late phase 2 of the Valsalva maneuver identified patients with the highest quartile of resting muscle sympathetic nerve activity (HyperPOTS) with 71% sensitivity and 85% specificity. In the treatment cohort, patients with HyperPOTS, identified by this clinical biomarker, more often reported clinical improvement (85% versus 44% in nonhyperadrenergic; P=0.016), had better orthostatic tolerance (∆Orthostatic Hypotension Daily Activities Scale: -1.9±0.9 versus 0.1±0.5; P=0.032), and reported less chronic fatigue (∆PROMIS Fatigue Short Form 7a: -12.9±2.7 versus -2.2±2.2; P=0.005) in response to guanfacine.

Conclusions: These results are consistent with the concept that POTS is caused by a central sympathetic activation in a subset of patients, which can be identified clinically by an exaggerated DBP increase during phase 2 of the Valsalva maneuver and improved by central sympatholytic therapy. These results support further clinical trials to determine the safety and efficacy of guanfacine in patients with POTS enriched for the presence of this clinical biomarker.

Background: There is a strong association between obstructive sleep apnea and hypertension, but the effects of obstructive sleep apnea symptoms on the risk of incident hypertension are not well documented. The aim of this prospective study was to examine whether snoring and sleepiness are associated with incident hypertension.

Methods: Data from the French population-based CONSTANCES cohort were analyzed. Normotensive participants, aged 18 to 69 years, were included between 2012 and 2016 and screened for snoring, morning fatigue, and daytime sleepiness in 2017 using items of the Berlin Questionnaire. We used Cox models, adjusted for multiple potential confounders, including body mass index, baseline blood pressure, sleep duration, and depressive symptoms, to compute hazards ratios of incidentally treated hypertension.

Results: Among 34 727 subjects, the prevalence of self-reported habitual snoring, morning fatigue, and excessive daytime sleepiness (≥3× a week for each) was 23.6%, 16.6%, and 19.1%, respectively. During a median follow-up of 3.1 years (interquartile range, 3.0-3.5), the incidence of treated hypertension was 3.8%. The risk of de novo treated hypertension was higher in participants who reported habitual snoring (adjusted hazard ratio, 1.17 [95% CI, 1.03-1.32]) and excessive daytime sleepiness (adjusted hazard ratio, 1.42 [95% CI, 1.24-1.62]), and increased with the weekly frequency of symptoms, with a dose-dependent relationship (P_trend≤0.02 for all symptoms).

Conclusions: Self-reported snoring and excessive daytime sleepiness are associated with an increased risk of developing hypertension. Identification of snoring and daytime sleepiness may be a useful public health screening tool in primary care for hypertension prevention.

Background: Preeclampsia poses a substantial clinical challenge, characterized by maternal hypertension, cardiac dysfunction, and persistent cardiovascular risks for both the mother and offspring. Despite the known roles of the estrogen receptor (GPER [G protein-coupled estrogen receptor]) in placental development, its impact on cardiovascular aspects within a preeclampsia animal model remains unexplored. We propose that G-1, a GPER agonist, could have the potential to regulate not only hypertension but also cardiac dysfunction in rats with preeclampsia.

Methods: To explore the influence of G-1 on preeclampsia, we used the reduced uterine perfusion pressure (RUPP) model. RUPP rats were administered either G-1 (100 µg/kg per day) or hydralazine (25 mg/kg per day). We conducted echocardiography to probe the intricate cardiac effects of G-1.

Results: The RUPP rat model revealed signs of hypertension and cardiac dysfunction and alterations in gene and protein expression within placental and heart tissues. G-1 treatment reduced blood pressure and reversed cardiac dysfunction in rats with preeclampsia. In contrast, administration of the vasodilator hydralazine reduced blood pressure without an improvement in cardiac function. In addition, while G-1 treatment restored the levels of sFLT-1 (soluble fms-like tyrosine kinase-1) in RUPP rats, hydralazine did not normalize this antiangiogenic factor.

Conclusions: The therapeutic intervention of G-1 significantly mitigated the cardiovascular dysfunction observed in the RUPP rat model of preeclampsia. This discovery underscores the broader significance of understanding GPER's role in the context of preeclampsia-related cardiovascular complications.

Background: Recent guidelines recommend antihypertensive drug treatment for prehypertensive individuals with blood pressure between 130/80 and 139/89 mm Hg. This study evaluates the cost-effectiveness of 3 interventions in Chinese prehypertensive adults: salt substitution, antihypertensive drug treatment, and their combination.

Methods: We developed a Markov cohort model to estimate cardiovascular disease (CVD) events, costs, and quality-adjusted life years (QALYs) over a lifetime. Data from the China Kadoorie Biobank informed the simulation. Costs and utilities were drawn from published sources. We evaluated the cost-effectiveness of salt substitution alone, antihypertensive drug treatment alone, and a combination of the 2, focusing on the overall prehypertensive population, those at high CVD risk, and different starting ages (40, 50, 60, and 70 years). Incremental cost-effectiveness ratios (ICERs) were calculated per QALY gained.

Results: Salt substitution at age 40 years is the only cost-effective strategy for prehypertensive individuals, with an ICER of $6413.62/QALY. For those at high CVD risk, the combination intervention starting at age 40 years is most cost-effective, with an ICER of $2913.30/QALY. Interventions initiated at younger ages yielded greater CVD reductions and lower ICERs. For example, a combined intervention at age 40 years reduces CVD events by 5.3% with an ICER of $2913.30/QALY, compared with 4.9% and $32 635.33/QALY at age 70 years. These results were consistent across sensitivity analyses.

Conclusions: In China, replacing usual salt with a salt substitute is more cost-effective than treating prehypertensive individuals over the age of 40 years with antihypertensive drugs. Furthermore, starting intervention at a younger age in prehypertensive adults can result in even greater cost savings.

Background: Endothelial cell TRPV4 (transient receptor potential vanilloid 4) channels provide a control point that is pivotal in regulating blood vessel diameter by mediating the Ca²⁺-dependent release of endothelial-derived vasoactive factors. In hypertension, TRPV4-mediated control of vascular function is disrupted, but the underlying mechanisms and precise physiological consequences remain controversial.

Methods: Here, using a comprehensive array of methodologies, endothelial TRPV4 channel function was examined in intact mesenteric resistance arteries from normotensive Wistar-Kyoto and spontaneously hypertensive rats.

Results: Our results show there is a notable shift in vascular reactivity in hypertension characterized by enhanced endothelium-dependent vasodilation at low levels of TRPV4 channel activation. However, at higher levels of TRPV4 activity, this vasodilatory response is reversed, contributing to the aberrant vascular tone observed in hypertension. The change in response, from dilation to constriction, was accompanied by a shift in intracellular Ca²⁺ signaling modalities arising from TRPV4 activity. Oscillatory TRPV4-evoked IP₃ (inositol triphosphate)-mediated Ca²⁺ release, which underlies dilation, decreased, while the contraction inducing sustained Ca²⁺ rise, arising from TRPV4-mediated Ca²⁺ influx, increased. Our findings also reveal that while the sensitivity of endothelial cell TRPV4 to activation was unchanged, expression of the channel is upregulated and IP₃ receptors are downregulated in hypertension.

Conclusions: These data highlight the intricate interplay between endothelial TRPV4 channel expression, intracellular Ca²⁺ signaling dynamics, and vascular reactivity. Moreover, the data support a new unifying hypothesis for the vascular impairment that accompanies hypertension. Specifically, endothelial cell TRPV4 channels play a dual role in modulating blood vessel function in hypertension.