American Journal of Hypertension最新文献

Background: Vitamin D may prevent the development of hypertension through down-regulation of renin-angiotensin system. However, epidemiologic studies assessing the interrelation of vitamin D-related biomarkers with hypertension are sparse.

Methods: We examined the prospective associations between vitamin D-related biomarkers and the risk of hypertension in a nested case-control study. In each of the Women's Health Study (WHS) and Physicians' Health Study (PHS) II, 500 incident hypertension cases and 500 age and race-matched controls were randomly selected. Baseline plasma 25(OH)-vitamin D [25(OH)D], parathyroid hormone (PTH), and total renin concentrations were measured.

Results: Among controls, 25(OH)D and PTH were inversely correlated, but neither was correlated with total renin. In the crude model, there was a trend of association between increasing quintiles of 25(OH)D and lower risk of hypertension in women, with relative risks and 95% CIs of 1.00, 1.24 (0.84-1.83), 0.82 (0.53-1.25), 0.75 (0.48-1.16), and 0.81 (0.52-1.27) (P, trend: .07). Adjustment for body mass index and other hypertension risk factors eliminated this association (relative risk of 5th quintile: 1.03). No associations were found in men. Baseline PTH and ratio of 25(OH)D to PTH were not associated with the risk of hypertension in women or men. When men and women were included in the same model, vitamin D insufficiency (defined as 25(OH)D <20 ng/mL) also was not associated with an increased risk of hypertension. No interactions were found across subgroups.

Conclusions: Our study found no association of baseline plasma 25(OH)D or PTH with the risk of hypertension or total renin concentration in middle-aged and older men and women.

Background: We aim to investigate the potential causal link between blood pressure (BP) levels and cerebral artery dissection (CAD) risk by employing a 2-sample Mendelian randomization (TSMR) framework.

Methods: Utilizing large-scale genome-wide association studies-retrieved data, we employed various Mendelian randomization (MR) techniques, including inverse variance weighted (IVW), MR-Egger regression, weighted median, and weighted mode, to ascertain BP's causal impact on CAD. The MR-Egger intercept was calculated to assess pleiotropy presence, determining heterogeneity by Cochran's Q statistic.

Results: The findings highlighted a significant association between elevated systolic BP (SBP; IVW: OR = 3.09, 95% CI: 1.11-8.61, P = 0.031) and increased diastolic BP (DBP; IVW: OR = 2.17, 95% CI: 1.14-6.21, P = 0.023) with CAD risk. Sensitivity analyses reinforced the robustness and reliability of these results.

Conclusions: The results from this TSMR study suggest a causal link between high SBP and DBP and the increased likelihood of CAD, which provides genetic evidence for a reduced risk of CAD under BP control.

Background: High fructose consumption increases blood pressure through microglia-related neuroinflammation in rats. Since intermediate-conductance calcium-activated potassium channels (KCa3.1) potentiates microglial reactivity, we examined whether the pretreatment with the KCa3.1 channel blocker TRAM-34 or minocycline prevents hypertension development in fructose-fed rats.

Methods: The study involved male Wistar rats that were given either high fructose (10% in drinking water) or tap water for 21 days. Fructose groups also received minocycline or TRAM-34 systemically for 21 days. We measured systolic and diastolic blood pressure (SBP and DBP), heart rate (HR) periodically with tail-cuff; proinflammatory cytokines, and insulin levels in plasma via Enzyme-linked immunosorbent assay (ELISA), and neuroinflammatory markers in the nucleus tractus solitarii (NTS) by qPCR at the end of 21 days. We also examined endothelium-dependent hyperpolarization (EDH)-type vasorelaxations in isolated mesenteric arteries of the rats ex vivo.

Results: SBP, DBP, and HR increased in the fructose group. Both minocycline and TRAM-34 significantly prevented these increases. Fructose intake also increased plasma interleukin-6, interleukin-1β, tumor necrosis factor-α, and insulin levels, whereas pretreatment with TRAM-34 prevented these increases as well. Iba-1, but not cluster of differentiation-86 levels were significantly higher in the NTS samples of fructose-fed hypertensive rats which implied microglial proliferation. EDH-type vasorelaxations mediated by endothelial KCa3.1 attenuated in the fructose group; however, TRAM-34 did not cause further deterioration in the relaxations.

Conclusions: TRAM-34 is as effective as minocycline in preventing fructose-induced hypertension without interfering with EDH-type vasodilation. Furthermore, TRAM-34 relieves high fructose-associated systemic inflammation.

Background: Evidence on the association of arterial stiffness and left ventricular (LV) concentric remodelling/LVH assessed by echocardiography, with abnormal blood pressure (BP) phenotypes, defined by office and ambulatory BP monitoring (ABPM) in the community is scanty. Thus, we investigated this issue in the participants to the Pressioni Monitorate E Loro Associazioni (PAMELA) study.

Methods: The present study included 491 participants who attended the second and third survey of the PAMELA study performed after 10 and 25 years from the initial evaluation. Data collection included medical history, anthropometric parameters, blood examinations, office, ABPM, echocardiographic and Cardio-Ankle Vascular Index (CAVI) measurements.

Results: In the whole study sample (age 66+10 years, 50% males), the prevalence rates of sustained normotension (NT), white coat hypertension (WCH), masked hypertension (MH), sustained hypertension (SH) and non-dipping (ND) were 31.2, 10.0, 24.2, 34.6, and 35.8% and respectively. The likelihood of having SH, the BP phenotype carrying the greatest CV risk, was four times higher (OR= 4.31, CI:2.39-7.76, p<0.0001) in participants with increased CAVI and LV remodelling/LVH compared to their counterparts without organ damage. This association showed an incremental value in discriminating SH compared to both isolated markers of organ damage (OR=1.92,p=0.03 for increased CAVI and OR= 2.02, p=0.02 for LV remodelling/LVH). The presence of isolated but also combined organ damage was unrelated to ND.

Conclusions: Our study provides new evidence of the incremental value of looking for both vascular and cardiac target organ damage to optimize the identification and clinical management of SH in the general population.

Background: There is insufficient evidence of how accurately hypertension is reported on death certificates, which are the primary evidence of causes of death. This study assesses the accuracy of reporting of hypertension on death certificates of decedents in Australia who previously had their blood pressure measured.

Methods: Blood pressure data from the 2014-2015 and 2017-2018 National Health Surveys were linked to death registration data from July 2015 to December 2021 (average 3.3 years from survey to death). The percentage of decedents with hypertension reported on the death certificate was calculated according to blood pressure level and previous diagnosis of hypertension.

Results: Hypertension was reported on the death certificate of 20.2% (95% confidence interval 12.1%-28.3%) of decedents who had very high to severe blood pressure (160/100 mm Hg and above), 14.5% (10.3%-18.8%) who had high blood pressure (140 to <160 / 90 to <100 mm Hg), 14.1% (10.8%-17.4%) who had normal to high blood pressure (<140/90 mm Hg) and who took hypertension medication, and 17.8% (13.6%-22.0%) who had been diagnosed with hypertension. Where the decedent had very high to severe blood pressure, hypertension was reported for 27.9% (14.1%-41.8%) of deaths if they had been diagnosed with hypertension, and 21.7% (9.6%-33.7%) where another cardiovascular disease was reported on the death certificate.

Conclusions: Hypertension mortality in Australia is only reported for a minority of deaths of people with high or very high to severe blood pressure; this is also found for those with a prior diagnosis of hypertension.

There is an increased prevalence of atherosclerotic cardiovascular disease (ASCVD) in patients with inflammatory rheumatic diseases (IRD) including rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, and systemic sclerosis. The mechanism for the development of ASCVD in these conditions has been linked not only to a higher prevalence and undertreatment of traditional cardiovascular (CV) risk factors but importantly to chronic inflammation and a dysregulated immune system which contribute to impaired endothelial and microvascular function, factors that may contribute to accelerated atherosclerosis. Accurate ASCVD risk stratification and optimal risk management remain challenging in this population with many barriers that include lack of validated risk calculators, the remitting and relapsing nature of underlying disease, deleterious effect of medications used to manage rheumatic diseases, multimorbidity, decreased mobility due to joint pain, and lack of clarity about who bears the responsibility of performing CV risk assessment and management (rheumatologist vs. primary care provider vs. cardiologist). Despite recent advances in this field, there remain significant gaps in knowledge regarding the best diagnostic and management approach. The evolving field of Cardio-Rheumatology focuses on optimization of cardiovascular care and research in this patient population through collaboration and coordination of care between rheumatologists, cardiologists, radiologists, and primary care providers. This review aims to provide an overview of current state of knowledge about ASCVD risk stratification in patients with IRD, contributing factors including effect of medications, and review of the current recommendations for cardiovascular risk management in patients with inflammatory disease with a focus on hypertension as a key risk factor.

Background: Elevated soluble stimulating factor 2 (sST2) level is observed in cardiovascular diseases, such as heart failure and acute coronary syndrome, which reflects myocardial fibrosis and hypertrophy, indicating adverse clinical outcomes. However, the association between sST2 and hypertensive heart disease are less understood. This study aimed to determine the relationship of sST2 with left ventricular hypertrophy (LVH) and geometric remodeling in essential hypertension (EH).

Methods: We enrolled 483 patients (aged 18-80 years; 51.35% female). sST2 measurements and echocardiographic analyses were performed.

Results: Stepwise multiple linear regression analysis showed significant associations among sST2, left ventricular (LV) mass, and LV mass index. The prevalence of LVH and concentric hypertrophy (CH) increased with higher sST2 grade levels (P for trend < 0.05). Logistic regression analysis suggested that the highest tertile of sST2 was significantly associated with increased LVH risk, compared with the lowest tertile (multivariate-adjusted odds ratio [OR] of highest group: 6.61; P < 0.001). Similar results were observed in the left ventricular geometric remodeling; the highest tertile of sST2 was significantly associated with increased CH risk (multivariate-adjusted OR of highest group: 5.80; P < 0.001). The receiver operating characteristic analysis results revealed that sST2 had potential predictive value for LVH (area under the curve [AUC]: 0.752, 95% confidence interval [CI]: 0.704-0.800) and CH (AUC: 0.750, 95% CI: 0.699-0.802) in patients with EH.

Conclusions: High sST2 level is strongly related to LVH and CH in patients with EH and can be used as a biomarker for the diagnosis and risk assessment of hypertensive heart disease.

Clinical trials registration: Trial Number ChiCTR2400082764.