American Journal of Hypertension最新文献

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.

Background: Vascular endothelial growth factor receptor inhibitors (VEGFRis) improve cancer patient survival by inhibiting tumor angiogenesis. However, VEGFRis induce treatment-limiting hypertension which has been associated with impaired vascular endothelial cell (EC) function and kidney damage. The mineralocorticoid receptor (MR) regulates blood pressure via effects on the vasculature and the kidney. Thus, we interrogated the role of the MR in EC dysfunction, renal impairment, and hypertension in a mouse model of VEGFRi-induced hypertension using sorafenib.

Methods: EC dysfunction in mesenteric arterioles was assessed by immunoblotting for phosphorylation of endothelial nitric oxide synthase (eNOS) at serine 1177. Renal damage was measured by assessing glomerular endotheliosis histologically. Blood pressure (BP) was measured using implanted radiotelemetry.

Results: Six days of sorafenib treatment significantly impaired mesenteric resistance vessel EC function, induced renal damage, and increased BP. Pharmacologic MR blockade with spironolactone prevented the sorafenib-induced decline in eNOS phosphorylation and the renal glomerular endotheliosis, without affecting systolic or diastolic BP. Mice with the MR knocked out specifically in ECs (EC-MR-KO) were protected from sorafenib-induced EC dysfunction and glomerular endotheliosis, whereas smooth muscle cell-specific MR (SMC-MR) knockout mice were not. Neither EC-MR knockout nor SMC-MR knockout affected the degree to which sorafenib increased systolic or diastolic BP.

Conclusions: These results reveal that the MR, specifically in EC but not in SMCs, is necessary for VEGFRi-induced renal and vascular injury. While ineffective at lowering SBP, these data suggest potential therapeutic benefits of MR antagonists, like spironolactone, to protect the vasculature and the kidneys from VEGFRi-induced injury.

Background: Prior studies have reported a decrease in the proportion of US adults with hypertension that had controlled blood pressure (BP).

Methods: We analyzed data from the National Health and Nutrition Examination Survey (n=25,128, ≥18 years of age) to determine changes in BP control from 2013-2014 to 2021-2023. Hypertension was defined as systolic BP ≥140 mmHg, diastolic BP ≥90 mmHg or antihypertensive medication use. BP control was defined as systolic BP <140 mmHg and diastolic BP <90 mmHg.

Results: The age-adjusted prevalence of hypertension (95%CI) was 32.8% (31.2%-34.4%) in 2013-2014 and 32.0% (30.1%-33.9%) in 2021-2023. Among US adults with hypertension, the age-adjusted proportion (95%CI) with controlled BP was 54.1% (49.1%-59.2%), 48.6% (44.5%-52.7%), and 48.3% (45.8%-50.8%) in 2013-2014, 2015-2016 and 2017-2020, respectively (p-trend=0.058), and 51.1% (47.9%-54.3%) in 2021-2023 (p-value=0.184 comparing 2021-2023 versus 2017-2020). The proportion (95%CI) of US adults taking antihypertensive medication with controlled BP was 72.0% (68.5%-75.5%), 66.7% (62.9%-70.5%), and 67.8% (65.3%-70.3%) in 2013-2014, 2015-2016, and 2017-2020, respectively (p-trend=0.085), and 68.3% (64.8%-71.9%) in 2021-2023 (p-value=0.654 comparing 2021-2023 versus 2017-2020). Among non-Hispanic Black adults, BP control increased from 37.4% (95%CI 33.6%-41.1%) to 49.6% (95%CI 42.3%-56.9%) between 2017-2020 and 2021-2023 for those with hypertension (p-value=0.005), and from 52.6% (95%CI 47.4%-57.8%) to 62.6% (95%CI 55.6%-69.7%) for those taking antihypertensive medication (p-value=0.033). There was no difference in BP control across race/ethnicity groups in 2021-2023.

Conclusions: The decline in BP control from 2013-2014 to 2017-2020 did not continue through 2021-2023. An increase in BP control occurred from 2017-2020 and 2021-2023 among non-Hispanic Black adults.

Background: Bladder dysfunction entails overactive bladder (OAB) defined as symptoms of urinary urgency, frequency, and/or nocturia with or without incontinence if there is no obvious pathology or infection or lower urinary tract symptoms (LUTS) that includes recognized causes of bladder dysfunction.

Methods: Literature search.

Results: Symptoms of OAB are reported in about 15% of the adult US population. This is increased 2- to 3- fold in patients with congestive heart failure (CHF), hypertension, cardiovascular disease (CVD), chronic kidney disease (CKD) or the elderly where it often accompanies prescription for short, rapid acting loop diuretics. However, less than 2% of patients seeking care for OAB receive treatment. The fear of urinary incontinence from short, rapid acting loop diuretics may contribute to medication nonadherence and less well controlled, apparently resistant hypertension. The bladder contracts to rapid stretch. Thus, less rapid acting diuretics such as thiazides or extended-release formulations of loop diuretics may be preferable for those with bladder dysfunction. Alternatively, the use of a mineralocorticosteroid receptor antagonist, angiotensin receptor antagonist/neprilysin inhibitor or sodium glucose linked transport type 2 inhibitor may allow a reduction in dose of a short, rapid acting loop diuretic for those with bladder dysfunction.

Conclusion: A worsening of symptoms from bladder dysfunction by short, rapid acting loop diuretics occurs frequently in patients with CVD, CHF, hypertension and CKD where it can contribute to impaired quality of life and poor adherence and thereby to worsening outcomes.

Background: Wide pulse pressure (PP) is associated with cardiovascular events and the progression of chronic kidney disease (CKD) to kidney failure. PP naturally widens with age, but it is unclear whether the risks associated with greater PP are the same across all ages.

Methods: We used Cox proportional hazards models to investigate the association of PP with (i) atherosclerotic cardiovascular disease (ASCVD) events or death and (ii) a 50% reduction in estimated glomerular filtration rate or kidney failure in the chronic renal insufficiency cohort (CRIC). We evaluated the association of time-updated PP with these outcomes, accounting for time-updated confounders using inverse probability weighting.

Results: Among 5,621 participants with CKD, every 10-mmHg greater PP was associated with a 6% higher risk of an ASCVD event or death (hazard ratio [HR] = 1.06, 95% CI 1.04, 1.08) and 17% higher risk of the composite kidney outcome (HR = 1.17, 95% CI 1.16, 1.18). Greater PP was associated with a higher risk of ASCVD events or death among participants in the lowest age tertile (21-61 years), but a higher risk of the composite kidney outcome in the oldest age tertile (71-79 years). While wide PP in participants that experienced the primary outcomes was predominantly driven by elevated SBP, PP remained significantly associated with the composite kidney outcome across all ages and with ASCVD events or death in the first age tertile when SBP was added to the Cox regression model.

Conclusions: Our findings suggest that the mechanism by which PP is associated with adverse outcomes may differ by age.

Background: Preeclampsia complicates 3-5% of all pregnancies and is associated with higher levels of asymmetric (ADMA) and symmetric (SDMA) dimethylarginines. Dimethylarginines are inhibitors of nitric oxide, which is a uterine smooth muscles relaxant. Women with hypertensive disorders experience a shorter labor duration compared to normotensive women. However, very little is known about the possible biochemical mechanisms behind differences in labor duration. In this study we aimed to investigate if women with preeclampsia had higher levels of arginines (ADMA, SDMA and L-arginine) at labor than controls, and also investigate the association between arginines and labor duration.

Methods: The study was based on data from the Swedish, Uppsala County population-based, prospective cohort BASIC, between 2009 and 2018. Arginines were analyzed by Ultra-High Performance Liquid Chromatography using plasma samples taken at labor from women with preeclampsia (n=47) and normotensive pregnancy (n=90). We also analyzed inflammation markers CRP, TNF-R1, TNF-R2 and GDF-15.

Results: Women with preeclampsia had higher levels of ADMA (p<0.001), SDMA (p<0.001), L-arginine (p<0.001), TNF-R1 (p<0.001), TNF-R2 (p=0.03) and GDF-15 (p<0.01) compared to controls. Further, ADMA and SDMA, not inflammation markers, were negatively correlated to labor duration in preeclampsia. No correlations were observed when comparing arginines and inflammation markers.

Conclusions: Among women with preeclampsia, our novel findings of higher level of arigines, negative correlation of arginines to duration of labor and absence of correlation of arginines to inflammation markers might support the theory that it is not inflammation but arginines which could be associated with shorter duration of labor in preeclampsia.

Background: The incidence of cardiovascular complications may be higher in unilateral than bilateral primary aldosteronism (PA). We compared noninvasive hemodynamics after targeted therapy of bilateral vs. unilateral PA.

Methods: Adrenal vein sampling was performed, and hemodynamics recorded using radial artery pulse wave analysis and whole-body impedance cardiography (n = 114). In 40 patients (adrenalectomy n = 20, spironolactone-based treatment n = 20), hemodynamic recordings were performed after 33 months of PA treatment.

Results: In initial cross-sectional analysis, 51 patients had bilateral and 63 unilateral PA. The mean ages were 50.6 and 54.3 years (P = 0.081), and body mass indexes 30.3 and 30.6 kg/m2 (P = 0.724), respectively. Aortic blood pressure (BP) and cardiac output did not differ between the groups, but left cardiac work was ~10% higher in unilateral PA (P = 0.022). In the follow-up study, initial and final BPs in the aorta were not significantly different, while initial cardiac output (+13%, P = 0.015) and left cardiac work (+17%, P = 0.009) were higher in unilateral than bilateral PA. After median treatment of 33 months, the differences in cardiac load were abolished, and extracellular water volume was reduced by 1.3 and 1.4 l in bilateral vs. unilateral PA, respectively (P = 0.814).

Conclusions: These results suggest that unilateral PA burdens the heart more than bilateral PA, providing a possible explanation for the higher incidence of cardiac complications in unilateral disease. A similar reduction in aldosterone-induced volume excess was obtained with targeted surgical and medical treatment of PA.