Journal of The American Society of Hypertension最新文献

The Systolic Blood Pressure Intervention Trial (SPRINT) trial demonstrated the efficacy and safety of targeting a systolic blood pressure of <120 mmHg compared to <140 mmHg in selected hypertensive patients. Some evidence, however, suggests a J-curve for; diastolic blood pressure (DBP) particularly in subjects with cardiovascular (CV) and chronic kidney disease. We evaluated the risk of events in SPRINT with focus on these subgroups according to DBP.

Mean DBP (±standard deviation) throughout follow-up time was calculated for each patient. Patients were then categorized into five groups according to mean DBP (<60 mmHg, 60–69 mmHg, 70–79 mmHg [reference], 80–89 mmHg, ≥90 mmHg); hazard ratio for outcomes was assessed overall and in the predefined subgroups.

A higher risk for CV events was observed in the lower DBP range overall (hazard ratio 1.46, confidential interval 95% 1.1–1.95, P < .001), but not in the absence of pre-existing CV or renal disease. Indeed, such risk significantly increased above 80 mmHg in patients with CV disease and below 70 mmHg in those with chronic kidney disease for selected outcomes. DBP<70 mmHg particularly affected renal outcomes irrespective of renal status.

Different risk profiles according to DBP appear to be related to specific clinical characteristics in SPRINT. These findings require further testing in dedicated trials with appropriate follow-up.

Evidence suggests that supplementation of vitamin D cannot decrease blood pressure in normal populations. However, in randomized controlled trials (RCTs) with vitamin D deficient participants (defined as baseline serum 25[OH]D levels <30 ng/mL or 50 nmol/L), this effect is inconsistent and under debate. Thus, we performed this systematic review and meta-analysis to evaluate whether vitamin D supplementation could affect blood pressure parameters in vitamin D–deficient subjects. The PubMed, Web of Science, ScienceDirect, and Cochrane library databases were searched. Extracted data were pooled as weighted mean differences with 95% confidence intervals to evaluate the effects. Subgroup analysis was further conducted according to the characteristics of included studies. Seven RCTs that contained 560 participants were included in our meta-analysis. The pooled weighted mean difference of peripheral diastolic blood pressure was −1.65 mm Hg (95% confidence interval: −3.05 to −0.25, I² = 30.3%). No significant effect of vitamin D supplementation was found on other parameters. Subgroup analysis showed a significant decrease in peripheral systolic blood pressure and diastolic blood pressure in Asia, 8 weeks of intervention, and more than 5000 IU of daily vitamin D supplementation subgroups. For vitamin D–deficient patients, there is a small but significant fall in peripheral blood pressure but no significant fall in other blood pressure parameters with vitamin D supplementation. Further RCTs with large numbers of participants is still warranted to confirm these effects.

It is not known whether combination of hypertension and high homocysteine (HHcy) impacts on stroke-related neurological severity. Our aim was to determine whether there is an interaction of hypertension and HHcy on neurological severity in first-ever ischemic stroke patients. We analyzed neurological severity among 189 consecutive first-ever ischemic stroke patients with or without hypertension or HHcy. Hypertension (odds ratio [OR]: 8.086, 95% confidence interval [CI]: 3.596–18.181, P < .001) and total homocysteine (OR: 1.403, 95% CI: 1.247–1.579, P < .001) were independently associated with neurological severity. In receiver-operating characteristic analysis, total homocysteine was a significant predictor of neurological severity (area under curve: 0.794; P < .001). A multiplicative interaction of hypertension and HHcy on more severe neurological severity was revealed by binary logistic regression (OR: 13.154, 95% CI: 5.293–32.691, P < .001). Analysis further identified a more than multiplicative interaction of hypertension and HHcy on neurological severity compared with patients without each condition (OR: 50.600, 95% CI: 14.775–173.285, P < .001). Interaction effect measured on an additive scale showed that 76.4% patients with moderate/severe neurological severity were attributed to interaction of hypertension and HHcy. Significant interaction of hypertension and HHcy on neurological severity was found on multiplicative and additive scale in first-ever Chinese ischemic stroke patients.

We evaluated the possible mechanisms underlying the oxidative stress induced by ethanol withdrawal. With this purpose, we verified the role of AT₁ receptors in such response. Male Wistar rats were treated with ethanol 3%–9% (vol./vol.) for 21 days. Ethanol withdrawal was induced by abrupt discontinuation of the treatment. Experiments were performed 48 hours after ethanol discontinuation. Increased plasma levels of angiotensin II were detected after ethanol withdrawal. Losartan (10 mg/kg; p.o. gavage), a selective AT₁ receptor antagonist, impeded the increase in blood pressure induced by ethanol withdrawal. Increased lipoperoxidation and superoxide anion (O₂⁻) levels were detected in aortas after ethanol withdrawal, and losartan prevented these responses. Decreased hydrogen peroxide and nitrate/nitrite concentration were detected in aortas after ethanol withdrawal, and losartan prevented these effects. Nitrotyrosine immunostaining in the rat aorta was increased after ethanol withdrawal, and AT₁ blockade impeded this response. Increased expression of PKCδ and p47^phox was detected after ethanol withdrawal, and treatment with losartan prevented these responses. Our study provides novel evidence that ethanol withdrawal increases vascular oxidative stress and blood pressure through AT₁-dependent mechanisms. These findings highlight the importance of angiotensin II in ethanol withdrawal–induced increase in blood pressure and vascular oxidative damage.

Hypertension is an established risk factor for subsequent cardiovascular and renal disease in children as well as adults. Sickle cell disease (SCD) is a genetic disorder associated with chronic hemolytic anemia with the major manifestation of vaso-occlusive crises. Although this disease entity involves most organ systems causing vascular and pulmonary injury, little is known about blood pressure (BP) levels or prevalence of hypertension in children with SCD. A cross-sectional study was conducted on 56 children with SCD (54 with hemoglobin SS disease; 2 with hemoglobin Sβ⁰ thalassemia; 29 females). Study participants underwent 24-hour ambulatory BP monitoring (ABPM). Serum creatinine and cystatin C were obtained to assess estimated glomerular filtration rate with age-based formulas. A random urine sample was obtained to estimate urine osmolality and urine albumin to creatinine ratio. Mean age range was 11.9 (±4.5) years. Seventeen participants (30%) met criteria for hypertension based on ABPM. Of the 17 participants classified with hypertension, three had office hypertension with ambulatory hypertension, and 14 had masked hypertension detected on ABPM. Another 28 participants (50%) had some abnormal ABPM parameters in the form of either prehypertension and/or lack of normal nocturnal dipping status. The prevalence of confirmed hypertension, largely manifest by masked hypertension, is high in children, as young as 6 years of age with SCD. Early identification of hypertension in SCD children can confer benefit as it is an important modifiable risk factor for progression of cardiovascular and renal disease.

The aim of this report is to demonstrate a 2-year-2-month-old child who presented with a history of malignant hypertension. He was made the diagnosis of Takayasu arteritis by laboratory tests and angiography; we initiated a treatment with sequential balloon predilation. The patient's blood pressure improved dramatically, and patency of renal artery was demonstrated with renal arteriography over 8 months after the balloon predilation.

The cardiovascular health (CVH) score constitutes a reliable and measurable indicator of CVH proposed by the American Heart Association (AHA) calculated based on seven fundamental parameters, that is, smoking, body mass index, physical activity, healthy diet score, blood pressure, blood cholesterol, and fasting plasma glucose. The size and activity of carotid body (CB) play an important role in the pathogenesis of the cardiovascular system. The objective of this study was to define the relationship between the AHA CVH score and the volume of CB (V_rCB+lCB) estimated based on computed tomography angiography (CTA) in patients with arterial hypertension. Studies were conducted on a group of 57 patients with arterial hypertension (age: 70.74 ± 8.21 years). The CVH score was calculated, and CTA of carotid arteries was carried out for all patients. The CB analysis was performed based on delayed phase imaging obtained from CTA of carotid arteries. Based on the CVH score value, CVH was determined as optimal (CVH score between 10 and 14 points), average (5 and 9 points), or inadequate (0 and 4 points). CVH score in the studied group of patients was 6.53 ± 1.81, whereas V_rCB+lCB value was 38.58 ± 18.43 mm³. Patients with an inadequate CVH score (0–4 points) have statistically significantly higher V_rCB+lCB, and they are fraught with V_rCB+lCB ≥ median much more often than patients with an optimal CVH score (10–14 points). The receiver operating characteristic curve indicated a CVH score value of 6 as an optimal cutoff point to predict V_rCB+lCB ≥ median. The CVH score ≤6 criterion indicates V_rCB+lCB ≥ median with sensitivity of 58.6% and specificity of 71.4%. In the regression analysis, it was indicated that lower partial scores for physical activity, healthy diet score, and blood pressure in the AHA CVH evaluation constitute independent risk factors for higher V_rCB+lCB. In the studied group of patients with arterial hypertension, an inversely proportional dependence between the CVH score and the size of CB is observed in CTA of carotid arteries.