American Journal of Hypertension最新文献

Background: Cuffless blood pressure (BP) devices are an emerging technology marketed as providing frequent, non-intrusive and reliable BP measurements. With the increasing interest in these devices, it is important for Hypertension Canada to provide a statement regarding the current place of cuffless BP measurements in hypertension management.

Methods: An overview of the technology in cuffless BP devices, the potential with this technology and the challenges related to determining the accuracy of these devices.

Results: Cuffless BP monitoring is an emerging field where various technologies are applied to measure BP without the use of a brachial cuff. None of the devices currently sold have been validated in static and dynamic conditions using a recognized validation standard. Important issues persist in regard to the accuracy and the place of these devices in clinical practice. Current data only support using validated cuff-based devices for the diagnosis and management of hypertension. Presently, readings from cuffless devices that are used for diagnosis or clinical management need to be confirmed using measurements obtained from a clinically validated BP device.

Conclusion: Cuffless BP devices are a developing technology designed to track BP in most daily-life activities. However, many steps remain before they should be used in clinical practice.

The diagnosis and management of hypertension have been based primarily on blood pressure (BP) measurement in the office setting. Higher out-of-office BP is associated with increased risk of cardiovascular disease, independent of office BP. Home BP monitoring (HBPM) consists of the measurement of BP by a person outside of the office at home and is a validated approach for out-of-office BP measurement. HBPM provides valuable data for diagnosing and managing hypertension. Another validated approach, ambulatory BP monitoring (ABPM), has been considered to be the reference standard of out-of-office BP measurement. However, HBPM offers potential advantages over ABPM including being a better measure of basal BP, wide availability to patients and clinicians, evidence supporting its use for better office BP control, and demonstrated efficacy when using telemonitoring along with HBPM. This state-of-the-art review examines the current state of HBPM and includes discussion of recent hypertension guidelines on HBPM, advantages of using telemonitoring with HBPM, use of self-titration of antihypertensive medication with HBPM, validation of HBPM devices, best practices for conducting HBPM in the clinical setting, how HBPM can be used as an implementation strategy approach to improve BP control in the US, health equity in HBPM use, and HBPM use among specific populations. Finally, research gaps and future directions of HBPM are reviewed.

Background: In a post-hoc analysis of a multinational, randomized trial, we investigated whether the efficacy and safety of nifedipine gastrointestinal therapeutic system (GITS) and ramipril differed between Chinese and European patients with hypertension.

Methods: Previously treated (after 2-week washout) and untreated patients with clinic blood pressure (BP) ≥140/90 mmHg (systolic/diastolic), daytime ambulatory BP ≥135/85 mmHg and standard deviation of home systolic BP >7 mmHg and/or daytime BP >12 mmHg were randomly assigned to treatment based on nifedipine GITS 30 mg or ramipril 10 mg for 12 months. Clinic, ambulatory and home BP were measured at baseline, 10 weeks and 12 months after randomization.

Results: A total of 67 Chinese and 101 European patients were analyzed and they differed in age (50.9 vs. 54.6 years, respectively), body mass index (24.5 vs. 27.0 kg/m2), clinic diastolic BP (87.9 vs. 92.5 mmHg), heart rate (75.0 vs. 70.8 beats/minute) and nighttime diastolic BP (79.3 vs. 75.9 mmHg) (all P<0.05). However, within each ethnicity, patients were comparable for clinical characteristics between the nifedipine GITS and ramipril groups (P>0.05). In both the Chinese and European patients, BP was similarly reduced with nifedipine GITS and ramipril, except that daytime systolic/diastolic BP reductions were 7.4/4.1 mmHg greater in the ramipril than nifedipine GITS group in Chinese (P=0.02). The safety profile differed between the Chinese and European patients (P for drug*ethnicity interaction ≤0.05) for all adverse events (lower incidence on nifedipine GITS in Chinese), ankle edema (higher on nifedipine GITS in Europeans) and dry cough (higher on ramipril in Chinese).

Conclusion: In the Chinese and European patients with hypertension, nifedipine GITS and ramipril had similar BP lowering efficacy, but different safety profile and tolerability.

Background: Increased circulating bilirubin attenuates angiotensin (Ang) II-induced hypertension and improves renal hemodynamics. However, the intrarenal mechanisms that mediate these effects are not known. The goal of the present study was to test the hypothesis that bilirubin generation in the renal medulla plays a protective role against Ang II-induced hypertension.

Methods: Twenty-week-old male C57Bl/6J mice were implanted with intrarenal medullary interstitial (IRMI) catheters following unilateral nephrectomy. After this time, biliverdin IXα was specifically infused into the kidney (3.6 mg/day) for 3 days before implantation with an osmotic minipump delivering Ang II (1000 ng/kg/min). BP was recorded for 3 days, 1 week after minipump infusion, in conscious mice. To further explore the antihypertensive role of renal medullary bilirubin generation, mice with specific deletion of biliverdin reductase-A (Blvra) in the thick ascending loop of Henle (TALH) were generated. At 20 weeks, BlvraTALHKO and control mice (Blvrafl/fl) were infused with Ang II for 2 weeks.

Results: IRMI infusion of biliverdin significantly decreased blood pressure compared to mice infused with vehicle (118 ± 4 vs. 158 ± 2 mmHg, p<0.05). Angiotensin-II infusion resulted in significantly higher blood pressure measured in conscious mice 7 days after implantation in BlvraTALHKO as compared to Blvrafl/fl mice (152 ± 2 vs. 140 ± 3 mmHg, p<0.05).

Conclusions: Together, these findings show that medullary bilirubin and biliverdin reductase can improve hypertension and that mechanisms that increase bilirubin and biliverdin reductase in the renal medulla could be an effective approach to treat hypertension.

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.