American Journal of Hypertension最新文献

Background: Lercanidipine, a newer-generation calcium channel blocker, is recognized for its effective antihypertensive properties and reduced side effects. This study aims to compare the effectiveness of lercanidipine and amlodipine in preventing major adverse cardiovascular events (MACE) in hypertensive patients.

Methods: A multicenter, retrospective observational study was conducted using the electronic medical records database from three tertiary hospitals in South Korea between 2017 and 2021. Hypertensive patients treated with either amlodipine or lercanidipine were analyzed. Propensity score matching (PSM) was utilized to minimize confounders, matching patients in a 3:1 ratio. The primary endpoint was the incidence of MACE, a composite of cardiovascular death, myocardial infarction, stroke, heart failure hospitalizations, and coronary revascularization over a 3-year follow-up period.

Results: A total of 47640 patients were evaluated, and 6029 patients were matched. Before PSM, the lercanidipine group had a higher cardiovascular risk (SCORE-2/SCORE-2OP value: 11.6% ± 9.2 vs 10.9% ± 8.8, p<0.01) and a higher incidence of MACE compared to the amlodipine group (4.1% vs 3.4%, p<0.01). After PSM, the incidence of MACE was numerically lower in the lercanidipine group compared to the amlodipine group (2.8% vs 4.1%, p=0.11), though this difference was not statistically significant. Blood pressure control remained comparable between the two groups over the 3-year follow-up period.

Conclusions: Lercanidipine demonstrated comparable effectiveness to amlodipine in preventing MACE among hypertensive patients. Given its comparable antihypertensive efficacy and potential for fewer side effects based on prior studies, lercanidipine may be considered a preferable option for hypertension management.

Background: During laboratory testing, participants rest quietly in a supine posture with little movement. However, it is rather common for participants to display various behaviors. The extent to which these common encounters influence cardiovascular measures is unknown.

Methods: Fifty-five adults (36±15 years) were studied during the following seven randomized conditions in the supine position: 1) quiet stationary rest (control), 2) while drowsy, 3) while and 4) after talking to investigators, 5) while and 6) after cell phone use for texting, and 7) lying on the side.

Results: Heart rate was greater when the participants were talking to investigators (+4 mmHg) and texting on cell phones (+5 mmHg) compared with quiet rest. Systolic blood pressure (BP) increased by 4 mmHg and diastolic BP by 3 mmHg while talking to investigators. Systolic BP was 6 mmHg and diastolic BP was 5 mmHg lower in the 'side lying' position compared with quiet rest. In the side-lying condition, carotid-femoral pulse wave velocity (PWV) was not able to be measured in 38% (n=16) of the participants while brachial-ankle PWV was not affected. Brachial-ankle PWV was greater while (+65 cm/s) and after (+29 cm/s) the participants were talking to investigators whereas carotid-femoral PWV was not able to be measured during talking. The drowsy behavior did not influence any of the BP and PWV measures.

Conclusion: Talking during the testing period significantly increases all the cardiovascular measures but cell phone use prior to the measures does not appear to influence them.

Transmural pressure and shear stress are mechanical forces that profoundly affect the smooth muscle cells (SMCs) comprising the vascular wall and the endothelial cells (ECs) lining the lumen. Pressure and flow are detected by mechanosensors in these cells and translated into appropriate responses to regulate blood pressure and flow. This review focuses on the role of the transient receptor potential (TRP) superfamily of cation channels in this process. We discuss how specific members of the TRP superfamily (TRPC6, TRPM4, TRPV1, TRPV4, and TRPP1) regulate the resting membrane and intracellular Ca2+ levels in SMCs and ECs to promote changes in vascular tone in response to intraluminal pressure and shear stress. Although TRP channels participate in vascular mechanotransduction, little evidence supports their intrinsic mechanosensitivity. Therefore, we also examine the evidence exploring the force-sensitive signal transduction pathways acting upstream of vascular TRP channels. Understanding the interplay between mechanosensors, force-induced signaling cascades, and TRP channels holds promise for the development of targeted therapies for diseases caused by vascular dysfunction.

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: 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: 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.