Essential hypertension is a notable threat for the older (age, ≥65 years) population. However, to the best of our knowledge, a real‑world study assessing olmesartan medoxomil‑amlodipine besylate (OM‑AML) tablets in older Chinese patients with essential hypertension has not been performed. Therefore, the present study aimed to evaluate the efficacy and safety of OM‑AML tablets in these patients. A total of 463 older Chinese patients with essential hypertension treated with OM‑AML (20/5 mg) tablets (Sevikar®) were analyzed in a prospective, single‑arm, multi‑center, real‑world study. Seated systolic blood pressure (SeSBP) and seated diastolic blood pressure (SeDBP) at baseline, and at week (W)4 and W8 after OM‑AML tablet administration were measured. The mean ± standard error change of SeSBP/SeDBP was ‑10.3±0.8/‑4.6±0.5 and ‑12.5±0.8/‑5.6±0.5 mmHg at W4 and W8, respectively. At W4, 74.1 and 26.8% of patients achieved BP target according to the China and American Heart Association (AHA) criteria, while at W8, 78.0 and 38.7% of patients reached these BP targets accordingly. Finally, 76.5 and 80.5% of patients achieved BP response at W4 and W8, respectively. Furthermore, home‑measured SeSBP and SeDBP were significantly decreased from W1 to W8 (both P<0.001). Additionally, the satisfaction of both patients and physicians was elevated at W8 compared with at W0 (both P<0.001). The medication possession rate from baseline to W4 and W8 was 95.5 and 92.5%. The most common drug‑associated adverse events by system organ classes were nervous system disorder (4.5%), vascular disorder (2.8%), and general disorder and administration site conditions (2.6%), which were generally mild. In conclusion, OM‑AML tablets may be considered effective and safe in lowering BP, enabling the achievement of guideline‑recommended BP targets in older Chinese patients with essential hypertension.
Atrial fibrillation (AF) is the most common persistent cardiac arrhythmia. This study aimed to estimate its prevalence and explore associated factors in adults aged 18 years or older in China.Study data were derived from a national sample from July 2020 to September 2021. Participants were recruited using a multistage stratified sampling method from twenty-two provinces, autonomous regions, and municipalities in China. AF was determined based on a history of diagnosed AF or electrocardiogram results.A total of 114,039 respondents were included in the final analysis with a mean age of 55 years (standard deviation 17), 52·1% of whom were women. The crude prevalence of AF was 2·3% (95% confidence interval [CI] 1·7-2·8) and increased with age. The age-standardized AF prevalence was 1·6% (95% CI 1·6-1·7%) overall, and 1·7% (1·6-1·8%), 1·4% (1·3-1·5%), 1·6% (95% CI 1·5-1·7%), and 1·7% (1·6-1·9%) in men, women, urban areas, and rural areas, respectively. The prevalence was higher in the central regions (2·5%, 2·3-2·7%) than in the western regions (1·5%, 1·0-2·0%) and eastern regions (1·1%, 1·0-1·2%) in the overall population, either in the gender or residency subgroups. The associated factors for AF included age (per 10 years; odds ratio 1·41 [95% CI 1·38-1·46]; p < 0·001), men (1·34 [1·24-1·45]; p < 0·001), hypertension (1·22 [1·12-1·33]; p < 0·001), coronary heart disease (1·44 [1·28-1·62]; p < 0·001), chronic heart failure (3·70 [3·22-4·26]; p < 0·001), valvular heart disease (2·13 [1·72-2·63]; p < 0·001), and transient ischaemic attack/stroke (1·22 [1·04-1·43]; p = 0·013).The prevalence of AF was 1.6% in the Chinese adult population and increased with age, with significant geographic variation. Older age, male sex, and cardiovascular disease were potent factors associated with AF. It is crucial to increase the awareness of AF and disseminate standardized treatment in clinical settings to reduce the disease burden.This research was supported the Nature Science Foundation of Hubei province (No: 2017CFB204).
Background: Atrial fibrillation (AF) is the most common persistent cardiac arrhythmia. Little is known about the national prevalence and risk factors for AF in adults aged 18 years or older in China.Methods: Study data were derived from a nationally representative sample from July 2020 to September 2021. Participants were recruited using a multistage stratified sampling method from twenty-two Chinese provinces. AF was determined based on a history of diagnosed AF or electrocardiogram results.Findings: A total of 114,039 respondents were included in the final analysis with a mean age of 55 years (standard deviation 17). In total, 52.1% of respondents were female. In total, 2.3% (95% CI 2.2-2.4) of the study sample had AF. The prevalence of AF was 2.6% (2.5-2.7%) among men, 2.0% (1.9-2.1%) among women, 2.3% (2.2-2.4%) among individuals living in urban areas and 2.3% (2.1-2.5%) among individuals living in rural areas. The age-standardized prevalence of AF was 1.6% (95% CI 1.6-1.7%) overall and 1.7% (1.6-1.8%), 1.4% (1.3-1.5%), 1.6% (95% CI 1.5-1.7%), and 1.7% (1.6-1.9%) in men, women, urban areas, and rural areas, respectively. The risk of AF was significantly associated with age (per 10 years), male sex, hypertension, hyperlipidaemia, coronary heart disease, chronic heart failure, and stroke/transient ischaemic attack.Interpretation: AF has increased substantially in the past two decades in China. It is crucial to increase the awareness of AF and disseminate standardized treatment in clinical settings to reduce the disease burden.Funding Information: This research was supported the Nature Science Foundation of Hubei province (No: 2017CFB204).Declaration of Interests: All authors declare no competing interests.Ethics Approval Statement: The study protocol was approved by the Institutional Committee on Human Research at Renmin Hospital of Wuhan University (Wuhan, China). Written informed consent was obtained from all study participants.
New Findings What is the central question of this study? Does oxidative stress induce impairment of autophagy that results in myocyte hypertrophy early after pressure overload? What is the main finding and its importance? In cultured myocytes, hydrogen peroxide decreased autophagy and increased hypertrophy, and inhibition of autophagy enhanced myocyte hypertrophy. In rats with early myocardial hypertrophy after pressure overload, myocyte autophagy was progressively decreased. The antioxidant N ‐acetyl‐cysteine or the superoxide dismutase mimic tempol prevented the decrease of myocyte autophagy and attenuated myocyte hypertrophy early after pressure overload. These findings suggest that oxidative stress impairs myocyte autophagy that results in myocyte hypertrophy. Abstract Insufficient or excessive myocyte autophagy is associated with left ventricular (LV) hypertrophy. Reactive oxygen species mediate myocyte hypertrophy in vitro and pressure overload‐induced LV hypertrophy in vivo . In the present study, we tested the hypothesis that oxidative stress induces an impairment of autophagy that results in myocyte hypertrophy. H9C2 cardiomyocytes pretreated with the autophagy inhibitor 3‐methyladenine were exposed to 10 and 50 μ m hydrogen peroxide (H 2 O 2 ) for 48 h. Male Sprague–Dawley rats underwent abdominal aortic constriction (AAC) or sham operation. The animals were killed 24, 48 or 72 h after surgery. In a separate group, the AAC and sham‐operated rats randomly received the antioxidant N ‐acetyl‐cysteine or the superoxide dismutase mimic tempol for 72 h. In H9C2 cardiomyocytes, H 2 O 2 decreased the ratio of microtubule‐associated protein light chain 3 (LC3) II to LC3 I and increased P62 and phosphorylated ERK (p‐ERK) proteins and myocyte surface area. 3‐Methyladenine further increased H 2 O 2 ‐induced p‐ERK expression. In rats after AAC, the heart to body weight ratio was progressively increased, the LC3 II/I ratio was progressively decreased, p62 and p‐ERK expression was increased, and expression of Beclin1, Atg5 and Atg12 was decreased. N ‐Acetyl‐cysteine or tempol prevented the decreases in the LC3 II/I ratio and Beclin1 and Atg5 expression and attenuated the increases in LV wall thickness, myocyte diameter and brain natriuretic peptide expression in AAC rats. In conclusion, oxidative stress decreases Beclin1 and Atg5 expression that results in impairment of autophagy, leading to myocyte hypertrophy. These findings suggest that antioxidants or restoration of autophagy might be of value in the prevention of early myocardial hypertrophy after pressure overload.
Abstract There lacks real‐world study with a large sample size assessing olmesartan medoxomil‐amlodipine besylate (OM‐AML) tablet. Therefore, this study aimed to evaluate the efficacy and safety of OM‐AML tablet in patients with essential hypertension. Totally, 1341 patients from 36 medical centers with essential hypertension who took OM‐AML (20/5 mg) tablet were analyzed in the current prospective, single‐arm, multi‐center, real‐world study (SVK study). Seated systolic blood pressure (SeSBP) and seated diastolic blood pressure (SeDBP) at baseline, week (W)4 and W8 were measured. The mean (±SE) change of SeSBP/SeDBP was ‐10.8 ± 0.4/‐6.6 ± 0.3 mmHg at W4 and ‐12.7 ± 0.5/‐7.6 ± 0.3 mmHg at W8, respectively. At W4, 78.8% and 29.0% patients achieved BP target by China and American Heart Association (AHA) criteria; at W8, 84.7% and 36.5% patients reached blood pressure (BP) target by China and AHA criteria, accordingly. Meanwhile, 80.2% and 86.4% patients achieved BP response at W4 and W8, respectively. Home‐measured SeSBP and SeDBP decreased from W1 to W8 (both p < .001). Besides, patients’ and physicians’ satisfaction were elevated at W8 compared with W0 (both p < .001). The medication possession rate was 94.8% from baseline to W4 and 91.3% from baseline to W8. The most common drug‐related adverse events were nervous system disorders (4.6%), vascular disorders (2.6%), and general disorders and administration site conditions (2.3%) by system organ class, which were generally mild and manageable. In conclusion, OM‐AML tablet is one of the best antihypertensive agents in patients with essential hypertension.
Sestrin2 (Sesn2) is involved in the progression of cardiovascular diseases, such as hypertension and myocardial infarction. This study aimed to examine Sesn2 expression in human calcific aortic valve disease (CAVD) and explore its possible mechanisms by which Sesn2 participates in this process. CAVD and normal aortic valves were collected. Sesn2 expression and sources were examined, and the results showed that Sesn2 expression was increased in aortic valves from patients with CAVD and was mainly secreted by macrophages. Additionally, U937 macrophages were pretreated with si-Sesn2 or cDNA-Sesn2 and further treated with oxidized low-density lipoprotein (ox-LDL); M1 macrophages and their markers were measured, and we found that pretreatment with si-Sesn2 increased ox-LDL-induced M1 macrophage polarization and marker mRNA levels, whereas pretreatment with cDNA-Sesn2 had the opposite effects. In ox-LDL-treated U937 macrophages, oxidative stress levels were increased in the si-Sesn2 pretreatment group and further increased by si-Nrf2 treatment, whereas oxidative stress levels were decreased in the cDNA-Sesn2 pretreatment group and significantly reversed by ML385, a specific Nrf2 inhibitor. The effects of Sesn2 on ox-LDL-induced oxidative stress and the osteogenic differentiation of ox-LDL-induced valvular interstitial cells (VICs) was examined by down-regulating Nrf2 pathway. When U937 macrophages were co-cultured with VICs, downregulation of Sesn2 increased ox-LDL-induced osteogenic differentiation in VICs, whereas overexpression of Sesn2 exerted the opposite effects. Our study suggests that Sesn2 is increased in CAVD aortic valves and may participate in the development of CAVD by regulating oxidative stress via the Nrf2 pathway.
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