Hypertension Research最新文献

Antihypertensive medications that can affect potassium homeostasis in the body. JGA, juxtaglomerular apparatus; ACEIs, angiotensin converting enzyme inhibitors; ARBs, angiotensin receptor blockers; MR, mineralocorticoid receptor.

Large-scale studies of the prognosis of resistant hypertension in Asian populations are limited, and the impact of poor adherence on clinical prognosis in patients with apparent treatment-resistant hypertension has not been studied. A nationwide cohort analysis was done utilizing the National Health Insurance Service database in Korea, covering patients who participated in health examinations from 2013 to 2018. A total of 935,002 patients were classified into apparent treatment-resistant (N = 69,372) or nonresistant (N = 865,630) hypertension based on blood pressure control and antihypertensive medication use. Medication adherence was assessed using the proportion of days covered. The primary composite outcome included all-cause mortality, myocardial infarction, stroke, and heart failure. Other outcomes were the development of atrial fibrillation and progression to end-stage renal disease (ESRD). The median follow-up duration was 6.0 (interquartile range [IQR], 4.1-7.0) years. Patients with apparent treatment-resistant hypertension were at a higher risk for the primary composite outcome than those with nonresistant hypertension (hazard ratio [HR], 1.32; 95% confidence interval [CI], 1.29-1.35). The incidence rates of ESRD were notably higher in the resistant hypertension group (HR, 3.02; 95% CI, 2.85-3.20). Among participants with resistant hypertension, 3852 (5.7%), 11,667 (17.3%), and 51,879 (77%) had poor, suboptimal, and optimal adherence, respectively. Poor medication adherence in apparent treatment-resistant hypertension was associated with a higher risk of the primary composite outcome compared to optimal adherence (HR, 1.49; 95% CI, 1.36-1.63). Apparent treatment-resistant hypertension is associated with significant cardiovascular risks in the Korean population. Poor adherence to antihypertensive medication significantly elevates the risk of adverse clinical outcomes in patients with apparent treatment-resistant hypertension, underscoring the need for stringent management of these patients.

Multiple sham-controlled clinical trials have demonstrated significant reductions in both office and 24-h blood pressure (BP) following radiofrequency renal denervation (RDN) in the uncontrolled hypertension population. Notably, the blood pressure response varies widely within individual participants, thus showing a clinical need to identify potential RDN "responders" prior to the procedure. Despite multiple analytic efforts, no single parameter, aside from baseline blood pressure, has been consistently associated with BP reduction following RDN. However, this failure may be due to limitations in empiric definitions of responders. Indeed, commonly applied responder definitions based on the difference between two point-in-time BP measurements are fraught due to visit-to-visit variability in office and 24-h blood pressure endpoints. Several factors should be considered to develop a more clinically useful operational definition of procedural response including relative changes in office and 24-h BP, consideration of the temporal response to RDN, as well as adjustment for baseline BP. The current evidence may provide incentives for future expert consensus to precisely define responders to hypertension treatments.

Cancer and cardiovascular disease (CVD) are the leading causes of death in Japan, with an increasingly recognized interrelationship. Both diseases share numerous risk factors and pathophysiological mechanisms, suggesting a bidirectional influence on onset and progression. Recent studies reveal that cancer survivors face elevated CVD risks, particularly shortly after diagnosis, while CVD may predispose individuals to cancer. Cancer treatments, including chemotherapy, can lead to cardiotoxicity and increased CVD complications. A study by Suzuki et al. demonstrates that individuals with hypertension and a history of cancer, especially those treated with chemotherapy, have a higher risk of developing CVD events. Despite limitations in study design and data specificity, these findings highlight the importance of long-term cardiovascular monitoring in cancer survivors. As cardio-oncology evolves, developing evidence-based guidelines and fostering collaboration between oncologists and cardiologists is crucial for optimizing patient care and outcomes in both cancer and CVD management.

This study aimed to investigate the characteristics of out-of-office blood pressure (BP) measurements in patients with apparent treatment-resistant hypertension (aRH) enrolled from 15 tertiary care centers in South Korea. aRH was defined as having uncontrolled office BP ≥ 130/80 mmHg despite receiving three classes of antihypertensive medication or any level of BP despite receiving ≥4 classes of antihypertensive medication. Patients with complete data for office BP, 24-h ambulatory BP monitoring (ABPM), and home BP measurements at baseline were included. BP control status between ABPM and home BP measurements was compared. Out of 1457 patients, 823 meeting the enrollment criteria were included (mean age: 59.9 ± 13.6 years; 57.5% male patients). Among them, 7.2% had controlled BP, 8.7% had whitecoat uncontrolled hypertension, 15.1% had masked uncontrolled hypertension, and 69% had sustained hypertension, as measured through baseline ABPM. Additionally, 43% of patients with controlled BP based on home BP measurement had nocturnal hypertension. Relying solely on home BP measurement may result in misclassifying 70% of patients as having either controlled BP or whitecoat uncontrolled BP. This study reaffirms the circadian pattern of resistant hypertension, characterized by a higher prevalence of non-dipping and rising patterns, even in patients with BP controlled based on ABPM. Considering the persistent difference between home BP measurement and ABPM, even at a lower home BP threshold, integrating both measurements into the management of aRH is advisable.

Maternal exercise during pregnancy is widely recognized as an effective means of promoting cardiovascular health in offspring. Few studies have explored how maternal exercise impacts vascular function and phenotypic switching in hypertensive offspring, despite the known involvement of vascular structural and functional remodeling in hypertension pathogenesis. Research indicates a significant relationship between elevated blood pressure and fibroblast growth factor 21 (FGF21) levels. It remains unclear whether maternal exercise during pregnancy can improve vascular function in hypertensive offspring by regulating FGF21 and its underlying mechanisms. In this study, pregnant spontaneously hypertensive rats and Wistar-Kyoto rats were randomly assigned to either a sedentary or exercise group. The exercise group underwent weightless swimming exercise from gestation day 1 (GD1) to GD20. The aim was to investigate the epigenetic modifications mediated by histone deacetylase sirtuin 1 (SIRT1) during the fetal period and the phenotypic changes in the mesenteric arteries (MAs) of hypertensive offspring. We found that maternal exercise significantly improved vascular remodeling in hypertensive offspring. Specifically, maternal exercise upregulated SIRT1 expression, which led to decreased H3K9ac (histone H3 lysine 9 acetylation) in the promoter region of the FGF21 gene. This epigenetic modification resulted in the transcriptional downregulation of FGF21 in the MAs of hypertensive fetuses. These results suggest that maternal exercise may lower blood pressure in hypertensive offspring by regulating deacetylation of the FGF21 gene promoter region through SIRT1, thereby reversing phenotypic switching and vascular structural remodeling.

Experimental and clinical studies have suggested atherosclerotic effects of uric acid (UA) on vascular smooth muscle cells (VSMCs). Nitroglycerine-induced vasodilation (NID), a control test for flow-mediated vasodilation, can be used as a possible marker of VSMC dysfunction. However, there is little information on the association between UA and NID. Therefore, we investigated the association between serum UA levels and NID according to sex. We measured NID of the brachial artery in 598 women (mean age: 66.2 ± 12.0 years) and 1008 men (mean age: 59.0 ± 18.0 years). In women, the mean serum UA level was 5.06 ± 1.24 mg/dL. Serum UA levels were negatively correlated with NID (p < 0.001), and NID significantly decreased with increasing serum UA levels (≤4.0 mg/dL, 13.4 ± 6.4%; 4.0 to ≤5.0 mg/dL, 11.4 ± 5.3%; 5.0 to ≤6.0 mg/dL, 10.8 ± 5.7%; >6.0 mg/dL, 9.7 ± 5.7%; p < 0.001). The prevalence of VSMC dysfunction, defined as NID < 8.4%, the division points for the lowest and middle tertiles of NID in women, increased with increasing serum UA levels ( ≤ 4.0 mg/dL, 23.3%; 4.0 to ≤5.0 mg/dL, 30.9%; 5.0 to ≤6.0 mg/dL, 36.4%; >6.0 mg/dL, 44.6%; p < 0.001). Multiple logistic regression analysis showed a significant association between serum UA levels and VSMC dysfunction (odds ratio, 1.21; 95% confidence interval, 1.02─1.43; p = 0.03). There was no interaction between age (<50 or ≥50 years) and the effect of serum UA levels on VSMC dysfunction (p interaction = 0.88). In contrast, no association was observed between serum UA levels and NID in men. Serum UA levels were significantly associated with VSMC dysfunction as assessed by NID in women.