Most of the systemic blood vessels are surrounded by the perivascular adipose tissue (PVAT). Healthy PVAT is anticontractile and anti-inflammatory, but a dysfunctional PVAT has been suggested to link cardiometabolic risk factors to vascular dysfunction. Vascular oxidative stress is an important pathophysiological event in cardiometabolic complications of obesity, type 2 diabetes, and hypertension. PVAT-derived adipocytes generate reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide that might signal to the vascular wall. Therefore, an abnormal generation of ROS by PVAT emerges as a potential pathophysiological mechanism underlying vascular injury. This review summarizes new findings describing ROS production in the PVAT of several vascular beds, major sources of ROS in this tissue including mitochondria, NADPH oxidase and eNOS uncoupled, and finally, changes in ROS production affecting vascular function in the presence of cardiometabolic risk factors and diseases.
Management of arterial hypertension in patients with chronic kidney disease (CKD) remains a major challenge due to its high prevalence and associations with cardiovascular disease (CVD) and CKD progression. Several clinical trials and meta-analyses have demonstrated that aggressive treatment of hypertension in patients with and without CKD lowers the risk of CVD and all-cause mortality, nevertheless the effects of blood pressure (BP) lowering in terms of renal protection or harm remain controversial. Both home and ambulatory BP estimation have shown that patients with CKD display abnormal BP patterns outside of the office and further investigation is required, so as to compare the association of ambulatory versus office BP measurements with hard outcomes and adjust treatment strategies accordingly. Although renin-angiotensin system blockade appears to be beneficial in patients with advanced CKD, especially in the setting of proteinuria, discontinuation of renin-angiotensin system inhibition should be considered in the setting of frequent episodes of acute kidney injury or hypotension while awaiting the results of ongoing trials. In light of the new evidence in favor of renal denervation in arterial hypertension, the indications and benefits of its application in individuals with CKD need to be clarified by future studies. Moreover, the clinical utility of the novel players in the pathophysiology of arterial hypertension and CKD, such as microRNAs and the gut microbiota, either as markers of disease or as therapeutic targets, remains a subject of intensive research.
Background: In the trial known as COPE (Combination Therapy of Hypertension to Prevent Cardiovascular Events), three benidipine (a Calcium Channel Blocker; CCB) regimens were compared. Hypertensive Japanese outpatients aged 40-85 years (n=3,293) who did not achieve the target blood pressure of <140/90 mmHg with benidipine 4 mg/day were treated with the diuretic thiazide (n=1,094) or a β-blocker (n=1,089) or an additional Angiotensin Receptor Blocker (ARB; n=1,110). A significantly higher incidence of hard cardiovascular composite endpoints and of fatal or non-fatal strokes was observed in the benidipine-β-blocker group compared to the benidipine-thiazide group.
Objective and methods: We further evaluated the treatment effects of the three benidipine-based regimens on vascular and renal events in a sub-analysis of the COPE patients.
Results: A total of 10 vascular events (0.8 per 1,000 person-years) including one aortic dissection (0.1 per 1,000 person-years) and nine cases of peripheral artery disease (0.8 per 1,000 person-years) were documented, as was a total of seven renal events (0.6 per 1,000 person-years). No significant differences in vascular and renal events were revealed among the three treatment groups: vascular events, p=0.92; renal events, p=0.16, log-rank test.
Conclusion: Blood pressure-lowering therapy with benidipine combined with an ARB, β-blocker, or thiazide was similarly effective in the prevention of vascular and renal events in hypertensive outpatients, although there are not enough events to compare the difference in the three treatment groups.
Background: Disruption of redox signaling is a common pathophysiological mechanism observed in several diseases. In hypertension, oxidative stress, resulted either from enhances in Reactive Oxygen Species (ROS) production or decreases in antioxidant defenses, is associated with increase in blood pressure, endothelial dysfunction and vascular remodeling. Although the role of oxidative stress in the development of hypertension is well known, it is still unclear if this process is a cause or a consequence of tissue changes in hypertension. Indeed, unbalanced ROS formation results in several detrimental effects that contribute to hypertension, including reduction in nitric oxide bioavailability and activation of metalloproteinases. Additionally, ROS may also directly react with lipids, proteins and DNA, thereby contributing to tissue damage associated with hypertension. Therefore, a deep understanding of the role of oxidative stress in hypertension is essential to comprehend its pathophysiology and to identify new therapeutic targets.
Conclusion: This mini-review discusses the main enzymatic sources of oxidants and the major antioxidant defenses in the vasculature, followed by the effects of oxidative stress in hypertension, highlighting endothelial dysfunction, vascular remodeling and tissue damage.
Hypertension is a significant risk factor for cardiovascular morbidity and mortality, not only in adults, but in youths also, as it is associated with long-term negative health effects. The predominant type of hypertension in children is the secondary hypertension, with the chronic kidney disease being the most common cause, however, nowadays, there is a rising incidence of primary hypertension due to the rising incidence of obesity in children. Although office blood pressure has guided patient management for many years, ambulatory blood pressure monitoring provides useful information, facilitates the diagnosis and management of hypertension in children and adolescents, by monitoring treatment and evaluation for secondary causes or specific phenotypes of hypertension. In the field of secondary hypertension, there are numerous studies, which have reported a strong association between different determinants of 24-hour blood pressure profile and the underlying cause. In addition, in children with secondary hypertension, ambulatory blood pressure monitoring parameters offer the unique advantage to identify pediatric low- and high-risk children for target organ damage. Novel insights in the pathogenesis of hypertension, including the role of perinatal factors or new cardiovascular biomarkers, such as fibroblast growth factor 23, need to be further evaluated in the near future.
Renovascular hypertension (RVH) remains among the most prevalent and important, but also potentially reversible, causes of secondary hypertension. The predominant causes of renal artery stenosis (RAS) are atherosclerotic renovascular arterial stenosis (ARAS) and renal fibromuscular dysplasia. This condition can lead to progressive renal injury, cardiovascular complications and 'flash pulmonary edema'. Duplex Doppler ultrasonography, computed tomographic angiography and magnetic resonance angiography are the most commonly used diagnostic methods. There are three therapeutic options available: medical therapy including renin-angiotensin-aldosterone system antagonists, lipid-lowering agents, and antiplatelet therapy, percutaneous angioplasty with or without stent placement and surgical revascularization. Three large trials failed to demonstrate the superiority of renal artery revascularization over pharmaceutical therapy in controlling blood pressure and preserving renal function. For this reason, today revascularization is only recommended for patients with progressive worsening of renal function, recurrent 'flash pulmonary edema' and rapid increase in antihypertensive requirement in patients with previously well-controlled hypertension. However, more properly designed trials are needed in order to identify which patient populations would probably benefit from renal revascularization.
Background: Primary aldosteronism is one of the most common causes of secondary hypertension. Patients with this endocrine syndrome are at increased cardiovascular risk, higher than hypertensive individuals with equal blood pressure levels.
Objectives: The study aimed to thoroughly present and critically discuss the novel insights into the field of primary aldosteronism, focusing on the clinically meaningful aspects.
Method: We meticulously evaluated existing data in the field of primary aldosteronism in order to summarize future perspectives in this narrative review.
Results: Novel data suggests that a subclinical form of primary aldosteronism might exist. Interesting findings might simplify the diagnostic procedure of the disease, especially for the localization of primary aldosteronism. The most promising progress has been noted in the field of the molecular basis of the disease, suggesting new potential therapeutic targets.
Conclusion: Several significant aspects are at early stages of evaluation. Future research is essential to investigate these well-promising perspectives.