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Study Objectives: To evaluate the available evidence on the putative relationships between sleep bruxism (SB) and, obstructive sleep apnea (OSA) to assess the extent of research on this topic, and to formulate suggestions for future research., Methods: A scoping review including studies examining temporal and overall association and prevalence of SB and OSA was performed. Six main databases and gray literature were searched. The studies selection was conducted by three independent reviewers. A narrative synthesis of the results was carried out., Results: Thirteen studies in adults and eight studies in children were finally included. The median of concomitant conditions prevalence was 39.3% in adults and 26.1% in children. Marked methodological variability was identified among studies in adults and even more when we compared detection methods in children. No significant association between OSA and SB emerged in most studies in adults, while an association may be possible in children., Conclusions: Based on the current literature, it is not possible to confirm that there is a relationship between SB and OSA in adults. In patients under pediatric care, although this association seems plausible, there is currently insufficient supportive evidence. Standardized validated methodologies for identifying SB should be consistently used in both populations before reaching any conclusion regarding such association. Furthermore, assessment of shared phenotypes between patients with SB and patients with OSA may reveal new insights that will contribute to personalized approaches aiming to optimize the management of such comorbidities., (© The Author(s) 2022. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: The effect of chronic use of renin-angiotensin-aldosterone system (RAAS) inhibitors on the severity of COVID-19 infection is still unclear in patients with hypertension. We aimed to investigate the association between chronic use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) and COVID-19-related outcomes in hypertensive patients., Methods: A single-center study was conducted on 133 consecutive hypertensive subjects presenting to the emergency department with acute respiratory symptoms and/or fever who were diagnosed with COVID-19 infection between 9 and 31 March 2020., Results: All patients were grouped according to their chronic antihypertensive medications (ACEIs, N = 40; ARBs, N = 42; not on RAAS inhibitors, N = 51). There was no statistical difference between ACEIs and ARBs groups in terms of hospital admission rate, oxygen therapy, and need for noninvasive ventilation. Patients chronically treated with RAAS inhibitors showed a significantly lower rate of admission to semi-intensive/intensive care units, when compared with the non-RAAS population (odds ratio (OR) 0.25, confidence interval (CI) 95% 0.09-0.66, P = 0.006). Similarly, the risk of mortality was lower in the former group, although not reaching statistical significance (OR 0.56, CI 95% 0.17-1.83, P = 0.341)., Conclusions: Our data suggest that chronic use of RAAS inhibitors does not negatively affect clinical course of COVID-19 in hypertensive patients. Further studies are needed to confirm this finding and determine whether RAAS inhibitors may have a protective effect on COVID-19-related morbidity and mortality., (© American Journal of Hypertension, Ltd 2020. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Several clinical studies reported an increased prevalence and accelerated progression of aortic valve calcification among patients with end-stage renal disease when compared with subjects with normal kidney function. Recently, mechanisms of calcific valve degeneration have been further elucidated and many of the pathways involved could be amplified in patients with decreased renal function. In particular, calcium-phosphate balance, MGP metabolism, OPG/RANK/RANKL triad, fetuin-A mineral complexes and FGF-23/Klotho axis have been shown to be impaired among patients with advanced chronic kidney disease and could play a role during vascular/valve calcification. The scope of the present review is to summarize the clinical data and the pathophysiological mechanisms potentially involved in the link between renal function decline and the progression of aortic valve disease.

Background: Angiotensin II (Ang II) is a powerful proinflammatory cytokine and growth factor that activates NF-kappaB, as well as NAD(P)H oxidase, and thus is a key factor for the induction and progression of cardiovascular diseases. Our previous studies have shown high Ang II and high blood pressure-driven proatherogenic remodelling in an animal model. To further explore Ang II in proatherogenic vascular remodelling independent of blood pressure, we used Bartter's/Gitelman's syndrome (BS/GS) patients given their elevated plasma Ang II, yet normo/hypotension, because extensive mechanistic studies in these patients suggest they are a good model to explore Ang II-mediated signalling., Methods: The study evaluated BS/GS patients for nitric oxide-dependent (FMD) and -independent vasodilation and intima-media thickness (IMT) of the carotid arteries compared with healthy subjects and essential hypertensive patients., Results: The results showed the absence of IMT growth in BS/GS patients as cumulative mean-IMT and mean maximum-IMT levels in BS/GS did not differ from normotensives: 0.58 +/- 0.09 mm versus 0.60 +/- 0.09 and 0.67 +/- 0.09 versus 0.70 +/- 0.13 respectively, P = ns, but were significantly lower compared with hypertensive patients: 0.69 +/- 0.13, P < 0.046 and 0.85 +/- 0.19, P < 0.018, respectively. FMD was increased in BS/GS versus hypertensives or normotensive controls (10.8 +/- 2.7% versus 6.5 +/- 2.3 and 8.7 +/- 1.9, P < 0.002 respectively) while endothelium-independent dilation did not differ (10.2 +/- 3.6% versus 7.2 +/- 1.9 and 8.2 +/- 3.3, P = ns) between groups., Conclusions: Our study in BS/GS provides to our knowledge the first clinical data that point to a direct proatherogenic role for Ang II. However, because the data are derived from findings in BS/GS and therefore are indirect, further studies in this and other models using more direct approaches should be pursued to demonstrate a direct proatherogenic effect of Ang II as well as further studies on Ang II type 2 receptor (AT2R) signalling that the spectrum of findings of this and other studies indicate as involved in the lack of vascular remodelling.

Objective: Mutations in the DAX-1 gene result in X-linked congenital adrenal hypoplasia. The classic clinical presentation is primary adrenal insufficiency in early life and hypogonadotropic hypogonadism at the time of expected puberty, but recent data have expanded the phenotypic spectrum of DAX-1 mutations. We report the occurrence of an ACTH-secreting adenoma in a patient with X-linked congenital adrenal hypoplasia., Design and Methods: Detailed clinical, radiological and pathological investigation of the pituitary adenoma. Genomic analysis of the DAX-1 gene in the patient and his mother., Results: In this patient, primary adrenal failure had been diagnosed at 3 years of age and, despite replacement therapy, at 30 years of age progressive pigmentation developed and impairment of the visual field followed. ACTH was 24 980 pg/ml and nuclear magnetic resonance disclosed a huge pituitary adenoma. Three transsphenoidal operations and radiotherapy were necessary to remove the tumor mass and control ACTH secretion. Histologically, the adenoma was composed of chromophobic and basophilic neoplastic cells with positive immunostaining for ACTH. Moreover, a novel mutation was found both in the patient and his mother: a 4 bp insertion (AGCG) at nucleotide 259, in exon 1 resulting in a frame shift and premature termination., Conclusions: This case suggests that in adrenal hypoplasia congenita the development of a pituitary adenoma should be considered when a sudden rise of ACTH occurs despite adequate steroid substitution.

Objectives: We report a female patient suffering from Takayasu arteritis (TA) who underwent surgical revascularization., Methods: By studying specimens obtained at surgery, we evaluated the cell composition of the arterial wall, along with the maturation pattern of vascular smooth muscle cells (VSMC) during the active phase of TA. Using TUNEL, we detected apoptotic cells within the tunica media., Results: The highest percentage of apoptotic cells was found in areas where inflammatory infiltrate was present and the medial structure was more or less damaged. Apoptotic cells were also found in structurally preserved areas, where VSMC but not inflammatory cells were present., Conclusions: Apoptosis involved not only inflammatory cells but also VSMC, particularly those of the immature type. We hypothesize a role for VSMC apoptosis in the development of TA.

The aim of the study was to investigate whether hypertension and physical training induce parallel changes in the arterial wall. Ninety-seven never-treated stage 1 hypertensive patients (HT) (systolic blood pressure 140 to 159 mm Hg or diastolic blood pressure 90 to 99 mm Hg) aged 18 to 45 years taking part in the Hypertension and Ambulatory Recording Venetia Study and 27 normotensive volunteers (NT) aged 30 +/- 9 years were studied. Data on physical or sports activity were collected and scored, and target organ involvement was investigated by assessing microalbuminuria, echocardiography, and carotid ultrasound study. The carotid arteries were examined according to the Atherosclerosis Risk in Communities protocol. Mean (m-IMT) and maximal (M-IMT) carotid intima-media thickness were measured at end-diastole in the far wall common carotid artery, in the bulb and internal carotid artery, in the lateral and posterior projection, averaging the left and right sides. A comparable level of physical activity was present in HT patients and NT subjects. Twenty-four-hour blood pressure and blood lipid levels, as well as target organ damage, were similar in physically active and sedentary HT. The m-IMT of the common carotid was greater in sedentary HT than in sedentary NT, as well as in active than in sedentary NT. The m-IMT of the internal carotid artery was also greater in active HT than in active NT, as well as in active than in sedentary HT. In logistic regression, comparing the first and fourth quartile of m-IMT, scored physical activity was a predictor of m-IMT in the internal carotid artery. No statistical interaction was found between physical activity and hypertension, indicating that these two items have a cumulative effect and act independently of each other. Sedentary HT had significantly greater levels of M-IMT than sedentary NT in all sites but the bulbs; in the internal and common carotid arteries, HT exercisers had significantly greater M-IMT than NT exercisers. Therefore, physical activity appears to be an early independent predictor of carotid wall thickness. This factor should be taken into consideration in population-based studies aimed at investigating supraortic vessels as it can act as a confounder.

The aim of this study was to evaluate the effect of anipamil, a phenyalkylamine-derived Ca(2+)-antagonist, on aortic intimal thickening and smooth muscle cell (SMC) phenotype in 2K-1C hypertensive rabbits. Monoclonal antimyosin antibodies [SM-E7, NM-G2, and NM-F6, which respectively, recognize smooth muscle (SM), A-type-, and B-type-like nonmuscle (NM) myosin heavy chains (MyHC)] identify different aortic SMC types: adult (SM-E7-positive), postnatal (SM-E7- and NM-G2-positive), and fetal (SM-E7-, NM-G2-, and NM-F6-positive). Twenty-four hypertensive rabbits were studied 2.5 months (n = 12) and 4 months (n = 12) after clipping. Six animals from each group were given anipamil (40 mg orally, once daily) immediately after surgery. The remaining 2K-1C were given a daily oral placebo. Normotensive age-matched controls were also studied. Transverse cryosections of aorta were taken for computerized morphometry and immunocytochemical studies. Primary and secondary SMC cultures were used to define potential changes in cell phenotype after adding anipamil to the culture medium. In untreated 2K-1C, intimal thickening, mainly composed of postnatal-type SMC, was found by 2.5 months after clipping. Morphometric and immunofluorescence studies in anipamil-treated 2K-1C rabbits revealed absent or negligible intimal thickening and a decrease of postnatal-type SMC from the underlying media. In culture experiments, growth inhibition of SMC by anipamil was accompanied by the expression of SM-MyHC in all SMC, ie, the appearance of a more differentiated cell phenotype compared to control cultures. In conclusion, prevention of intimal thickening in anipamil-treated 2K-1C was achieved through selective reduction in the media of the postnatal-type SMC. This could be achieved by reducing NM-MyHC content or increasing synthesis of SM-MyHC expression. As blood pressure was not significantly lowered by anipamil treatment, a direct and specific antiproliferative action of this drug on medial SMC is likely to take place.

In this review we have analyzed the present knowledge about the differentiation and growth processes in vascular smooth muscle cells (SMC) in hypertension. The study of smooth muscle (SM) and nonmuscle (NM) myosin isoform expression has permitted us to identify a three-stage specific maturational pathway, namely, fetal, postnatal, and adult. In the renovascular (rabbit) and genetic (rat) models of hypertension, adaptive changes occurring in hypertensive vessels make SMC resemble those found in the early stages of development (smooth muscle plasticity). In fact, based on SM- and NM-myosin isoform distribution, postnatal-type SMC predominate in the arterial media during the early remodeling of the arterial wall that occurs in hypertension, whereas postnatal- and fetal-type SMC predominate in the intimal thickening. Locally produced or activated autocrine/paracrine factors, such as growth factors or cytokines, along with circulating hormones, seem to be involved in the growth response or changes in the differentiation pattern of SMC. Thus, these factors not only play a specific role in the regulation of blood pressure, but also are likely to be responsible for the remodeling of the arterial wall in hypertension.

Twenty-seven mild to moderate essential hypertensive patients were treated with captopril alone or combined with hydrochlorothiazide and left ventricular echocardiographic changes were evaluated after 1, 3 and 6 months. The left ventricular mass decreased slightly after 3 months, together with mean wall stress and total peripheral resistance, while the cardiac performance, as measured by fractional shortening and cardiac output, was unaffected. A high degree of individual variability was observed, and only 9 out of 20 patients examined after 3 months had a consistent reduction in left ventricular mass. The effect of captopril on the isomyosin composition was also evaluated in 4 normotensive rats after 12 weeks of drug administration. No interference with the physiological pattern was observed and no modifications of the biochemical and structural properties of the myocardium were detected.