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OBJECTIVES Hypertension phenotypes differ between Africans and Europeans, with a greater prevalence of low renin salt-sensitive hypertension and greater predisposition to adverse cardiac remodelling in Africans. To elucidate the roles of inheritance and environment in determining hypertension phenotypes in sub-Saharan Africans and white-Europeans, we compared phenotypes in white individuals in the UK (n = 132) and in African individuals in the UK (n = 158) and Nigeria (n = 179). METHODS Biochemistry, blood pressure, left ventricular structure (echocardiography) and 24-h urinary collections of sodium and potassium were measured. RESULTS Twenty-four-hour urinary sodium/potassium ratio was lower in individuals living in Europe (both African and white: 2.32 ± 0.15 and 2.28 ± 0.17) than in individuals in Nigeria (4.09 ± 0.26, both P

Thiazide diuretics have been the cornerstone of hypertension treatment for >5 decades. Most recent European and American guidelines recommend both thiazide‐type and thiazide‐like diuretics as first‐line drugs for all patients with hypertension. In contrast, diuretics are not regarded as first‐line treatment in the UK and in patients who are to be initiated on a diuretic treatment, thiazide‐like molecules, such as chlortalidone and indapamide are the preferred option. This review examines the prescribing trend of the 4 most commonly prescribed thiazide diuretics for the treatment of hypertension in the UK. Prescription cost analysis data were obtained for both 2010 and 2016/2017 for each region of the UK to analyse the impact of the 2011 National Institute for Health and Care Excellence hypertension guidelines on the trend in thiazide diuretic prescribing. Overall, the prescriptions of thiazide diuretics declined over the years. Bendroflumethiazide is the most commonly prescribed diuretic in the UK and despite some geographical differences, thiazide‐type diuretics are more widely used than thiazide‐like. The use of indapamide increased significantly between 2010 and 2016/2017 while chlortalidone was rarely employed. Of the many factors affecting trends in prescriptions, clinical inertia, treatment adherence, availability of the products and the lack of fixed dose combinations may play a role.

We investigated the sensitivity and reproducibility of inferior vena cava (IVC) diameters and superior vena cava (SVC) flow velocities in detecting changes in cardiac preload in clinically euvolemic subjects with hypertension.Measurements were obtained during passive leg raising (PLR) and lower limb venous occlusion (LVO), interventions which respectively transiently increase and decrease cardiac preload. Measurements were made in 36 subjects and repeated on two separate occasions to examine reproducibility.During PLR, there was no significant change in IVC diameters, but peak flow velocity of the SVC S wave increased by 6.5 (95% confidence interval 1.6-11.3) cm/s (Despite suboptimal reproducibility of baseline measurements, high agreeability between the changes in IVC diameter and SVC flow after LVO suggests that these indices can be used to monitor changes in cardiac preload.

Supressed plasma renin in patients with primary hypertension is thought to be an indirect marker of sodium-induced volume expansion which is associated with more severe hypertension and hypertension-mediated organ damage. A novel test for erythrocyte glycocalyx sensitivity to sodium (eGCSS) has been proposed as a direct measure of sodium-induced damage on erythrocyte surfaces and a marker of sensitivity of the endothelium to salt in humans. Here we explore if eGCSS relates to plasma renin and other clinical and biochemical characteristics in a cohort of patients with primary hypertension. Hypertensive subjects (n = 85, 54% male) were characterised by blood biochemistry (including plasma renin/aldosterone), urine analysis for albumin-creatinine ratio (ACR), 24-h urine sodium/potassium excretion. eGCSS was measured using a commercially available kit. Correlations between eGCSS and clinical and biochemical characteristics were explored using Spearman’s correlation coefficient and characteristics compared across tertiles of eGCSS. eGCSS was inversely correlated with renin (p p = 0.012). eGCSS was positively correlated with ACR (p p

Aim: Different to inhibitory drugs of the renin-angiotensin-aldosterone system (RAAS), diuretics are known to decrease blood pressure (BP) and stimulate renin release by the kidneys. Despite plasma aldosterone (PA) level is mostly regulated by the RAAS activity, serum potassium has been shown to be an important factor in animal models and humans. Here we perform a systematic review and meta-analysis of randomized-controlled trials investigating the effects of diuretic therapy on PA and its correlation with change in potassium and BP. Methods: Three databases were searched: MEDLINE, EMBASE and The Cochrane Central Register of Controlled Trials (CENTRAL). Titles were firstly screened by title and abstract for relevancy before full-text articles were assessed for eligibility according to a pre-defined inclusion/exclusion criteria. Results: A total of 1139 articles were retrieved of which 45 met the pre-specified inclusion/exclusion criteria. The average standardised difference in mean PA change was similar for all classes of diuretic (mean, 95% CI); thiazide/thiazide-like 0.304 (0.169, 0.440), loop 0.927 (0.37, 1.49), MRA/potassium-sparing 0.264 (0.174, 0.355) and combination 0.466 (0.142, 0.789), Q = 6.475, P = 0.091. In subjects previously untreated with another antihypertensive, there was a significant relationship between PA change and change in systolic BP but no relationship with the change in potassium. Conclusion: In RCTs of diuretic therapy in hypertension, there is an increase in PA with all classes of diuretic and no between-class heterogeneity. Change in PA is not related with potassium but correlates to the change in BP in subjects previously untreated with another antihypertensive medication.

Purpose Heat stress exacerbates post-exercise hypotension (PEH) and cardiovascular disturbances from elevated body temperature may contribute to exertion-related incapacity. Mast cell degranulation and muscle mass are possible modifiers, though these hypotheses lack practical evidence. This study had three aims: (1) to characterise pre–post-responses in histamine and mast cell tryptase (MCT), (2) to investigate relationships between whole body muscle mass (WBMM) and changes in blood pressure post-marathon, (3) to identify any differences in incapacitated runners. Methods 24 recreational runners were recruited and successfully completed the 2019 Brighton Marathon (COMPLETION). WBMM was measured at baseline. A further eight participants were recruited from incapacitated runners (COLLAPSE). Histamine, MCT, blood pressure, heart rate, body temperature and echocardiographic measures were taken before and after exercise (COMPLETION) and upon incapacitation (COLLAPSE). Results In completion, MCT increased by nearly 50% from baseline (p = 0.0049), whereas histamine and body temperature did not vary (p > 0.946). Systolic (SBP), diastolic (DBP) and mean (MAP) arterial blood pressures and systemic vascular resistance (SVR) declined (p $$\Delta $$ Δ SBP (r = − 0.43, p = 0.046). For collapse versus completion, there were significant elevations in MCT (1.77 ± 0.25 μg/L vs 1.18 ± 0.43 μg/L, p = 0.001) and body temperature (39.8 ± 1.3 °C vs 36.2 ± 0.8 °C, p p = 0.107) and significantly lower MAP, DBP and SVR (p Conclusion These data support the hypothesis that mast cell degranulation is a vasodilatory mechanism underlying PEH and exercise associated collapse. The magnitude of PEH is inversely proportional to the muscle mass and enhanced by concomitant body heating.

Heat stress exacerbates post-exercise hypotension (PEH) and cardiovascular disturbances from elevated body temperature may contribute to exertion-related incapacity. Mast cell degranulation and muscle mass are possible modifiers, though these hypotheses lack practical evidence. This study had three aims: (1) to characterise pre-post-responses in histamine and mast cell tryptase (MCT), (2) to investigate relationships between whole body muscle mass (WBMM) and changes in blood pressure post-marathon, (3) to identify any differences in incapacitated runners.24 recreational runners were recruited and successfully completed the 2019 Brighton Marathon (COMPLETION). WBMM was measured at baseline. A further eight participants were recruited from incapacitated runners (COLLAPSE). Histamine, MCT, blood pressure, heart rate, body temperature and echocardiographic measures were taken before and after exercise (COMPLETION) and upon incapacitation (COLLAPSE).In completion, MCT increased by nearly 50% from baseline (p = 0.0049), whereas histamine and body temperature did not vary (p 0.946). Systolic (SBP), diastolic (DBP) and mean (MAP) arterial blood pressures and systemic vascular resistance (SVR) declined (p 0.019). WBMM negatively correlated with Δ SBP (r = - 0.43, p = 0.046). For collapse versus completion, there were significant elevations in MCT (1.77 ± 0.25 μg/L vs 1.18 ± 0.43 μg/L, p = 0.001) and body temperature (39.8 ± 1.3 °C vs 36.2 ± 0.8 °C, p 0.0001) with a non-significant rise in histamine (9.6 ± 17.9 μg/L vs 13.7 ± 33.9 μg/L, p = 0.107) and significantly lower MAP, DBP and SVR (p 0.033).These data support the hypothesis that mast cell degranulation is a vasodilatory mechanism underlying PEH and exercise associated collapse. The magnitude of PEH is inversely proportional to the muscle mass and enhanced by concomitant body heating.

AIMS Plasma renin activity (PRA) is regarded as a marker of sodium and fluid homeostasis in patients with primary hypertension. Whether effects of diuretics on PRA differ according to class of diuretic, whether diuretics lead to a sustained increase in PRA, and whether changes in PRA relate to those in blood pressure (BP) is unknown. We performed a systematic review and meta-analysis of trials investigating the antihypertensive effects of diuretic therapy in which PRA and/or other biomarkers of fluid homeostasis were measured before and after treatment. METHODS Three databases were searched: MEDLINE, EMBASE and The Cochrane Central Register of Controlled Trials. Titles were firstly screened by title and abstract for relevancy before full-text articles were assessed for eligibility according to a predefined inclusion/exclusion criteria. RESULTS A total of 1684 articles were retrieved of which 61 met the prespecified inclusion/exclusion criteria. PRA was measured in 30/61 studies. Diuretics led to a sustained increase in PRA which was similar for different classes of diuretic (standardised mean difference [95% confidence interval] 0.481 [0.362, 0.601], 0.729 [0.181, 1.28], 0.541 [0.253, 0.830] and 0.548 [0.159, 0.937] for thiazide, loop, mineralocorticoid receptor antagonists/potassium-sparing and combination diuretics respectively, Q = 0.897, P = .826), and did not relate to the average decrease in blood pressure. CONCLUSION In antihypertensive drug trials, diuretics lead to a sustained increase in average PRA, which is similar across different classes of diuretic and unrelated to the average reduction in blood pressure.

Background: Effects of afterload and blood pressure (BP) on pulse wave velocity (PWV) have been investigated using vasoactive drugs but effects of cardiac pre-load have not previously been studied. Methods: Transient mechanical reduction of cardiac pre-load (lower limb venous occlusion, LVO) and expansion of cardiac pre-load (intravenous infusion of 2 litres of saline solution, SST) were performed in patients with hypertension. BP, carotid-femoral PWV (Sphygmocor, AtCor Medical, Asutralia), cardiac stroke volume (SV) and total peripheral resistance (TPR) derived by transthoracic echocardiography were recorded during LVO and SST. Peak flow velocity in superior vena cava (SVCx) was used to asses change in pre-load. Results: 35 subjects were studied. SVCx decreased during LVO (n = 20) by mean (95% confidence-intervals) 7.6 (2.8–11.6) cm/s and increased during SST (n = 15) by 7.1 (−0.3–14.6) cm/s. LVO produced a small but significant reduction in mean arterial BP (MAP) of 1.5 (0.0–3.1) mmHg and SV of 6.7 (2.2–11.3) mL; while TPR and PWV increased by 236.9 (51.7–422.1) dynes-sec/cm5 and 0.7 (0.3–1.1) m/s respectively. SST produced a decrease of MAP of 4.3 (0.4–8.0) mmHg while SV increased by 4.8 (0.7–9.1) mL. TPR and PWV were reduced by 255.7 (15.4–490.5) dynes-sec/cm5 and 0.7 (0.1–1.0) m/s, respectively. All p < 0.05. Conclusion: Modulation of cardiac pre-load affect PWV beyond the effects on afterload and BP. The reciprocal changes of BP, PWV, SV and TPR could be explained by a role of the autonomic nervous system in the regulation of vascular tone in response to change of pre-load.

Background Effects of short‐term interventions on large‐artery stiffness assessed by pulse wave velocity ( PWV ) have mainly been explained by concomitant changes in blood pressure ( BP ). However, lower body negative pressure, which increases sympathetic activity and has other hemodynamic effects, has a specific effect on PWV in healthy volunteers. Methods and Results We examined effects of lower‐limb venous occlusion ( LVO ), a similar intervention to lower‐body negative pressure that reduces BP but increases sympathetic activity and device‐guided breathing ( DGB ), which reduces both BP and sympathetic activity, on PWV in patients with essential hypertension (n=70 after LVO , n=45 after DGB and LVO in random order). The short‐acting calcium channel antagonist nifedipine was used as a control for changes in BP . LVO produced a small but significant reduction in mean arterial pressure of 1.8 (95% CI 0.3–3.4) mm Hg. Despite this, aortic and carotid‐femoral PWV increased during LVO by 0.8 (0.2–1.4) m/s and 0.7 (0.3–1.05) m/s, respectively. DGB reduced PWV by 1.2 (0.9–1.4) m/s, to a greater extent than did nifedipine 10 mg (reduction of 0.7 [0.1–1.3] m/s, P DGB ). This occurred despite a greater decrease in BP with nifedipine compared with DGB . Conclusions Arterial stiffness can be modulated independently of BP over the short term. The mechanism could involve alterations in sympathetic activity or other as yet uncharacterized effects of LVO and DGB .

Obstructive Sleep Apnoea (OSA) is a breathing disorder characterized by narrowing of the upper airway that impairs normal ventilation during sleep. OSA is a highly prevalent condition which is associated with several Cardiovascular (CV) risk factors and CV diseases. Despite this clear association, Randomized Controlled Trials (RCTs) have provided equivocal data that treatment of sleep apnoea can improve CV outcomes regardless of its ability to reduce blood pressure. Here, we critically review the evidence that supports role of OSA as a risk factor for increased arterial stiffness which represents an early manifestation of vascular damage often preceding major CV events. Additionally, we examined evidence from interventional RCTs to assess if treatment of OSA by continuous positive airway pressure can affect arterial stiffness measured as carotid-femoral pulse wave velocity. Overall, a large body of evidence supports the role of OSA as a risk factor for increased arterial stiffness and several pathophysiological mechanisms, including activation of the autonomic nervous system, may help to explain the link between breathing disorders and vascular alterations (here mainly examined as functional properties). Whether the causal relationship between OSA and vascular damage exists or is mostly explained by confounders and whether OSA treatment can improve vascular stiffening is still debated.

Objective: Blood pressure (BP) can be divided into steady state (mean arterial pressure, MAP) and pulsatile (pulse pressure, PP) components that are differentially associated with target organ damage and cardiovascular events. Here, we tested the effects of non-pharmacological interventions that reduce sympathetic activity (SA) and cardiac pre-load on MAP and PP. Material and Methods: Pulse-wave analysis of the radial artery (SphygmoCor, AtCor Medical, Sydney, Australia), calibrated from 3 consecutive readings of brachial BP, was used for the evaluation of central PP and MAP. Measurements were obtained before and after supervised device-guided paced breathing (DGB), and bilateral lower limb venous occlusion (LVO, performed non-invasively using thigh cuffs), in random order. DGB reduces SA whereas LVO produces an acute reduction in pre-load. High resolution heart rate variability (HRV) as log-ratio of low-frequency/high-frequency range (LF/HF),( Schiller Medilog AR12plus, United States) was used to assess the effects of DGB on SA, while reduction of pre-load was evaluated by inferior vena cava diameter (IVCd) measured with cardiac ultrasound. Results: Thirty six HT patients (16 female) age (mean±SD) 46±12 years, BP 144.8±17.7/88.2±10.3 mmHg were studied. DGB decreased log LF/HF from 0.306±0.27 to 0.171±0.3 and LVO decreased IVCd from 15.16±3.96 mm to 12.39±3.43mm. Reduction of brachial BP was greater during DGB compared to LVO: (mean (95% confidence interval)):-9.7(-11.6,-7.8) mmHg vs -3.8(-5.8,-1.7) mmHg for systolic BP and -4.1(-5.6,-2.5) mmHg vs 1.1(-0.1, 2.2) mmHg for diastolic BP, respectively ( P . Effects of DGB and LVO were similar on PP: -3.5(-4.8,-2.3) mmHg for DBG and -3.1(-5.5,-0.7) mmHg for LVO, P>0.1. MAP reduction was significant only during DBG (-6.4 (-8.1,-4.7) mmHg) compared to LVO (-1.2 (-2.7, 0.1) mmHg, P between the interventions. Conclusion: Reducing sympathetic activity via DGB decreases both steady state and pulsatile components of BP whereas pre-load reduction selectively decreases PP. Depending on individual BP components, interventions targeting sympathetic activity and/or pre-load might be used to personalized treatment.

Objective: Mental stress is detrimental to cardiovascular health, being a risk factor for coronary heart disease and a trigger for cardiac events. However, it is not currently routinely assessed. The aim of this study was to identify features of the photoplethysmogram (PPG) pulse wave which are indicative of mental stress. Approach: A numerical model of pulse wave propagation was used to simulate blood pressure signals, from which simulated PPG pulse waves were estimated using a transfer function. Pulse waves were simulated at six levels of stress by changing the model input parameters both simultaneously and individually, in accordance with haemodynamic changes associated with stress. Thirty-two feature measurements were extracted from pulse waves at three measurement sites: the brachial, radial and temporal arteries. Features which changed significantly with stress were identified using the Mann–Kendall monotonic trend test. Main results: Seventeen features exhibited significant trends with stress in measurements from at least one site. Three features showed significant trends at all three sites: the time from pulse onset to peak, the time from the dicrotic notch to pulse end, and the pulse rate. More features showed significant trends at the radial artery (15) than the brachial (8) or temporal (7) arteries. Most features were influenced by multiple input parameters. Significance: The features identified in this study could be used to monitor stress in healthcare and consumer devices. Measurements at the radial artery may provide superior performance than the brachial or temporal arteries. In vivo studies are required to confirm these observations.

Objective:Arterial stiffness (AS) measured as carotid-femoral pulse wave velocity (cfPWV) is an important determinant of cardiovascular risk closely related to brachial blood pressure (BP). Whether it can be changed independently of BP in the short term is uncertain but recent observations suggest t

Europe’s population is becoming increasingly ethnically diverse, and epidemiological studies indicate that there are remarkable differences in cardio-metabolic risk factors between ethnic groups living in the same area. Variations observed in the distribution of cardiovascular risk factors in these communities may therefore help explain—at least in part—the different burdens on cardiovascular diseases. So far, the underlying pathophysiology leading to ethnic variations in the prevalence of cardio-metabolic risk factors is still poorly understood but it is likely to represent the complex interactions from several innate and environmental factors. Tailored prevention and treatment strategies should therefore be implemented in those “high-risk populations,” but data derived from randomized clinical trials are still limited. This article will provide an overview on the role of ethnicity on cardio-metabolic risk factors and cardiovascular diseases, focusing on type 2 diabetes and dyslipidemia based mainly on Dutch and British data.

Objective: To test if arterial stiffness (AS) can be modulated by the autonomic nervous system (ANS) independently of blood pressure (BP) in hypertensive patients. Material and methods: AS was measured by carotid-femoral pulse wave velocity (cfPWV) using the SphygmoCor device (AtCor Medical, Australia). Mean arterial pressure (MAP) was obtained by pulse-wave analysis of the radial artery and ANS activity was estimated by heart rate variability (HRV) as log-ratio of low-frequency/high-frequency heart rate components (Schiller Medilog AR12plus, United States) in hypertensive subjects (n = 43, 17 female, mean ± SD age 45 ± 13 years, brachial BP 145 ± 17/87 ± 10 mmHg) at rest. All measurements were subsequently repeated during supervised device-guided paced breathing (DGB) and reduction of cardiac pre-load by lower limb venous occlusion (LVO). These interventions, which are known to decrease and increase sympathetic activity, were performed in random order. Results: DGB reduced HRV by 0.14 [0.07, 0.20] (Mean [95% confidence intervals]) and LVO increased HRV by 0.13 [0.08, 0.18] (both P