Why are there ethnic differences in cardio-metabolic risk factors and cardiovascular diseases?

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

Ventricular and vascular stiffening in aging and hypertension

The assessment of arterial stiffness, a common feature of aging, exacerbated by pathological conditions like hypertension, has become an attractive tool for identifying structural and functional changes of the arteries even in an early stage of the atherosclerotic disease. Arterial stiffness has been recognized as an important physio-pathological determinant for the age-related rise in systolic blood pressure, demonstrating also an independent predictive value for cardiovascular events. In the recent decades, many techniques and indices to evaluate vascular stiffness have been developed and extensive data concerning their prognostic value have been collected. Moreover, it has become clear that vessel and heart must be considered as a unique system, in which combined stiffness of vessel and heart interacts to limit cardiovascular performance. In this review, main methods and indices used to estimate arterial and ventricular stiffness are presented, focusing on their alteration in physiological aging and arterial hypertension. Furthermore, the concept of ventricular-arterial coupling is explained in order to give an insight to the interplay between arterial and ventricular stiffness in aging and hypertension

5B.03:ARTERIAL-VENTRICULAR COUPLING AND PARAMETERS OF VASCULAR STIFFNESS IN HYPERTENSIVE PATIENTS: ROLE OF GENDER

The present study was designed to investigate the relationship between left ventricular elastance (ELV), arterial elastance (EA), parameters of vascular stiffness and the influence of gender in a population of hypertensive individuals at high cardiovascular (CV) risk

Post-exertional increase in first-phase ejection fraction in recreational marathon runners

Objectives Running a marathon has been equivocally associated with acute changes in cardiac performance. First-phase ejection fraction is a novel integrated echocardiographic measure of left ventricular contractility and systo-diastolic coupling which has never been studied in the context of physical activity. The aim of this study was to assess first-phase ejection fraction following recreational marathon running along with standard echocardiographic indices of systolic and diastolic function. Design and participants: Runners (n = 25, 17 males), age (mean ± standard deviation) 39 ± 9 years, were assessed before and immediately after a marathon race which was completed in 4 h, 10 min ± 47 min. Main outcome measures Central hemodynamics were estimated with applanation tonometry; cardiac performance was assessed using standard M-mode two-dimensional Doppler, tissue-doppler imaging and speckle-tracking echocardiography. First-phase ejection fraction was calculated as the percentage change in left ventricular volume from end-diastole to the time of peak aortic blood flow. Results Conventional indices of systolic function and cardiac performance were similar pre- and post-race while aortic systolic blood pressure decreased by 9 ± 8 mmHg (P < 0.001) and first-phase ejection fraction increased by approximately 48% from 16.3 ± 3.9% to 22.9 ± 2.5% (P < 0.001). The ratio of left ventricular transmitral Doppler early velocity (E) to tissue-doppler imaging early annular velocity (e′) increased from 5.1 ± 1.8 to 6.2 ± 1.3 (P < 0.01). Conclusion In recreational marathon runners, there is a marked increase in first-phase ejection fraction after the race despite no other significant change in cardiac performance or conventional measure of systolic function. More detailed physiological studies are required to elucidate the mechanism of this increase

Lessons Learned in Vineyard Monitoring and Protection from a Ground Autonomous Vehicle

Vineyard protection is a key task for winegrowers to maximize crop yield. Control of plagues, fungi and other threats are recurrent tasks in winery. This project is focused on the improvement of plague control tasks, specifically on the distribution and placement of pheromone dispensers for matting disruption, currently a labour-intensive and time consuming task. The operators walk through the vineyard hanging the dispensers in a regular distribution pattern. Grape project aims to automate the dispenser distribution in the vineyard using an outdoor autonomous ground platform with a robotic arm. Furthermore our platform is used to monitor the vineyard status and retrieve this information to the producer in order to to provide timely and precise information from the field

Diagnosis and management of primary hyperaldosteronism in patients with hypertension: a practical approach endorsed by the British and Irish Hypertension Society.

Alongside the lack of homogeneity among international guidelines and consensus documents on primary hyperaldosteronism, the National UK guidelines on hypertension do not provide extensive recommendations regarding the diagnosis and management of this condition. Local guidelines vary from area to area, and this is reflected in the current clinical practice in the UK. In an attempt to provide support to the clinicians involved in the screening of subjects with hypertension and clinical management of suspected cases of primary hyperaldosteronism the following document has been prepared on the behalf of the BIHS Guidelines and Information Service Standing Committee. Through remote video conferences, the authors of this document reviewed an initial draft which was then circulated among the BIHS Executive members for feedback. A survey among members of the BIHS was carried out in 2022 to assess screening strategies and clinical management of primary hyperaldosteronism in the different regions of the UK. Feedback and results of the survey were then discussed and incorporated in the final document which was approved by the panel after consensus was achieved considering critical review of existing literature and expert opinions. Grading of recommendations was not performed in light of the limited available data from properly designed randomized controlled trials

Does Treatment for Obstructive Sleep Apnoea Improve Arterial Stiffness? Evidence from Randomized Clinical Trials on Carotid-femoral Pulse Wave Velocity

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. (C) 2020 Association for Research into Arterial Structure and Physiology. Publishing services by Atlantis Press International B.V

Post-exertional hypotension and collapse in marathon runners; the role of muscle mass, histamine and mast cell tryptase

Introduction Post-exertional hypotension is the sustained reduction in arterial blood pressure (BP) following exercise which, if severe enough, can lead to syncope and exercise-induced collapse particularly following the cessation of exercise. Elevations in skeletal muscle blood flow, coupled with an inactive muscle pump lead to marked reductions in venous return which is exacerbated in hot environments. Exercise also generates a sustained post-exertional vasodilation within the vascular beds of previously active skeletal muscle driven through activation of histamine receptors. Previous studies have demonstrated that the use of histamine receptor antagonists blocks 80% of post-exercise vasodilation. Several possible mechanisms may increase intramuscular histamine during recovery from exercise. Mast cells located within the connective tissue layer surrounding skeletal muscle fascicles or near blood vessels may degranulate, releasing histamine locally in response to exercise related factors. Histamine can also be formed de novo without storage in mast cells through histidine decarboxylase. Previous studies have found no change in circulating plasma histamine concentrations however. Method Twenty-four runners were recruited as controls prior to completing a standard marathon. A resting transthoracic echocardiogram (TTE) was performed at baseline and immediately following completion of the marathon in conjunction with bioelectrical impedance, blood pressure (BP), heart rate (HR), plasma histamine and mast cell tryptase levels. Eight runners who collapsed during, or following, the marathon were recruited with blood pressure, heart rate, plasma mast cell tryptase and plasma histamine measured as soon as possible following collapse. Results Control participants (n=24) had a significantly increased plasma mast cell tryptase (pre; 806±386ng/L, post; 1179±422ng/L, p=0.012) post marathon in comparison to baseline with a significantly decreased IVCd (p=0.0004), stroke volume (p <0.0001), body mass (p <0.0001), fat mass (p=0.006), muscle mass (p=0.044) and mean arterial pressure (MAP) (p=0.0052). Control participants’ systolic BP (r= -0.440, p=0.046), diastolic BP (r= -0.60, p=0.0043) and MAP (r=-0.60, p=0.0039) were all significantly negatively correlated with their muscle mass post marathon. In comparing collapse and control participants, collapsed participants had a significantly higher histamine (9.6±16.6μg/L) compared to control pre-marathon measures (0.45± μg/L, p=0.016). Compared to control post-marathon measures the collapsed groups had a significantly lower MAP (collapse; 68.2±7.7mmHg, control 76.64±7.92, p=0.031) and a significantly higher mast cell tryptase (collapse; 1769±244ng/L, control; 1179±422ng/L, p=0.001). Conclusion These data confirm that following a marathon there is a significant rise in plasma mast cell tryptase. The degree of post exertional hypotension is significantly correlated with participants muscle mass. Collapsed participants, whom have a significantly lower MAP than post-marathon controls, have a significantly higher mast cell tryptase. These findings support the hypothesis that skeletal muscle vasodilation by histamine release, probably through mast cell degranulation, is contributory to post-exertional hypotension