1,721,027 research outputs found
The aerobic exercise training in hypertension: A matter of baking ingredients
No full textExercise training is worldwide considered pivotal for maintaining and restoring general population health. Its potential beneficial effects touch several domains: metabolic, haemodynamic, psychological, and social. The European guidelines for hypertension recom- mend physical activity among the nonpharmacological interventions to manage ‘all patients with hypertension’, and the harder effort is advocated in order to fight against sedentary living. In the domain of the exercise training, there are nonetheless many features to be consid- ered. Indeed, haemodynamic modifications linked to exer- cise strictly depend on the type and the duration of the effort as well as the background of the individual who is going to be trained (i.e. age, sex, hypertensive or not, previously trained, or sedentary ...). In literature, since several years, many attempts have been made to investigate the haemodynamic response to different exercise-training programs, with not always coherent conclusions. In 1987, Douglas et al. reported on the effect of prolonged and high-intensity exercise (triathlon) on left ventricular func- tion and found that immediately after the competition, the athletes presented reduced fractional shortening, driven by altered contractility and preload. These alterations recov- ered 1 day after the exercise, suggesting cardiac ‘fatigue.’ Similarly, 20 years later, Aslani et al. demonstrated that the Ranger training program (consisting in 8 weeks of exhaustive exercise) was associated with impaired left ventricular function. As such, from the available data, it appears that high-intensity exercise is acutely and chroni- cally associated with impaired haemodynamics. In addition, even aerobic exercise, when extremely vigorous like the marathon, is chronically associated with increased arterial stiffness
Arterial pulsatility: The undisclosed driver of microvascular impairment?
No full textThe relationship between chronic kidney disease (CKD) and hypertension has been widely investi- gated, however it is not well established whether
hypertension precedes microvascular kidney impairment or vice versa. One insight on this issue comes from a study by Woodard et al. [1], in which the authors found that increased arterial stiffness would increase the transmission of the pulsatile energy into the kidney microcirculation, contributing to the loss of the kidney function. On
The Association Between Orthostatic Symptoms and Orthostatic Hypotension: Does it Really Matter?
No full textOrthostatic hypotension (OH) is a clinical condition arbi- trarily defined by consensus as a fall in systolic/diastolic blood pressures (BPs) of 20/10 mmHg passing from the supine to the upright position during the first 3 minutes. The observation of a BP drop during standing is a frequent condition, mainly in elderly people, associated with different pathophysiological mechanisms and with potential prog- nostic value in several population settings. There are not univocal data from the literature about the prognostic role of OH, mainly concerning cardiovascular risk. Some studies found a significant association between OH and the risk of fall, syncope, mortality and cardiovascular disease, or risk of dementia, but this association is not always confirmed. In general, there is some agreement about the fact that OH could be more a marker of frailty and underling disease leading to increased mortality or cardiovascular risk than a causal condition. The association between symptoms and OH has been investigated in literature. A study systematically testing for OH found that most of the patients presenting OH are asymptomatic. Indeed, even the presence of asymptomatic OH has been shown to be independently associated with mortality and cardiovascular disease, but again, this seems linked to the presence of underlying disease
Non-invasive estimation of aortic blood pressures: A close look at current devices and methods
No full textWhile for years clinicians have used cuff pressure to assess patients’ cardiovascular risk, recent evidences has shown that aortic pressure, or more specifically aortic systolic and aortic pulse pressures, have a better prognostic value to predict cardiovascular events and mortality. This led to the emergence of multiple methods and devices to assess aortic pressure non-invasively. Some use scaled waveforms measured at the carotid level with tonometry, or ultrasounds. Others use transfer function or mathematical modelling from radial or brachial traces acquired from volume plethsymography or applanation tonometry. Not all these techniques are equivalent and most of them have the major flaw of using brachial cuff pressure to scale their results. The purpose of this review is to present the strengths and weaknesses of techniques and various commercial devices to estimate aortic systolic pressure
The Impact of Uric Acid and Hyperuricemia on Cardiovascular and Renal Systems.
No full textThe description of gout dates back almost 5000 years, and scientific interest in uric acid increased when it was found to be involved in the pathogenesis of gout. Since then, many basic and clinical studies have assessed the implications of uric acid for the oxidative system, inflammation, and cardiovascular and renal outcomes. Uric acid-lowering therapy failed to improve clinical hard outcomes in asymptomatic hyperuricemia, and it is retained in symptomatic hyperuricemia. Dietary and lifestyle modifications are critical to manage hyperuricemia. More studies are warranted to investigate the role of uric acid-lowering drugs on cardiovascular outcomes
Advances in pharmacotherapies for hyperuricemia
No full textIntroduction: Hyperuricemia is an overlooked cardiovascular and renal risk factor. Epidemiological and genetic studies have shown an independent role of uric acid in the risk of coronary artery disease, heart failure, chronic kidney disease, and cardiovascular mortality. Treatment options include xanthine oxidase inhibitors, uricosuric medications, and the recombinant uricases. Whether to treat asymptomatic hyperuricemia, and to which target, remains debated. However, the results of recent trials and meta-analysis seem to support this therapeutic strategy. Areas covered: In the present review, we summarized current therapeutic indications and options for the treatment of symptomatic and asymptomatic hyperuricemia. Furthermore, we searched the recent literature (last 5 years: 2018 to 2022) to report the results of randomized controlled trials and meta-analysis on cardiovascular and nephroprotective effects of hypouricemic agents. Expert opinion: Future large well-designed clinical trials on the role of hypouricemic agents in nephroprotection and cardiovascular prevention and treatment are warranted and may extend their indications and use, with a direct impact on morbidity and mortality. Differentiating between hyperproducing and hypoexcreting phenotypes may help designing future trials improving the consistency of results. Finally, medications with cardio and nephroprotective properties have shown to reduce serum uric acid levels and may be used in patients with hyperuricemia and other cardiovascular complications
Efficacia clinica dei bloccanti dei recettori dell'angiotensina II: il ruolo dell'irbesartan.
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Visit-to-visit variability: Prognostic significance?
No full textHypertension is the most prevalent treatable risk factor for stroke. Treatment of hypertension is based on usual blood pressure, which is evaluated by repeated measurement. When only few measurements show high blood pressure, this is considered as a background noise generally due to white coat effect. Rothwell et al. challenged this notion and presented data from post-hoc analyses of three randomized trials and one meta-analysis, where 3 parameters are strongly associated with the risk of stroke: visit-to-visit variability of systolic blood pressure, increased residual variability in treated patients, and episodic hypertension. These findings are not proof of a causal link between variability and vascular risk. However, a new window has been opened in clinical practice, giving new implications in the choice of treatment, and, for next trials, highlighting the importance of including variability and patients with episodic hypertension. © 2012 Elsevier Masson SAS
Hypertension and Dyslipidemia Combined Therapeutic Approaches
Full text linkTreating blood pressure (BP) alone may provide only limited benefits while it is recommendable to manage the total cardiovascular risk. To date, several studies have shown that concomitant treatment of hypertension and dyslipidemia with non-pharmacological approaches and/or metabolically neutral antihypertensive drugs and statins produce a significantly greater reduction of the risk of developing cardiovascular disease. Thus, in this review article, we summarize the available evidence regarding non-pharmacological and pharmacological approaches with a favourable effect on both BP and lipids
Effects of Antihypertensive Drugs on Central Blood Pressure in Humans: A Preliminary Observation
No full textBACKGROUND: Central blood pressure (BP) is considered a better predictor of cardiovascular events than brachial BP. Modifications of central, beyond brachial BP, can be assessed by pressure amplification, a potential new cardiovascular risk factor. Comparison between drugs' effect on central hemodynamics has been poorly studied. Our aim was to assess the hemodynamic effect of a 12-week treatment with amlodipine 5mg, or candesartan 8mg, or indapamide sustained-release 1.5mg, in comparison with placebo.
METHODS: We analyzed 145 out-patients with essential hypertension in primary prevention enrolled in the Natrilix SR Versus Candesartan and Amlodipine in the Reduction of Systolic Blood Pressure in Hypertensive Patients (X-CELLENT) study, a multicenter, randomized, double-blinded, placebo-controlled trial. Arterial stiffness, central BP, pressure amplification, and wave reflection were measured by applanation tonometry.
RESULTS: Baseline characteristics of patients were homogeneous between groups. After treatment, we found that active drugs produced similar reduction of both central and peripheral BPs, with no significant interdrug differences (all P < 0.05; excluded peripheral pulse pressure, compared with placebo). Second, amlodipine (1.9% ± 15.3%), candesartan (3.0% ± 14.6%) and indapamide (4.1% ± 14.4%) all increased pulse pressure amplification, but only indapamide was statistically different from placebo (P = 0.02). Finally, no significant changes were observed on pulse wave velocity, heart rate, and augmentation index.
CONCLUSIONS: The 3 antihypertensive drugs similarly reduced peripheral and central BP, as compared with placebo, but a significant increase in pulse pressure amplification was obtained only with indapamide, independently of arterial stiffness modifications
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