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1.
Obes Surg ; 2020 Mar 04.
Artículo en Inglés | MEDLINE | ID: mdl-32133587

RESUMEN

INTRODUCTION: Postprandial hypoglycemia (PPHG) is a well-known complication after bariatric surgery (BS). However, it is not known whether PPHG affects weight loss after BS. AIMS: To assess the impact of PPHG on weight loss after BS in subjects without and with type 2 diabetes mellitus (T2D). METHODS: Data from 338 subjects who had undergone gastric bypass (RYGB) or sleeve gastrectomy (LSG) and were followed up for at least 2 years were analyzed. At each follow-up visit, the patient's anthropometric and biochemical characteristics were recorded and the Edinburgh Questionnaire was performed to evaluate the presence of PPHG symptoms. RESULTS: Before surgery: younger age and lower BMI predicted PPHG after BS (p = 0.02 and p = 0.0008, respectively). Also, the baseline OGTT indicated that subjects who developed PPHG had an earlier glucose peak and more often had low glucose levels at 2 h compared with the no-PPHG group (p = 0.03 and p = 0.004, respectively). After surgery: Mild-to-moderate PPHG occurred equally after RYGB and LSG (38% vs 25%, p = ns when accounting for confounders), and in T2D who achieved remission and those who did not (29.5% vs 28.6%, ns). At the 2-year follow-up, occurrence of PPHG was independently associated with smaller weight loss (p = 0.0006). CONCLUSIONS: Mild-to-moderate PPHG is a frequent complication after bariatric surgery and results in smaller weight loss after 2 years. Age, baseline BMI, and an earlier glucose peak during OGTT predict PPHG after bariatric surgery.

2.
Artículo en Inglés | MEDLINE | ID: mdl-32157642

RESUMEN

Renal denervation is a device-based procedure for hypertension for which safety and efficacy has been demonstrated. At present, its clinical use is still matter of debate, despite the most recent clinical trials have shown promising results with new-generation devices in various hypertensive populations. This position paper was deemed necessary by the Italian Society of Arterial Hypertension, in order to provide indications about the applications of renal denervation in the clinical setting. A state-of-the art review of the literature, focusing on safety and efficacy data, is provided. Furthermore, based on current evidence and expert consensus, clinical profiles of possible candidates for renal denervation are proposed. The selection process should take into account not only blood pressure values, global cardiovascular risk profile, but also drug adherence and tolerability and patient preferences. This position paper also defines minimum requirements for renal denervation selection centers and a flowchart for the difficult-to-treat hypertensive patient. Further studies are needed to support these preliminary indications, which are based on expert-consensus only.

3.
Obesity (Silver Spring) ; 28(3): 609-615, 2020 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-32020775

RESUMEN

OBJECTIVE: Interleukin (IL)-1ß is involved in obesity-associated inflammation and in the pathogenesis of type 2 diabetes (T2D) mellitus. Our aim was to correlate serum IL-1ß and caspase-1 levels with weight loss, glucose metabolism, and insulin resistance (IR) after bariatric surgery. METHODS: A total of 32 patients with morbid obesity and T2D (Ob-T2D) and 29 patients with morbid obesity and normal glucose tolerance (Ob-NGT), treated by Roux-en-Y gastric bypass, were studied before and 1 year after surgery. Sixteen healthy individuals served as a control (HC) group. IR was assessed by the oral glucose insulin sensitivity method. Plasma IL-1ß levels and caspase-1 were measured. RESULTS: Presurgery BMI was similar in Ob-NGT and Ob-T2D. IR was progressively impaired in Ob-NGT and Ob-T2D (P < 0.0001). Fasting plasma IL-1ß and caspase-1 levels were lower in HCs than in patients with Ob-NGT or Ob-T2D (P < 0.02; P = 0.05), and both were inversely correlated with IR (P = 0.01; P = 0.02). After surgery, BMI decreased and IR improved to a similar extent in Ob-NGT and Ob-T2D (P < 0.0001). Plasma caspase-1 concentrations normalized in both groups (P < 0.0001), whereas plasma IL-1ß levels normalized only in Ob-NGT. CONCLUSIONS: Plasma IL-1ß and caspase-1 levels were inversely correlated with IR. Caspase-1 levels normalized after weight loss, whereas IL-1ß normalized only in people without T2D, suggesting the persistence of a systemic inflammatory condition in people with T2D.

4.
Heart Fail Rev ; 25(1): 31-42, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31512149

RESUMEN

The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in the regulation of blood pressure and volume homeostasis, promoting critical structural changes in every component of the cardiovascular system, including the heart and blood vessels. Consequently, the RAAS is a crucial therapeutic target for several chronic diseases of the cardiovascular system, spanning from arterial hypertension (AH) to heart failure (HF). AH represents a leading risk factor for the development of symptomatic HF, particularly with left ventricle (LV) preserved ejection fraction (HFpEF). LV diastolic dysfunction and cardiac remodelling are the first discernible manifestations of heart disease in patients with AH. Typically, AH develops many years before the diagnosis of overt HF, providing a therapeutic target for preventive strategies. Treatment of AH is based on different classes of antihypertensive drugs, which show differences in their capacity to prevent the evolution towards HF. The blockers of the RAAS are effective drugs to treat AH and prevent HF with reduced ejection fraction (HFrEF), but the evidence of the potential benefits in patients with HFpEF remains limited. In this review, the authors summarise data from several clinical trials of HFpEF and HFrEF, focusing on the mechanisms leading the transition from AH to HF and late complications.

5.
Cardiovasc Res ; 116(2): 429-437, 2020 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-31220219

RESUMEN

AIMS: The relationship between resistance artery remodelling and endothelial function remains unknown. In this study, we assessed (i) the capacity of endothelial function and nitric oxide (NO) availability to provide more information on the severity of resistance artery remodelling than common cardiovascular risk factors in subjects at low or high cardiovascular risk; and (ii) differences between patterns of resistance artery remodelling associated with deficit of NO availability and with exposure to cardiovascular risk factors. METHODS AND RESULTS: All analyses were conducted on the microvascular data set of the Italian Society for Arterial Hypertension (SIIA) that includes 356 patients with measures of small resistance arteries remodelling acquired with pressure or wire myography. Information on endothelial function and NO availability were also available in 116 patients. The European Heart Score (HS) was used to define the total cardiovascular risk of each patient. Endothelial function was inversely related with the severity of the resistance artery remodelling, and this association remained significant after adjustment for the HS. By contrast, the HS lost its significant association with the media-to-lumen (M/L) ratio and the media cross-sectional area after adjustment for endothelial function. The strength of these associations was similar in subjects at high and low cardiovascular risk. The addition of endothelial function and NO availability to the HS significantly improved the identification of subjects at more and less severe resistance artery remodelling. A severe deficit of NO availability was associated with hypertrophic remodelling, while a higher HS was more clearly associated with eutrophic remodelling. CONCLUSION: Resistance artery endothelial function and NO availability might represent important factors involved in resistance artery remodelling, independently from cardiovascular risk factor exposure.

6.
Diabetes Obes Metab ; 21(12): 2587-2598, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31282073

RESUMEN

AIM: To investigate the associations of blood pressure variability (BPV), expressed as long-term (visit-to-visit) and short-term (ambulatory blood pressure monitoring [ABPM] and home blood pressure monitoring [HBPM]) and all-cause mortality, major adverse cardiovascular events (MACEs), extended MACEs, microvascular complications (MiCs) and hypertension-mediated organ damage (HMOD) in adult patients with type 2 diabetes. MATERIALS AND METHODS: PubMed, Medline, Embase, Cinahl, Web of Science, ClinicalTrials.gov and grey literature databases were searched for studies including patients with type 2 diabetes, at least one variable of BPV (visit-to-visit, HBPM, ABPM) and evaluation of the incidence of at least one of the following outcomes: all-cause mortality, MACEs, extended MACEs and/or MiCs and/or HMOD. The extracted information was analyzed using random effects meta-analysis and meta-regression. RESULTS: Data from a total of 377 305 patients were analyzed. Systolic blood pressure (SBP) variability was associated with a significantly increased risk of all-cause mortality (HR 1.12, 95% CI 1.04-1.21), MACEs (HR 1.01, 95% CI 1.04-1.17), extended MACEs (HR 1.07, 95% CI 1.03-1.11) and MiCs (HR 1. 12, 95% CI 1.01-1.24), while diastolic blood pressure was not. Associations were mainly driven from studies on long-term SBP variability. Qualitative analysis showed that BPV was associated with the presence of HMOD expressed as carotid intima-media thickness, pulse wave velocity and left ventricular hypertrophy. Results were independent of mean blood pressure, glycaemic control and serum creatinine levels. CONCLUSIONS: Our results suggest that BPV might provide additional information rather than mean blood pressure on the risk of cardiovascular disease in patients with type 2 diabetes.

7.
High Blood Press Cardiovasc Prev ; 26(4): 321-329, 2019 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-31325087

RESUMEN

Cardiovascular disease (CVD) remains the leading cause of morbility and mortality worldwide. The identification of common cardiovascular risk factors has led to the development of effective treatments that enabled a significant reduction of the global cardiovascular disease burden. However, a significant proportion of cardiovascular risk remains unexplained by these risk factors leaving many individuals at risk of cardiovascular events despite good control of the risk factors. Recent randomized clinical trials and Mendelian randomization studies have suggested that inflammation explains a significant proportion of the residual cardiovascular risk in subjects with good control of risk factors. An accelerated process of vascular ageing is increasingly recognized as a potential mechanism by which inflammation might increase the risk of CVD. In turn, cellular ageing represents an important source of inflammation within the vascular wall, potentially creating a vicious cycle that might promote progression of atherosclerosis, independently from the individual cardiovascular risk factor burden. In this review, we summarise current evidence suggesting a role for biological ageing in CVD and how inflammation might act as a key mediator of this association.


Asunto(s)
Envejecimiento/metabolismo , Enfermedades Cardiovasculares/metabolismo , Mediadores de Inflamación/metabolismo , Inflamación/metabolismo , Telómero/metabolismo , Factores de Edad , Envejecimiento/genética , Envejecimiento/patología , Animales , Enfermedades Cardiovasculares/genética , Enfermedades Cardiovasculares/patología , Enfermedades Cardiovasculares/fisiopatología , Senescencia Celular , Humanos , Inflamación/genética , Inflamación/patología , Inflamación/fisiopatología , Medición de Riesgo , Factores de Riesgo , Transducción de Señal , Telómero/genética , Telómero/patología , Homeostasis del Telómero , Acortamiento del Telómero , Factores de Tiempo
8.
Vascul Pharmacol ; 120: 106576, 2019 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-31279096

RESUMEN

Smooth muscle function is explored by sublingual glyceryl trinitrate (GTN) administration to compare with endothelium-dependent vasodilation of the brachial artery by flow-mediated-dilation (FMD). This study compared the hemodynamic and autonomic effects of the two most often used GTN dosages. In 80 essential hypertensive patients (HT) and 60 normotensive subjects (NT), FMD of the brachial artery and endothelium-independent response to sublingual GTN (25 µg and 400 µg) were evaluated by high-resolution ultrasound and automated image analysis. In 10 HT, muscle sympathetic nerve activity (MSNA) was also assessed by microneurography. HT showed significantly (p < .01) lower FMD (5.5 ±â€¯3.3%) compared to NT (6.9 ±â€¯2.2%). The response to GTN 25 µg tended to be lower (HT:7.2 ±â€¯3.3%; NT:7.9 ±â€¯2.9%; p = .06), whereas response to GTN 400 µg was similar (HT:14.3 ±â€¯4.8%, NT:14.5 ±â€¯4.7%, p = ns). Blood pressure (BP) reduction induced by GTN 400 µg (systolic-BP:-3.2 ±â€¯7.7 mm Hg, diastolic-BP:-4.7 ±â€¯5.0 mm Hg) was greater (p < .001) compared to GTN 25 µg (systolic-BP:-0.7 ±â€¯5.8 mm Hg, diastolic-BP:-0.7 ±â€¯4.4 mm Hg). Changes in heart rate were also greater (+5.6 ±â€¯6.4 bpm versus -0.2 ±â€¯5.4 bpm, p < .001). This behaviour was similar in either NT or HT. MSNA was significantly increased by GTN 400 µg (31 ±â€¯7bursts/min to 41 ±â€¯6bursts/min, p < .001) but not by 25 µg (33 ±â€¯9bursts/min to 37 ±â€¯11bursts/min, p = .19). In conclusion, the administration of low-dose GTN allows exploring endothelium-independent vasodilation in FMD protocols, inducing only modest hemodynamic and sympathetic responses.

9.
J Clin Endocrinol Metab ; 104(10): 4253-4263, 2019 Oct 01.
Artículo en Inglés | MEDLINE | ID: mdl-31162549

RESUMEN

CONTEXT: Mechanisms mediating the cardiovascular and renal protection exerted by SGLT2 inhibitors are still partially unknown. We investigated whether dapagliflozin modulates systemic and renal vascular function and structure, and induces epigenetic modifications. SUBJECTS AND METHODS: Forty hypertensive patients with type 2 diabetes were randomly assigned to 4-week treatment with dapagliflozin 10 mg or hydrochlorothiazide (HCT) 12.5 mg. Routine analyses; plasma renin activity; aldosterone, catecholamine, and 24-hour urinary electrolyte levels; flow-mediated dilation (FMD) of the brachial artery; carotid-femoral pulse-wave velocity (PWV); augmentation index; and resistive index and dynamic renal resistive index (DRIN) were measured at baseline and after treatment. Circulating miRNAs (miRs) related to heart failure (miR30e-5p, miR199a-3p), endothelial dysfunction (miR27b and miR200b), and renal function (miR130b-3p, miR21-5p) were assessed and related to the effects of treatments. RESULTS: Dapagliflozin and HCT marginally lowered blood pressure. Fasting glucose was lowered, whereas 24-hour diuresis, glycosuria, and osmolar clearance were increased by dapagliflozin (P < 0.001 for all), without affecting sodium excretion and glomerular filtration rate. Magnesium levels significantly increased after dapagliflozin treatment (P = 0.02). Neither dapagliflozin nor HCT modified FMD or PWV. DRIN did not vary in the dapagliflozin group, whereas it increased in the HCT group (P = 0.047 for time by treatment interaction). Both treatments induced variations in the expression of some miRs; dapagliflozin, but not HCT, significantly up-regulated miR30e-5p and downregulated miR199a-3p. CONCLUSION: A putative epigenetic regulation of the protecting cardiovascular effect exerted by SGLT2 inhibitors was found. Dapagliflozin might exert nephroprotection by preserving renal vasodilating capacity.

10.
Eur Heart J ; 40(30): 2534-2547, 2019 Aug 07.
Artículo en Inglés | MEDLINE | ID: mdl-31211361

RESUMEN

Endothelial dysfunction is involved in the development of atherosclerosis, which precedes asymptomatic structural vascular alterations as well as clinical manifestations of cardiovascular disease (CVD). Endothelial function can be assessed non-invasively using the flow-mediated dilation (FMD) technique. Flow-mediated dilation represents an endothelium-dependent, largely nitric oxide (NO)-mediated dilatation of conduit arteries in response to an imposed increase in blood flow and shear stress. Flow-mediated dilation is affected by cardiovascular (CV) risk factors, relates to coronary artery endothelial function, and independently predicts CVD outcome. Accordingly, FMD is a tool for examining the pathophysiology of CVD and possibly identifying subjects at increased risk for future CV events. Moreover, it has merit in examining the acute and long-term impact of physiological and pharmacological interventions in humans. Despite concerns about its reproducibility, the available evidence shows that highly reliable FMD measurements can be achieved when specialized laboratories follow standardized protocols. For this purpose, updated expert consensus guidelines for the performance of FMD are presented, which are based on critical appraisal of novel technical approaches, development of analysis software, and studies exploring the physiological principles underlying the technique. Uniformity in FMD performance will (i) improve comparability between studies, (ii) contribute to construction of reference values, and (iii) offer an easy accessible and early marker of atherosclerosis that could complement clinical symptoms of structural arterial disease and facilitate early diagnosis and prediction of CVD outcomes.

12.
Curr Hypertens Rep ; 21(4): 32, 2019 04 04.
Artículo en Inglés | MEDLINE | ID: mdl-30949772

RESUMEN

PURPOSE OF REVIEW: To examine the state of the art on the pathogenesis of endothelial dysfunction in the microcirculation of patients with obesity, focusing on the complex relationship between the consolidated and the novel mechanisms involved in this alteration. RECENT FINDINGS: Human obesity is associated with vascular endothelial dysfunction, caused by a reduced nitric oxide availability secondary to an enhanced oxidative stress production. Pro-inflammatory cytokine generation, secreted by perivascular adipose tissue, is a major mechanism whereby obesity is associated with a reduced vascular NO availability. Vasculature also represents a source of low-grade inflammation and oxidative stress which contribute to endothelial dysfunction in obese patients. Recently, a direct influence of arginase on endothelial function by reducing nitric oxide availability was demonstrated in small vessels from patients with severe obesity. This effect is modulated by ageing and related to the high levels of vascular oxidative stress. Oxidative stress, inflammation, and enzymatic pathways are important players in the pathophysiology of obesity-related vascular disease. The identification of new therapeutic approaches able to interfere with these mechanisms will result in more effective prevention of the cardiovascular complications associated with obesity.

14.
Vascul Pharmacol ; 115: 84-88, 2019 04.
Artículo en Inglés | MEDLINE | ID: mdl-30822569

RESUMEN

Arterial hypertension remains the world's leading mortality risk factor and despite overwhelming evidence that blood pressure-lowering strategies greatly reduce the cardiovascular risk, a substantial proportion of hypertensive individuals worldwide fail to achieve an optimal blood pressure control under treatment. Among the causes responsible for the gap existing between blood pressure lowering potential of the different antihypertensive treatments and real-life practice is the presence of drug-induced hypertension. Many therapeutic agents or substances may directly favour an increment of blood pressure values or counteract the blood pressure lowering effects of antihypertensive drugs. Excessive water and sodium retention, direct vasoconstriction or sympathomimetic activation are major mechanisms of action of such substances. The present manuscript will review medications and other substances that may increase blood pressure, also suggesting the choice of the more appropriate antihypertensive agents to employ when withdrawal of the substance or drug causing an elevation of blood pressure values is not possible.


Asunto(s)
Antihipertensivos/uso terapéutico , Presión Arterial/efectos de los fármacos , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/tratamiento farmacológico , Hipertensión/tratamiento farmacológico , Antihipertensivos/efectos adversos , Toma de Decisiones Clínicas , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/diagnóstico , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/etiología , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/fisiopatología , Humanos , Hipertensión/inducido químicamente , Hipertensión/diagnóstico , Hipertensión/fisiopatología , Factores de Riesgo , Resultado del Tratamiento
15.
Eur J Prev Cardiol ; 26(10): 1092-1095, 2019 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-30776914
16.
J Clin Endocrinol Metab ; 104(2): 341-348, 2019 02 01.
Artículo en Inglés | MEDLINE | ID: mdl-30165404

RESUMEN

Context: Endothelium guarantees vascular homeostasis by the opposite action of substances by vasodilating/antithrombogenic and vasoconstricting/prothrombotic activities. Obesity is characterized by endothelial dysfunction associated with a condition of vascular low-grade inflammation. Evidence Acquisition: Analysis of available basic or clinical papers published in peer-reviewed international journals on microcirculation and obesity. Evidence Synthesis: Vascular low-grade inflammation, which characterizes obesity, is secondary to abnormal production of proinflammatory cytokines, including TNF-α. TNF-α, generated either in small vessels or within the perivascular adipose tissue (PVAT) of patients with obesity, stimulates reactive oxygen species generation, mainly through NAD(P)H oxidase activation, which in turn reduces nitric oxide (NO) availability. These aspects are highlighted by the insulin resistance status and macronutrient intake that characterize the obesity condition. Oxidant excess has also been proposed as a mechanism whereby TNF-α interferes with the endothelin-1/NO system at the level of small vessels from patients with obesity. Conclusions: In obesity, microvasculature from visceral fat is an important source of low-grade inflammation and oxidative stress that, together with the PVAT, directly contribute to vascular changes, favoring the development and acceleration of the vascular atherothrombotic process in this clinical condition.


Asunto(s)
Endotelio Vascular/fisiopatología , Obesidad/fisiopatología , Factor de Necrosis Tumoral alfa/fisiología , Tejido Adiposo/fisiopatología , Endotelina-1/fisiología , Humanos , Inflamación/etiología , Inflamación/fisiopatología , Insulina/fisiología , Resistencia a la Insulina/fisiología , Microvasos/fisiopatología , Obesidad/complicaciones , Estrés Oxidativo/fisiología
17.
Eur Heart J ; 40(4): 383-391, 2019 Jan 21.
Artículo en Inglés | MEDLINE | ID: mdl-29077881

RESUMEN

Aims: Accumulation of reactive oxygen species (ROS) promotes vascular disease in obesity, but the underlying molecular mechanisms remain poorly understood. The adaptor p66Shc is emerging as a key molecule responsible for ROS generation and vascular damage. This study investigates whether epigenetic regulation of p66Shc contributes to obesity-related vascular disease. Methods and results: ROS-driven endothelial dysfunction was observed in visceral fat arteries (VFAs) isolated from obese subjects when compared with normal weight controls. Gene profiling of chromatin-modifying enzymes in VFA revealed a significant dysregulation of methyltransferase SUV39H1 (fold change, -6.9, P < 0.01), demethylase JMJD2C (fold change, 3.2, P < 0.01), and acetyltransferase SRC-1 (fold change, 5.8, P < 0.01) in obese vs. control VFA. These changes were associated with reduced di-(H3K9me2) and trimethylation (H3K9me3) as well as acetylation (H3K9ac) of histone 3 lysine 9 (H3K9) on p66Shc promoter. Reprogramming SUV39H1, JMJD2C, and SRC-1 in isolated endothelial cells as well as in aortas from obese mice (LepOb/Ob) suppressed p66Shc-derived ROS, restored nitric oxide levels, and rescued endothelial dysfunction. Consistently, in vivo editing of chromatin remodellers blunted obesity-related vascular p66Shc expression. We show that SUV39H1 is the upstream effector orchestrating JMJD2C/SRC-1 recruitment to p66Shc promoter. Indeed, SUV39H1 overexpression in obese mice erased H3K9-related changes on p66Shc promoter, while SUV39H1 genetic deletion in lean mice recapitulated obesity-induced H3K9 remodelling and p66Shc transcription. Conclusion: These results uncover a novel epigenetic mechanism underlying endothelial dysfunction in obesity. Targeting SUV39H1 may attenuate oxidative transcriptional programmes and thus prevent vascular disease in obese individuals.

18.
Obesity (Silver Spring) ; 27(1): 68-74, 2019 01.
Artículo en Inglés | MEDLINE | ID: mdl-30516353

RESUMEN

OBJECTIVE: Bariatric surgery may ameliorate renal function through vascular mechanisms. This study tested surgery's ability to improve measured glomerular filtration rate (mGFR) and identified clinical, renal, and systemic vascular predictors of such improvement. METHODS: Twenty-five nondiabetic subjects with severe obesity were studied before and 1 year after Roux-en-Y gastric bypass, evaluating mGFR and renal plasma flow, basal renal resistive index (RI) and dynamic renal RI, renal visceral fat, and systemic vascular parameters, including flow-mediated dilation, aortic pulse wave velocity, and carotid intima media thickness and stiffness. RESULTS: After Roux-en-Y gastric bypass, BMI decreased by 31%. At follow-up, body surface area (BSA)-adjusted mGFR increased (from 86.9 ± 15.2 to 109.0 ± 18.2 mL/min/1.73 m2 , P <  0.001), whereas the absolute mGFR did not change. Renal plasma flow did not vary. RI decreased; flow-mediated dilation, pulse wave velocity, carotid intima media thickness, and carotid stiffness improved. mGFR changes after surgery (ΔmGFR/BSA) were associated with younger age and lower fasting glucose. Among vascular variables, an improved ΔmGFR/BSA was associated with smaller brachial artery diameter, lower intima media thickness, and lower RI; this latter association remained after adjusting for covariates. No measure of adiposity was associated with ΔmGFR. CONCLUSIONS: In subjects with obesity and normal renal function, bariatric surgery improves mGFR/BSA (although absolute mGFR is unchanged) and renal and systemic vascular function. Lower renal intravascular resistance can predict these improvements, maximizing them in relatively young individuals.


Asunto(s)
Cirugía Bariátrica/efectos adversos , Riñón/fisiopatología , Obesidad Mórbida/cirugía , Obesidad/complicaciones , Insuficiencia Renal Crónica/etiología , Cirugía Bariátrica/métodos , Femenino , Tasa de Filtración Glomerular , Humanos , Masculino , Persona de Mediana Edad , Obesidad/cirugía , Insuficiencia Renal Crónica/patología
19.
Minerva Med ; 110(6): 546-554, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31965780

RESUMEN

The 2018 ESH/ESC guidelines indicate that the first-choice therapy in the majority of hypertensive patients should be a fixed combination of a drug that blocks the renin-angiotensin-aldosterone system and a calcium antagonist or a diuretic. Evidence from the meta-analysis of controlled clinical trials, however, indicates that the classes of drugs that block the renin-angiotensin-aldosterone system should not be considered equivalent as ACE inhibitors have been clearly shown to outperform AT-1 antagonists in preventing myocardial infarction and total mortality. Moreover, studies such as ASCOT and ACCOMPLISH demonstrate a superiority of the ACE-inhibitor/calcium antagonist association over beta-blocker/diuretic associations and especially towards the ACE-inhibitor/diuretic combination, whereas there is no scientific evidence of efficacy with respect to cardiovascular events on the part of AT-1 antagonist/calcium antagonist combinations. Drugs such as ramipril and amlodipine are undoubtedly the reference molecules within their respective classes as numerous controlled clinical studies have demonstrated their effectiveness on cardiovascular events. It is therefore obvious that the availability of a fixed combination with both molecules is a great opportunity for the therapy of the hypertensive patient, considering also the availability of studies that demonstrate its effectiveness on intermediate endpoints associated with high tolerability. So, in accordance with the 2018 ESH/ESC guidelines, the fixed combination ramipril/amlodipine represents a first choice therapy for hypertension.


Asunto(s)
Inhibidores de la Enzima Convertidora de Angiotensina/administración & dosificación , Bloqueadores de los Canales de Calcio/administración & dosificación , Hipertensión/tratamiento farmacológico , Amlodipino/administración & dosificación , Antihipertensivos/administración & dosificación , Combinación de Medicamentos , Humanos , Guías de Práctica Clínica como Asunto , Ramipril/administración & dosificación , Resultado del Tratamiento
20.
Arterioscler Thromb Vasc Biol ; 38(10): 2474-2483, 2018 10.
Artículo en Inglés | MEDLINE | ID: mdl-30354211

RESUMEN

Objective- Arginase can reduce NO availability. In this study, we explored arginase as a determinant of endothelial dysfunction in small arteries from obese patients and its relationship with aging and microvascular remodeling. Approach and Results- Small arteries were dissected after subcutaneous fat biopsies and evaluated on a pressurized micromyograph. Endothelium-dependent vasodilation was assessed by acetylcholine, repeated under L-NAME ( N G-nitro-L-arginine-methyl ester), N(ω)-hydroxy-nor-l-arginine (arginase inhibitor) and gp91ds-tat (NADPH [nicotinamide adenine dinucleotide phosphate oxidase] oxidase inhibitor) in vessels from young (age <30 years) control and obese and old (>30 years) control and obese subjects. Media-lumen ratio and amount of vascular wall fibrosis were used as markers of vascular remodeling. Amount of vascular superoxide anions and NO production were determined with immunofluorescence, whereas arginase expression was quantified using Western blot and quantitative polymerase chain reaction. Obese and older age groups had lower vascular NO, as well as higher media-lumen ratio, wall fibrosis, intravascular superoxide, and blunted inhibitory effect of L-NAME on acetylcholine versus controls and younger age groups. N(ω)-hydroxy-nor-l-arginine restored the acetylcholine-induced vasodilation in young and, to a lesser extent, in old obese subjects. This effect was abolished by addition of L-NAME. Gp91ds-tat increased the vasodilatory response to N(ω)-hydroxy-nor-l-arginine in old obese. Superoxide anions and arginase I/II levels were higher in the vascular wall of obese versus controls. Conclusions- Arginase contributes to microvascular endothelial dysfunction in obesity. Its impact is reduced by aging because of higher levels of vascular oxidative stress. Obesity is accompanied by accelerated microvascular remodeling, the extent of which is related to the amount of arginase in the vascular wall.


Asunto(s)
Envejecimiento/metabolismo , Arginasa/metabolismo , Arterias/enzimología , Óxido Nítrico/metabolismo , Obesidad/enzimología , Grasa Subcutánea/irrigación sanguínea , Vasodilatación , Adulto , Factores de Edad , Arginasa/antagonistas & inhibidores , Arterias/efectos de los fármacos , Arterias/fisiopatología , Estudios de Casos y Controles , Inhibidores Enzimáticos/farmacología , Femenino , Humanos , Masculino , Persona de Mediana Edad , NADPH Oxidasas/metabolismo , Obesidad/diagnóstico , Obesidad/fisiopatología , Estrés Oxidativo , Transducción de Señal , Superóxidos/metabolismo , Remodelación Vascular , Vasodilatación/efectos de los fármacos , Vasodilatadores/farmacología , Adulto Joven
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