Remodelado vascular excéntrico: su relación con trastornos metabólicos y el incremento de la masa corporal / Eccentric Vascular Remodeling: Its Relationship with Metabolic Disorders and Increased Body Mass

RESUMEN Introducción: Existe evidencia reciente que establecería a la hipoperfusión muscular como causa primaria de trastornos metabólicos en respuesta a la sobrealimentación. Esta concepción centrípeta del desarrollo de trastornos metabólicos podría implicar no solo alteraciones en la microvasculatura, sino también afectación en las arterias de conductancia. Objetivos: 1) Determinar la asociación entre diámetro basal de la arteria humeral (D-Hum) y la vasodilatación mediada por flujo (VDMF) 2) Analizar la asociación de ambos parámetros conforme aumenta de la masa corporal 3) Evaluar asociaciones entre el D-Hum/VDMF con componentes del síndrome metabólico (SM) 4) Evaluar la asociación independiente de ambas variables con el SM. Material y métodos: Se evaluaron 3493 pacientes. Se excluyeron pacientes < 18 y >80 años, con patología cardiovascular previa, insuficiencia renal crónica (IRC), colagenopatías, y tratados con estatinas. Se determinó presión arterial (PA), parámetros antropométricos y perfil metabólico, y se clasificó a los sujetos de acuerdo con la presencia de SM según AHA/NHLBI 2019. Se midieron D-Hum en mm y VDMF en %. Se analizó la asociación lineal entre D-Hum y VDMF y se analizaron ambas variables según decilos de índice de masa corporal (IMC). Se evaluaron asociaciones entre D-Hum/VDMF con la PA, glucemia (Glu), triglicéridos (TG) y colesterol de alta densidad (HDLc). Se realizaron dos regresiones logísticas con SM como variable dependiente y D-Hum o VDMF más edad, sexo, IMC y factores de riesgo coronario (FRC) como independientes. Resultados: Ingresaron 1995 pacientes (48,2 ± 11 años, 56 % hombres). El D-Hum y la VDMF presentaron una asociación inversa (r= -0,42; p < 0,0001). El D-Hum aumentó según decilos del IMC (p < 0,000001); la VDMF mostró relación inversa con los decilos crecientes de IMC (p < 0,000001). El D-Hum presentó correlación directa con PA, Glu y TG; e inversa con HDLc (p < 0,05 en todos los casos). La VDMF mostró correlación inversa con PA, Glu y TG; y directa con HDLc (p < 0,05 en todos los casos). El D-Hum se asoció en forma independiente con el SM ajustado por edad, sexo, IMC y FRC (OR 1,42, p = 0,0019), mientras que la VDMF no (OR 0,98, p = 0,217). Conclusión: El remodelado vascular excéntrico se asoció con un compromiso en la adaptación vascular ante aumentos en la demanda de flujo sanguíneo y con alteraciones metabólicas a lo largo del incremento de la masa corporal. Así, el compromiso dinámico de la vasculatura podría tener un rol determinante en el desarrollo de alteraciones metabólicas en forma sincrónica con la ganancia de peso.

ABSTRACT Background: Recent evidence would establish muscle hypoperfusion as the primary cause of metabolic disorders in response to overfeeding. This centripetal concept on the development of metabolic disorders could involve not only alterations in the microvasculature, but also affect the conductance arteries. Objectives: The aim of this study was 1) to determine the association between baseline brachial artery diameter (BAD) and flow-mediated vasodilation (FMVD), 2) To analyze the association of both parameters throughout the increase in body mass, 3) To evaluate associations between BAD/FMVD with components of the metabolic syndrome (MS) and 4) To evaluate the independent association of both variables with MS. Methods: A total of 3493 patients were evaluated. Patients <18 and >80 years old, those with previous cardiovascular disease, chronic kidney disease (CKD), collagenopathies, or treated with statins were excluded from the study. Blood pressure (BP), anthropometric parameters and metabolic profile were determined, and the subjects were classified according to the presence of MS conforming AHA/NHLBI 2019 criteria. BAD was measured in mm and FMVD as percentage. The linear association between BAD and FMVD was assessed, and both variables were analyzed according to deciles of body mass index (BMI). Associations between BAD/FMVD with BP, glucose (Glu), triglycerides (TG) and high-density cholesterol (HDL-C) levels were evaluated. Two logistic regression analyses were performed with MS as dependent variable and BAD or FMVD plus age, gender, BMI, and coronary risk factors (CRF) as independent variables. Results: A total of 1995 patients (48.2 ± 11 years, 56% men) were admitted in the study. An inverse correlation was found between BAD and FMVD (r= -0.42; p < 0.0001). BAD increased according to deciles of BMI (p < 0.000001), while FMVD showed an inverse relationship with increasing deciles of BMI (p < 0.000001). BAD exhibited a direct correlation with BP, Glu and TG; and an inverse relationship with HDL-C (p < 0.05 in all cases). FMVD presented an inverse correlation with BP, Glu and TG; and a direct correlation with HDL-C (p < 0.05 in all cases). BAD was independently associated with MS adjusted for age, gender, BMI and CRF (OR 1.42, p=0.0019), while FMVD was not (OR 0.98, p = 0.217). Conclusion: Eccentric vascular remodeling was associated with vascular adaptation to increased blood flow demand and with metabolic alterations throughout the increase in body mass. Thus, the dynamic compromise of vasculature could play a decisive role in the development of metabolic alterations occurring synchronously with weight gain.

Prevalence and Burden of Carotid and Femoral Atherosclerosis in Subjects Without Known Cardiovascular Disease in a Large Community Hospital in South-America.

INTRODUCTION: Clinical guidelines recommend measurement of arterial (carotid and femoral) plaque burden by vascular ultrasound (VUS) as a risk modifier in individuals at low or moderate risk without known atherosclerotic cardiovascular disease (ASCVD). AIM: To evaluate the prevalence of carotid and femoral plaques by age and sex, the burden of subclinical atherosclerosis (SA), and its association with classic CVRF in subjects over 30 years of age without ASCVD. METHODS: We prospectively enrolled 5775 consecutive subjects referred for cardiovascular evaluation and determined the prevalence and burden of SA using 2D-VUS in carotid and femoral arteries. RESULTS: Sixty-one percent were men with a mean age of 51.3 (SD 10.6) years. Overall, plaque prevalence was 51% in carotid arteries, 39.3% in femoral arteries, 62.4% in carotid or femoral arteries, and 37.6% in neither. The prevalence of plaques and SA burden showed an increasing trend with age, being higher in men than in women and starting before the age of 40, both in the carotid and femoral sites. There was also an increasing prevalence of plaques according to the number of CVRF, and interestingly we found a high prevalence of plaques in subjects with 0 or 1 classic CVRF. CONCLUSIONS: We observed an increased prevalence and burden of carotid or femoral SA, higher in men, beginning before the fourth decade of life and increasing with age. Despite a significant association with classic CVRF, a significant number of subjects with low CVRF were diagnosed with SA.

Chronic Kidney Disease and Arterial Stiffness: A Two-Way Path.

The kidney-heart relationship has raised interest for the medical population since its vast and complex interaction significantly impacts health. Chronic kidney disease (CKD) generates vascular structure and function changes, with significant hemodynamic effects. The early arterial stiffening in CKD patients is a consequence of the interaction between oxidative stress and chronic vascular inflammation, leading to an accelerated deterioration of left ventricular function and alteration in tissue perfusion. CKD amplifies the inflammatory cascade's activation and is responsible for altering the endothelium function, increasing the vascular tone, wall thickening, and favors calcium deposits in the arterial wall. Simultaneously, the autonomic imbalance, and alteration in other hormonal systems, also favor the overactivation of inflammatory and fibrotic mediators. Thus, hormonal disarrangement also contributes to structural and functional lesions throughout the arterial wall. On the other hand, a rise in arterial stiffening and volume overload generates high left ventricular afterload. It increases the left ventricular burden with consequent myocardial remodeling, development of left ventricular hypertrophy and, in turn, heart failure. It is noteworthy that reduction in glomerular mass of renal diseases generates a compensatory glomerular filtration overdriven associated with large-arteries stiffness and high cardiovascular events. Furthermore, we consider that the consequent alterations of the arterial system's mechanical properties are crucial for altering tissue perfusion, mainly in low resistance. Thus, increasing the knowledge of these processes may help the reader to integrate them from a pathophysiological perspective, providing a comprehensive idea of this two-way path between arterial stiffness and renal dysfunction and their impact at the cardiovascular level.

La Vasculatura Sistémica En La Enfermedad Renal Crónica. Tercera Parte / Systemic Vasculature In Chronic Kidney Disease. Third Part

Resumen En esta revisión de la literatura presentamos diversos mecanismos terapéuticos para tratar la rigidez vascular en pacientes con enfermedad renal crónica. En el ámbito de la terapéutica no farmacológica la restricción de sodio y la indicación de dieta mediterránea han demostrado efectos benéficos, mientras que acerca de la indicación de actividad física aún no hay evidencia clara sobre su utilidad para disminuir la rigidez vascular en este grupo específico de pacientes. Es con el tratamiento farmacológico donde se evidencian los mayores beneficios, tanto en la rigidez vascular como en los eventos cardiovasculares asociados. Está ampliamente demostrada la efectividad de los inhibidores del sistema renina-angiotensina-aldosterona y de los fármacos antialdosterónicos para disminuir la presión y la rigidez arterial. Otras drogas, como los bloqueadores del receptor de endotelina, han demostrado sus efectos protectores sobre la pared arterial, aunque no están carentes de potenciales efectos adversos. También repasamos los resultados obtenidos con el uso de las nuevas drogas antidiabéticas, en particular los iSLGT2 y los aGLP-1, y su efecto sobre la presión arterial y la rigidez vascular, en particular en pacientes con enfermedad renal crónica. Se revisan además la utilidad de aquellas drogas con efecto sobre la cascada inflamatoria y sobre las calcificaciones vasculares, muy propensas durante los tratamientos sustitutivos de la función renal. Este trabajo se enfoca, en síntesis, en las diversas intervenciones terapéuticas sobre la rigidez arterial, con énfasis en la disminución de eventos cardiovasculares y de la mortalidad en pacientes con enfermedad renal crónica.

Abstract In this literature review we present various therapeutic alternatives for vascular stiffness in patients with chronic kidney disease. Here we discussed the role of non-pharmacological treatments with evidence of the benefit of sodium restriction on vascular stiffness, the positive effects in that sense shown by the Mediterranean diet, and the small benefits of physical activity on vascular stiffness in this group of patients. Is in the pharmacological treatment where the best benefits are evidenced; both, on vascular stiffness and on the associated cardiovascular events. The effectiveness of renin-angiotensin-aldosterone system inhibitors and antialdosteronic drugs to decrease blood pressure and stiffness has been widely demonstrated. Other drugs, such as endothelin receptor blockers, showed their protective effects on the arterial wall, but with potential adverse effects. This article also reviews the effects of new anti-diabetic drugs, iSLGT2 and aGLP-1 in particular, and their effect on blood pressure and vascular stiffness, particularly in patients with chronic kidney disease. The utility of drugs with effects on the inflammatory cascade and drugs with a potential effect on vascular calcification, complication occurring frequently during renal function replacement treatment, are also reviewed. In short, this work focuses in the therapeutic interventions on arterial stiffness, with emphasis on the reduction of cardiovascular events and mortality in patients with chronic kidney disease.

Blood pressure control is not enough to normalize endothelial repair by progenitor cells.

Patients presenting with classical cardiovascular risk factors within acceptable or average value ranges often develop cardiovascular disease, suggesting that other risk factors need to be considered. Considering that endothelial progenitor cells (EPCs) contribute to endothelial repair, we investigated whether EPCs might be such a factor. We compared the ability of peripheral blood EPCs to attach to extracellular matrix proteins and to grow and function in culture, between controlled hypertensive patients exhibiting a Framingham score (FS) of <10% while showing severe vascular impairment (intima-media thickness/diameter, carotid-femoral pulse wave velocity, brachial artery flow-mediated dilation, carotid and femoral atherosclerotic plaque presence; vulnerable group, N = 30) and those with an FS of ≥10% and scarce vascular changes (protected group, N = 30). When compared with vulnerable patients, protected patients had significantly higher early and late-EPC and early and late-tunneling nanotube (TNT) numbers. Significant negative associations were found between vascular damage severity and early EPC, late-EPC, or late-TNT numbers, whereas EPC or TNT numbers and patient characteristics or cardiovascular risk factors were not associated. Except for protected patients, in all controlled hypertensive patients, early and late-EPC and early and late-TNT counts were significantly lower than those in the normotensive subjects studied (N = 30). We found that the disparity in vascular status between patients presenting with both an FS of ≥10% and scarce vascular changes and those presenting with both an FS of <10% and severe vascular impairment is related to differences in peripheral blood EPC and TNT numbers. These observations support the role of EPCs as contributors to vascular injury repair and suggest that EPC numbers may be a potential cardiovascular risk factor to be included in the FS calculation.NEW & NOTEWORTHY As individuals who present with risk factors within acceptable or average value ranges often develop cardiovascular (CV) disease, it has been suggested that other CV risk factors need to be considered in addition to those that are commonly combined in the Framingham score (FS) to estimate the risk of general CV disease. We investigated whether peripheral endothelial progenitor cells (EPCs) and tunneling nanotubes (TNTs) deserve to be considered. Here we report that EPCs and TNTs are significantly lower in controlled hypertensive patients versus normotensive subjects and that the disparity in vascular status between patients presenting with an FS of ≥10% with scarce vascular changes and those presenting with an FS of <10% with severe vascular impairment is related to differences in EPC and TNT numbers. These data point to EPC and TNT numbers as potential CV risk factors to be included in the FS calculation.

La Vasculatura Sistémica En La Enfermedad Renal Crónica. Segunda Parte / Systemic Vasculature In Chronic Kidney Disease. Second Part

Resumen Existen cambios estructurales importantes de la pared arterial en, prácticamente, todas las etapas clínicas de la enfermedad renal crónica. Son un marcador pronóstico y, al mismo tiempo, un factor de progresión y de eventos, tanto cardiovasculares como renales. Es por ello que tener una estimación del daño vascular y, mejor aún, un diagnóstico adecuado es esencial. La evaluación vascular en la consulta clínica, mediante la determinación de la presión del pulso y el índice de presión arterial sistólica tobillo-brazo, sirven como una orientación inicial del daño arterial de estos pacientes. Hoy podemos valorar, de manera accesible, las lesiones estructurales de las arterias mediante la cuantificación y caracterización, por ecografía vascular, de las placas ateroscleróticas de carótidas y femorales y por la velocidad de onda del pulso. En la gran mayoría de los pacientes renales la velocidad de onda del pulso está muy aumentada, comparada con poblaciones sanas, como consecuencia de múltiples mecanismos patogénicos. Las alteraciones vasculares, tanto de los grandes vasos como de la microcirculación, están fuertemente vinculados con la progresión de la enfermedad renal crónica, así como con complicaciones y eventos renales, cardiacos y cerebrales. En conclusión, en individuos con riesgo de desarrollar enfermedad renal crónica, o en quienes ya la padecen, la medición de la rigidez arterial y de los daños ateroscleróticos de la pared vascular serían parámetros centrales para su evaluación y uno de los objetivos a considerar al diseñar estrategias preventivas del deterioro de los órganos blanco y eventos.

Abstract There exist significant structural changes in the artery wall in almost all clinical stages of chronic kidney disease. They constitute a prognostic marker and, at the same time, a progression factor and an event factor, both cardiovascular and renal. For that reason, it is essential to have an estimation of vascular damage and, even better, an accurate diagnosis. Vascular evaluation during clinical consultation by means of determining pulse pressure and ankle-brachial pressure index are a helpful initial orientation of these patient´s artery damage. Today we can assess, in an accessible way, the structural lesions of the arteries by means of quantification and characterization, through vascular ultrasound, of carotid and femoral atherosclerotic plaques and through the pulse wave velocity. The vast majority of renal patients show increased pulse wave velocity, compared to healthy populations, as a result of multiple pathogenic mechanisms. Vascular alterations, both of large arteries and at the microcirculation level, are strongly linked to the progression of chronic kidney disease, as well as renal, cardiac and cerebral complications and events. In individuals at risk of developing chronic kidney disease, or in those who already suffer from it, the measurement of arterial stiffness and of atherosclerotic damage to the vascular wall is a central parameter for evaluation and one of the objectives to consider when designing preventive strategies against deterioration of target organs and events.

Evaluation of ventricular-arterial coupling by impedance cardiography in healthy volunteers.

BACKGROUND: The interplay between cardiac function and the arterial system is currently defined as ventricular-arterial coupling (VAC) and it is an expression of global cardiovascular efficiency. VAC involves a variety of complex interactions between the heart and the vasculature. A basic index of VAC is the ratio of effective arterial elastance (Ea)/ end-systolic elastance (Ees). While this is often done with echocardiography, obtaining Ea/Ees using impedance cardiography is feasible, although this possibility has not been explored so far. OBJECTIVE: The aim of this study was to compare the Ea/Ees values obtained using echocardiography and impedance cardiography. APPROACH: Two independent operators estimated Ea/Ees in 91 (41 ± 14 years old, women 51%) untreated apparently healthy individuals using (1) Doppler echocardiography with the single-beat method developed by Chen et al (2001 J. Am. Coll. Cardiol. 38 2028-34); and (2) data provided by impedance cardiography. The differences between Ea/Ees values were compared and correlation between both methods was estimated. MAIN RESULTS: Although Ea and Ees values calculated by impedance cardiography were lower than those estimated by echocardiography (-0.201 ± 0.457 mmHg ml-1 and -0.193 ± 0.413 mmHg ml-1), Ea/Ees ratio values were similar. Thus, there was no significant difference between the mean values of Ea/Ees estimated by impedance cardiography or echocardiography (Ea/Ees impedance cardiography - Ea/Ees echocardiography = -0.015 ± 0.096, p  = 0.150). Ea/Ees values calculated by both methods were highly correlated (r = 0.85, p  < 0.001), as well as the pre-ejection and left ventricular ejection time (r = 0.83 and r = 0.91, respectively). SIGNIFICANCE: In healthy individuals, estimation of Ea/Ees by impedance cardiography yielded similar values to those obtained using echocardiography.

Comportamiento de la rigidez arterial en diferentes condiciones clínicas utilizando el método oscilométrico / Behavior of arterial stiffness in different clinical conditions using the oscillometric method

Resumen El estudio de la rigidez arterial, en los últimos años ha sido de gran interés en la comunidad científica, siendo un indicador importante de riesgo cardiovascular y de mortalidad, además es un predictor de progresión para ciertas enfermedades crónicas. Con el fin de comprender la interpretación de la medición de la rigidez vascular, se describen 12 casos de pacientes con diferentes condiciones fisiopatológicas, que reflejan la práctica clínica diaria, en los que se evaluó la rigidez arterial mediante un método oscilométrico (Arteriograph®, TensioMed, Budapest-Hungría, Ltd.), calculando la velocidad de onda de pulso, presiones arteriales periféricas y centrales, presión de pulso, e índices de aumentación. La medición e interpretación adecuada de esta información puede ayudar a entender y resolver dudas frente a diferentes condiciones fisiopatológicas asociadas a las enfermedades cardiovasculares, mejorando la toma de decisiones terapéuticas, el seguimiento de pacientes y optimizar la prevención cardiovascular.

Abstract The study of arterial stiffness has been in recent years of great interest in the scientific community, being an important indicator of cardiovascular risk and mortality, in addition to being a predictor of progression for certain chronic diseases. In order to understand the interpretation of the measurement of vascular rigidity, 12 cases of patients with different physiopathological conditions are described, thus reflecting the daily clinical practice, in which the arterial stiffness was evaluated by means of an oscillometric method (Arteriograph®, TensioMed , Budapest-Hungary, Ltd.), calculating the pulse wave velocity, peripheral and central arterial pressures, pulse pressure, and augmentation indices. The adequate measurement and interpretation of this information can help to understand and resolve doubts in the face of different physiopathological conditions associated with cardiovascular diseases, improving therapeutic decision-making, following-up of patients and optimizing cardiovascular prevention.

Cuantificación de la rigidez arterial: de lo básico a lo clínico / Quantification of arterial stiffness: From basic to clinical

La población mundial está envejeciendo, y por tanto el número de pacientes mayores está aumentando continuamente en todas las especialidades, sobre todo en las relacionadas con la Cardiología y la Cirugía cardiovascular. El aumento de la edad se acompaña de una serie de cambios en la estructura y en la función arterial que conducen progresivamente, entre otros deterioros, a un incremento de la rigidez arterial. En la búsqueda del daño de órgano blanco en pacientes en riesgo cardiovascular asintomáticos, como una fase intermedia en el curso de la enfermedad vascular y como factor determinante del riesgo cardiovascular global, la observación de que cualquiera de estos 4 marcadores principales ­microalbuminuria, aumento de velocidad de onda de pulso carótido-femoral [ VOP c-f], hipertrofia ventricular izquierda y presencia de placas carotídeas­ puede predecir la mortalidad cardiovascular independientemente y con mayor precisión que la estratificación con diferentes escalas de riesgo, es un argumento importante a favor del uso de la evaluación integral clínica y vascular en la práctica clínica diaria. De igual forma, ayuda a identificar quienes responden a la terapéutica o quienes requieren mayor control de sus otros factores de riesgo asociados, en caso de observarse una disminución o no de estos parámetros.

Sympathetic predominance is associated with impaired endothelial progenitor cells and tunneling nanotubes in controlled-hypertensive patients.

Early endothelial progenitor cells (early EPC) and late EPC are involved in endothelial repair and can rescue damaged endothelial cells by transferring organelles through tunneling nanotubes (TNT). In rodents, EPC mobilization from the bone marrow depends on sympathetic nervous system activity. Indirect evidence suggests a relation between autonomic derangements and human EPC mobilization. We aimed at testing whether hypertension-related autonomic imbalances are associated with EPC impairment. Thirty controlled-essential hypertensive patients [systolic blood pressure/diastolic blood pressure = 130(120-137)/85(61-88) mmHg; 81.8% male] and 20 healthy normotensive subjects [114(107-119)/75(64-79) mmHg; 80% male] were studied. Mononuclear cells were cultured on fibronectin- and collagen-coated dishes for early EPC and late EPC, respectively. Low (LF)- and high (HF)-frequency components of short-term heart rate variability were analyzed during a 5-min rest, an expiration/inspiration maneuver, and a Stroop color-word test. Modulations of cardiac sympathetic and parasympathetic activities were evaluated by LF/HF (%) and HF power (ms(2)), respectively. In controlled-hypertensive patients, the numbers of early EPC, early EPC that emitted TNT, late EPC, and late EPC that emitted TNT were 41, 77, 50, and 88% lower than in normotensive subjects (P < 0.008), respectively. In controlled-hypertensive patients, late EPC number was positively associated with cardiac parasympathetic reserve during the expiration/inspiration maneuver (rho = 0.45, P = 0.031) and early EPC with brachial flow-mediated dilation (rho = 0.655; P = 0.049); also, late TNT number was inversely related to cardiac sympathetic response during the stress test (rho = -0.426, P = 0.045). EPC exposure to epinephrine or norepinephrine showed negative dose-response relationships on cell adhesion to fibronectin and collagen; both catecholamines stimulated early EPC growth, but epinephrine inhibited late EPC growth. In controlled-hypertensive patients, sympathetic overactivity/parasympathetic underactivity were negatively associated with EPC, suggesting that reducing sympathetic/increasing parasympathetic activation might favor endothelial repair.

Lack of RAAS inhibition by high-salt intake is associated with arterial stiffness in hypertensive patients.

HYPOTHESIS/INTRODUCTION: The relationship between salt intake, blood pressure and RAAS activation is still controversial, being that both high- and low-salt intakes are associated with cardiovascular events in a J-shaped curve pattern. We hypothesized that different patterns of RAAS response to dietary salt intake among hypertensives could be identified, while vascular damage would be related to high-salt intake plus absence of expected RAAS inhibition. OBJECTIVE: We aim to assess the relationship between sodium intake, RAAS and vascular stiffness in hypertension. MATERIALS AND METHODS: We screened 681 hypertensive patients for urinary/plasma electrolytes, renin, aldosterone and pulse wave velocity (PWV) under their usual salt intake level. RESULTS: After applying exclusion criteria, an inverse relation between urinary sodium and RAAS was observed in the 300 remaining subjects. Additionally, four types of response were identified: 1) Low (L) sodium (S)-Low RAAS, 2) LS-High (H) SRAAS, 3) HS-Low RAAS, 4) HS-High RAAS. We found no differences in age/BP among groups, but type 4 response individuals included more females and a higher pulse wave velocity. CONCLUSIONS: We showed a) an inverse salt-RAAS relation, b) an association between HS plus high RAAS with increased PWV that could identify a higher-risk hypertensive condition.

Sodium intake is associated with parasympathetic tone and metabolic parameters in mild hypertension.

BACKGROUND: Although the impairment of parasympathetic cardiac control was described in hypertensives submitted to a high salt diet, the impact of this autonomic abnormality on metabolic and inflammation markers in patients with mild hypertension has not been explored. METHODS: Four hundred and ninety mild essential hypertensive patients (144 ± 9/94 ± 9 mm Hg, 49.5 ± 13.9 years, 67.9 % male) were studied. Dietary sodium intake was estimated by measuring 24-h urinary sodium excretion (UNa), and the patients were classified according to UNa levels as follows: low (<50 mEq/l), medium (50-99 mEq/l), and high UNa (≥100 mEq/l). Parasympathetic tone was evaluated by assessing heart rate recovery (HRR) after an exercise stress test. HRR, plasma lipids, glucose metabolism, and inflammatory biomarkers were compared across UNa groups. RESULTS: HRR and high-density lipoprotein (HDL)-cholesterol were progressively lower, and insulin (INS), homeostasis model assessment of insulin resistance (HOMAir), ultrasensitive-C-reactive protein (usCRP) were progressively higher across increasing UNa groups. In the low and medium UNa groups, HDL-cholesterol was higher and CRP was lower than that in high UNa (P < 0.01 and P < 0.05, respectively) (Dunnett post-hoc test). In the low UNa group, triglycerides (TGs), INS, and HOMAir were lower than that in high UNa (P < 0.05). Multiple linear regression analysis showed that UNa, HOMAir, and heart rate (HR) were negatively associated with HRR (P < 0.0001, P < 0.0001, and P = 0.001, respectively). CONCLUSIONS: In the essential hypertensive patients studied high sodium intake is associated with parasympathetic inhibition, lipid disturbances, and inflammation. Studies designed to assess causality between sodium intake and metabolic and autonomic status are needed to evaluate the relevance of controlling sodium intake, especially in hypertensive patients.

Identificación no invasiva de ateroesclerosis subclínica en individuos con psoriasis / Non-invasive identification of subclinical atheroesclerosis

Antecedentes. La psoriasis es una enfermedad inflamatoria crónica multisistémica que implica un riesgo cardiovascular aumentado, incluidos enfermedad coronaria, infarto de miocardio y muerte de causa cardiovascular, sobre todo en pacientes jóvenes y con psoriasis más graves. Esto se debe a una aterogénesis precoz y en ocasiones subclínica, que podría ser identificada de manera no invasiva mediante estudios vasculares de vasos periféricos. Objetivos. a) identificar la presencia de ateroesclerosis subclínica en pacientes con psoriasis; b) establecer su valor predictivo independientemente de otros factores de riesgo cardiovascular. Diseño. Estudio de cohorte, prospectivo, controlado. Métodos. Se incluyeron 175 pacientes consecutivos, un grupo con psoriasis (GP, n:35) y un grupo control (GC, n:140), a quienes se les efectuó estudios de identificación de placas de ateroesclerosis y de elasticidad arterial en vasos carotídeos extracraneales y femorales. Resultados. El score de Framingham en los pacientes de ambos grupos fue bajo (7 ± 2,3

vs. 5,7 ± 1,8

; GP vs. GC respectivamente; p = .003), mientras que el score de riesgo vascular determinado según la alteración de parámetros de ateroesclerosis subclínica evaluados fue mayor en el GP (2,9 ± 1,2 vs. 2,2 ± 0.08; p = .002). La rigidez de la pared arterial se halló significativamente incrementada en el GP (EIM 0,7 ± 0,2 vs. 0,63 ± 0,1 mm, p< 0.001), donde se observó una prevalencia mayor de placas ateroescleróticas (94

vs. 62,5

Background. Psoriasis is a chronic multisystem inflammatory disease that involves an increasedcardiovascular risk as heart disease, myocardial infarction and cardiovascular death, especially inyounger patients and severe psoriasis. This is due to early atherogenesis, and sometimes to a subclinicalcourse, which could be identified by non invasive vascular studies of peripheral vessels.Objectives. a) Identify the presence of subclinical atherosclerosis in patients with psoriasis; b)Determine its predictive value independently of other cardiovascular risk factors.Design. Cohort, prospective, controlled trial. Methods. 175 consecutive patients were included, a Psoriatic Group (PG, n:35) and a Control Group(CG, n:140) where identified, and submited to studies for identification of atherosclerotic plaquesand arterial elasticity in extracranial carotids and femoral vessels.Results. The Framingham scores in patients of both groups was low (7 ± 2.3

vs. 5.7 ± 1.8

;GP vs. GC respectively, p = .003) while the vascular risk score, determined by the alteration ofsubclinical atherosclerosis parameters, was higher in the GP (2.9 ± 1.2 vs. 2.2 ± 0.08, p = .002).The arterial wall stiffness was found significantly increased in the GP (EIM 0.7 ± 0.2 vs 0.63 ± 0.1mm, p< 0.001), where a higher prevalence of atherosclerotic plaques (94

vs. 62.5

, p = .001) la mayoría de alta vulnerabilidad. Conclusiones. El uso de técnicas no invasivas que faciliten la detección precoz de pacientes psoriásicos con enfermedad subclínica de la pared arterial, permitiría evaluar correctamente el riesgo, que puede ser subestimado si sólo se realizan estudios clínicos de los factores de riesgoconvencionales. (AU)

, p = .001),mostly of high vulnerability, was also observed.Conclusions. The use of non invasive techniques that facilitate early detection of psoriaticindividuals with subclinical arterial wall disease, would allow a proper assessment of risk whichmay be underestimates by only clinical assessment of conventional risk factors.(AU)

Identificación no invasiva de ateroesclerosis subclínica en individuos con psoriasis / Non-invasive identification of subclinical atheroesclerosis

Antecedentes. La psoriasis es una enfermedad inflamatoria crónica multisistémica que implica un riesgo cardiovascular aumentado, incluidos enfermedad coronaria, infarto de miocardio y muerte de causa cardiovascular, sobre todo en pacientes jóvenes y con psoriasis más graves. Esto se debe a una aterogénesis precoz y en ocasiones subclínica, que podría ser identificada de manera no invasiva mediante estudios vasculares de vasos periféricos. Objetivos. a) identificar la presencia de ateroesclerosis subclínica en pacientes con psoriasis; b) establecer su valor predictivo independientemente de otros factores de riesgo cardiovascular. Diseño. Estudio de cohorte, prospectivo, controlado. Métodos. Se incluyeron 175 pacientes consecutivos, un grupo con psoriasis (GP, n:35) y un grupo control (GC, n:140), a quienes se les efectuó estudios de identificación de placas de ateroesclerosis y de elasticidad arterial en vasos carotídeos extracraneales y femorales. Resultados. El score de Framingham en los pacientes de ambos grupos fue bajo (7 ± 2,3% vs. 5,7 ± 1,8%; GP vs. GC respectivamente; p = .003), mientras que el score de riesgo vascular determinado según la alteración de parámetros de ateroesclerosis subclínica evaluados fue mayor en el GP (2,9 ± 1,2 vs. 2,2 ± 0.08; p = .002). La rigidez de la pared arterial se halló significativamente incrementada en el GP (EIM 0,7 ± 0,2 vs. 0,63 ± 0,1 mm, p< 0.001), donde se observó una prevalencia mayor de placas ateroescleróticas (94% vs. 62,5%, p = .001) la mayoría de alta vulnerabilidad. Conclusiones. El uso de técnicas no invasivas que faciliten la detección precoz de pacientes psoriásicos con enfermedad subclínica de la pared arterial, permitiría evaluar correctamente el riesgo, que puede ser subestimado si sólo se realizan estudios clínicos de los factores de riesgoconvencionales.

Background. Psoriasis is a chronic multisystem inflammatory disease that involves an increasedcardiovascular risk as heart disease, myocardial infarction and cardiovascular death, especially inyounger patients and severe psoriasis. This is due to early atherogenesis, and sometimes to a subclinicalcourse, which could be identified by non invasive vascular studies of peripheral vessels.Objectives. a) Identify the presence of subclinical atherosclerosis in patients with psoriasis; b)Determine its predictive value independently of other cardiovascular risk factors.Design. Cohort, prospective, controlled trial. Methods. 175 consecutive patients were included, a Psoriatic Group (PG, n:35) and a Control Group(CG, n:140) where identified, and submited to studies for identification of atherosclerotic plaquesand arterial elasticity in extracranial carotids and femoral vessels.Results. The Framingham scores in patients of both groups was low (7 ± 2.3% vs. 5.7 ± 1.8%;GP vs. GC respectively, p = .003) while the vascular risk score, determined by the alteration ofsubclinical atherosclerosis parameters, was higher in the GP (2.9 ± 1.2 vs. 2.2 ± 0.08, p = .002).The arterial wall stiffness was found significantly increased in the GP (EIM 0.7 ± 0.2 vs 0.63 ± 0.1mm, p< 0.001), where a higher prevalence of atherosclerotic plaques (94% vs. 62.5%, p = .001),mostly of high vulnerability, was also observed.Conclusions. The use of non invasive techniques that facilitate early detection of psoriaticindividuals with subclinical arterial wall disease, would allow a proper assessment of risk whichmay be underestimates by only clinical assessment of conventional risk factors.

Non invasive vascular evaluation and subclinical atherosclerosis: a new perspective to evaluate cardiovascular risk.

Techniques as Intima Media Thickness (IMT) and (Pulse Wave velocity) PWV have been strongly suggested by European and American Guidelines to assess subclinical ahterosclerotic vascular disease as target organ damage, and when they are present, they have been clearly associated to an increased risk of cardiovascular complications and death.

Estrés psicosocial y baja resiliencia, un factor de riesgo de hipertensión arterial / Psychosocial Stress and Low Resilience: a Risk Factor for Hypertension

Introducción El estrés psicosocial crónico (EPC) fue propuesto como un factor de riesgo cardiovascular (FRC); sin embargo, la complejidad y la falta de medidas objetivas para evaluarlo, unidas al hecho de que no todas las personas reaccionan ante él de igual manera, determinaron que en la actualidad no se cuente con estudios concluyentes al respecto. Objetivos Determinar si la baja resiliencia (BR) frente al EPC se asocia con hipertensión arterial y daño de órgano blanco en pacientes ambulatorios libres de tratamiento que concurren a realizarse un examen periódico de salud y comprobar si esta asociación tiene relación con el patrón de activación neurohormonal. Material y métodos Se realizó un estudio preliminar, observacional transversal, en el que se enrolaron en forma consecutiva 53 individuos, 32 varones y 21 mujeres. Los pacientes completaron dos cuestionarios: uno para medir EPC y el otro, la Escala de Resiliencia de Connor-Davidson. Quedaron divididos en cuatro grupos: 1, sin EPC y con resiliencia normal (RN); 2, sin EPC y con baja resiliencia (BR); 3, con EPC y RN; 4, con EPC y BR. Resultados El porcentaje de hipertensos fue superior en el grupo 4 (p < 0,001), como también el de individuos con incremento de la circunferencia de la cintura (ICC) (p = 0,05). Si bien los niveles de noradrenalina, cortisol y ácido vanililmandélico fueron ligeramente superiores en el grupo 4, las diferencias no alcanzaron significación estadística. Para determinar si el EPC unido a BR es un factor de riesgo para el desarrollo de hipertensión arterial se empleó un modelo de regresión logística, controlado por confundidores; el odds ratio fue de 10,9 con intervalos de confianza del 95%, inferior de 1,8 y superior de 65,2. Conclusiones Datos preliminares sugieren que individuos con EPC unido a BR tienen un riesgo alto para el desarrollo de hipertensión arterial.

Background Chronic psychosocial stress (CPSS) has been proposed as a risk factor for cardiovascular disease (CVD); yet there are not conclusive studies supporting this theory due to the complexity and the lack of objective assessment measures, together with the absence of homogeneous reactions towards CPSS. Objectives To determine the presence of an association between low resilience (LR) to chronic PSS and hypertension and target organ damage in untreated outpatients undergoing a routine health examination, and to determine whether this association is related to the pattern of neurohumoral activation. Material and Methods We conducted a preliminary observational and cross-sectional study that enrolled 53 consecutive patients, 32 men and 21 women. The patients answered two questionnaires: one measured CPSS and the other the Connor-Davidson Resilience Scale. Patients were divided into four groups: 1, no CPSS and normal resilience (NR); 2, no CPPS and low resilience (LR) 3, with CPSS and NR; 4 with CPSS and LR. Results The prevalence of hypertension and increased waist circumference (IWC) was greater in group 4 (p<0.001 and p=0.05, respectively). The plasma levels of norepinephrine, cortisol and vanillyl mandelic acid were slightly increased in group 4, yet these differences were not significant. A logistic regression model was used to control for confounding in order to determine whether CPPS together with LR constitute a risk factor for the development of hypertension; odds ratio, 10.9, 95% CI: 1.7-65.2. Conclusions These preliminary data suggest that subjects with CPPS and LR have high risk for the development of hypertension.