Rápida cicatrización de la úlcera venosa con técnica TAPIRS (ecoesclerosis del eje axial, perforantes y terminal insuficientes) más vendaje multicapa. Ensayo clínico / Rapid healing of venous ulcers with terminal, axial and perforator interruption of the reflux source (TAPIRS) plus multilayer bandage: A clinical trial

INTRODUCCIÓN: Las úlceras venosas (UV) son las úlceras más frecuentes de las extremidades, y generan morbilidad importante y altos costos para los sistemas de salud. Las técnicas quirúrgicas usadas para el control de la hipertensión venosa han venido siendo remplazadas con mayor frecuencia por procedimientos mínimamente invasivos como la escleroespuma. OBJETIVO: Determinar el tiempo de cicatrización de la UV con un protocolo de manejo que incluyó la oclusión venosa endoluminal con escleroespuma ecoguiada del eje axial, perforantes y terminal insuficientes (técnica TAPIRS) más curaciones con vendaje multicapas (VM) hasta la cicatrización de la herida. MATERIAL Y MÉTODOS: Ensayo clínico prospectivo no controlado (cuasiexperimental) en pacientes con UV (CEAP C6) realizado en la consulta externa de cirugía vascular, durante 2013-2014. Se incluye a 17 pacientes mayores de 18 años, portadores de una UV con eje axial insuficiente, e índice tobillo-brazo mayor a 0,8. Se analizaron en total 17 extremidades. Se realizó inyección de escleroespuma (técnica de Tessari) usando polidocanol al 3% en el sistema venoso superficial con oclusión del eje venoso axial, perforantes y terminal asociados al lecho de la úlcera, guiada por ecodoppler junto con aplicación de VM y curación según las condiciones de la herida. Se realizaron controles clínicos y fotográficos en cada curación, aplicación de VM hasta el cierre de la UV y controles ecográficos a la 4 y 12 semanas. RESULTADOS: El promedio de edad fue de 56,4 años, la duración de la úlcera activa previamente al tratamiento fue de 2,96 años, todas las UV cicatrizaron antes de las 7 semanas, con una tasa de cierre de 3,92 cm2/semana y el tiempo de cierre de la úlcera fue de 3,92 semanas (24 días). CONCLUSIÓN: La oclusión endoluminal venosa usando la técnica TAPIRS (cierre de los ejes axiales, perforantes y terminales insuficientes con escleroespuma ecoguiada) junto a la aplicación de VM es una técnica que favorece la rápida cicatrización de las UV

INTRODUCTION: Chronic venous ulcers (CVU) are the most common ulcers occurring in the lower limbs, having a high morbidity and place a high financial strain on the health system. The traditional surgical techniques are being replaced by minimally invasive procedures, such as foam sclerotherapy. OBJECTIVE: The aim of this study was to determine CVU healing times and rates using the terminal, axial and perforator interruption of the reflux source (TAPIRS) protocol, which included an endoluminal venous occlusion with ultrasound-guided foam and a multilayer bandage system until achieving ulcer healing. MATERIAL AND METHODS: A prospective uncontrolled trial was conducted on patients with chronic venous leg ulcers (CEAP [clinical, etiological, anatomical and pathological elements] C6) during 2013 and 2014. A total of 17 patients aged 18 years and over, presenting with venous insufficiency, CVU, and an ankle-brachial index greater than 0.8, were included, and total of 17 limbs were analysed. All of the patients were subjected to endoluminal occlusion with ultrasoundguided foam in the axial superficial venous system and perforator and terminal veins near to the ulcer, using Tessari method with 3% polidocanol. Follow-up was carried out at every week and a doppler test was conducted after 4 and 12 weeks. RESULTS: The mean age of the patients was 56.4 years. The active ulcer duration prior to treatment was 2.96 years. The study showed that all CVU were healing before 7 weeks, the healing rate was 3.92 cm2/week, and the time until the ulcer was healed was 3.53 weeks (24 days). CONCLUSIONS: The minimally invasive ablation of terminal, axial and perforator reflux with compression in patients is a technique that leads to faster healing times of CVU

Estudio de la insuficiencia venosa crónica mediante ecografía Doppler y realización de cartografía venosa / Doppler ultrasound study and venous mapping in chronic venous insufficiency

La insuficiencia venosa crónica (IVC) de las extremidades inferiores es una enfermedad muy prevalente. La ecografía Doppler se ha establecido en las últimas décadas como el método de elección en el estudio de esta patología, por lo que resulta imprescindible ante una eventual indicación quirúrgica. El objetivo de este trabajo es establecer una metodología en la exploración, incluyendo la realización de cartografía y el marcaje prequirúrgico. Para ello revisaremos la anatomía venosa de los miembros inferiores y la fisiopatología de la IVC explicando los conceptos hemodinámicos básicos y la terminología necesarios para la realización de un informe radiológico que permita una adecuada planificación terapéutica y comunicación con otros especialistas. Explicaremos brevemente la estrategia CHIVA (cura hemodinámica de la insuficiencia venosa ambulatoria), método quirúrgico mínimamente invasivo que tiene como objetivo restaurar la hemodinámica venosa sin extirpar la vena safena (AU)

Chronic venous insufficiency of the lower limbs is very prevalent. In recent decades, Doppler ultrasound has become the method of choice to study this condition, and it is considered essential when surgery is indicated. This article aims to establish a method for the examination, including venous mapping and preoperative marking. To this end, we review the venous anatomy of the lower limbs and the pathophysiology of chronic venous insufficiency and explain the basic hemodynamic concepts and the terminology required to elaborate a radiological report that will enable appropriate treatment planning and communication with other specialists. We briefly explain the CHIVA (the acronym for the French term "cure conservatrice et hémodynamique de l'insuffisance veineuse en ambulatoire" = conservative hemodynamic treatment for chronic venous insufficiency) strategy, a minimally invasive surgical strategy that aims to restore correct venous hemodynamics without resecting the saphenous vein (AU)

G-CSF induced arteriogenesis in humans: molecular insights into a randomized controlled trial.

AIMS: Recent data have demonstrated the feasibility of therapeutic induction of coronary collateral growth (arteriogenesis); however, mechanisms of action of such therapeutic collateral stimulation in humans are unknown. The aim of this study was to evaluate potential mechanisms, especially the involvement of arteriogenesis-relevant genes. METHODS AND RESULTS: A total of 52 patients were randomized into two groups: subcutaneous G-CSF (10 µg/kg; n=26) or placebo (n=26). Before and after this 2-week treatment, collateral-flow index (CFI) was determined by simultaneous measurement of mean aortic, distal coronary occlusive and central venous pressure. CD34+ endothelial progenitor cells (EPC) and monocytes were quantified before, during and after treatment; gene-expression analysis of monocytes was performed with real-time polymerase chain reaction (RT-PCR). G-CSF lead to a significant increase of EPC and monocytes (4.8 and 2.6 fold, p < 0.05); for both cell types, the extent of increase correlated with CFI increase (r=0.23 and 0.14, p < 0.05). G-CSF also induced a change in gene expression of pro-and anti-arteriogenic genes in monocytes. Among nine assessed genes, three were found to be differentially regulated (IL8, JAK2, and PNPLa4; p < 0.05). CONCLUSIONS: The mechanism of induction of collateral growth by G-CSF is related to an increase of EPC and of peripheral monocytes. It also leads to a change toward a pro-arteriogenic gene expression in peripheral monocytes.

Heritability of venous biomechanics.

OBJECTIVE: Altered venous biomechanics may contribute to the pathogenesis of venous diseases, and their heritability is less known. METHODS AND RESULTS: Seventy-eight monozygotic twin pairs (aged 42.4 ± 16.8 years) and 24 same-sex dizygotic twin pairs (aged 50.5 ± 16.1 years) were examined. Anteroposterior and mediolateral diameters of the common femoral vein were measured by ultrasonography. Measurements were made both in supine and in standing body positions, with or without controlled forced expiration (Valsalva test). High correlation of diameter, capacity, and distensibility values was found between twin pairs. The univariate heritability (A), shared (C), and unshared (E) environmental effects model has shown 39.3% genetic component of the variance of low pressure, 37.9% of high-pressure venous capacity, and 36.4% of maximal capacity changes, even after elimination of sex, age, and body weight effects. Bivariate Cholesky analysis revealed substantial covariance of inherited body weight and venous capacity components (57.0%-81.4%). CONCLUSIONS: Femoral vein capacity and elasticity depend ≈30% to 40% on genetic factors, and this value in the standing body position can reach 50%. A relatively high genetic covariance was found between weight and femoral vein capacity and elasticity. Our work might yield some new insights into the inheritance of venous diseases that are associated with altered venous biomechanics and help elucidate the involved genes.

The heart communicates with the endothelium through the guanylyl cyclase-A receptor: acute handling of intravascular volume in response to volume expansion.

Atrial natriuretic peptide (ANP) regulates arterial blood pressure and volume. Its guanylyl cyclase-A (GC-A) receptor is expressed in vascular endothelium and mediates increases in cGMP, but the functional relevance is controversial. Notably, mice with endothelial-restricted GC-A deletion [EC GC-A knockout (KO) mice] exhibit significant chronic hypervolemic hypertension. The present study aimed to characterize the endothelial effects of ANP and their relevance for the acute regulation of intravascular fluid volume. We studied the effect of ANP on microvascular permeability to fluorescein isothiocyanate-labeled albumin (BSA) using intravital microscopy on mouse dorsal skinfold chambers. Local superfusion of ANP (100 nm) increased microvascular fluorescein isothiocyanate-BSA extravasation in control but not EC GC-A KO mice. Intravenous infusion of synthetic ANP (500 ng/kg x min) caused immediate increases in hematocrit in control mice, indicating intravascular volume contraction. In EC GC-A KO mice, the hematocrit responses were not only abolished but even reversed. Furthermore, acute vascular volume expansion, which caused release of endogenous cardiac ANP, did not affect resting central venous pressure of control mice but rapidly and significantly increased central venous pressure of EC GC-A KO mice. In cultured lung endothelial cells, ANP provoked cGMP-dependent protein kinase I-mediated phosphorylation of vasodilator-stimulated phosphoprotein. We conclude that ANP, via GC-A, enhances microvascular endothelial macromolecule permeability in vivo. This effect might be mediated by cGMP-dependent protein kinase I-dependent phosphorylation of vasodilator-stimulated phosphoprotein. Modulation of transcapillary protein and fluid transport may represent one of the most important hypovolemic actions of ANP.