Microcirculatory Dysfunction in Chronic Venous Insufficiency (CVI)

Abstract

The elevated ambulatory pressure in the peripheral venous system of chronic venous insufficiency (CVI) patients manifests itself not only in the form of disturbed macrocirculation but also and particularly in microangiopathic changes. For this reason, it is closely correlated with trophic disorders of the skin and can ultimately lead to ulceration. Using microcirculation research techniques, we are able to provide clear evidence of a typical microangiopathy in chronic venous insufficiency. Fifty CVI patients in Widmer stages I, II, and III were examined with fluorescence video microscopy, intravital video capillaroscopy, transcutaneous oxygen partial pressure measurement, TcpO2 and laser Doppler flowmetry. The effects of compression therapy with individually fitted compression stockings on capillary morphology were studied over a period of 4 weeks in 20 CVI patients in Widmer stages I and II. The capillary pressure was measured during simulated muscle contraction using a servo‐null micropressure system. We periodically drew blood from the dorsalis pedis vein and a brachial vein of 11 healthy test persons and 8 patients with stage III CVI during experimental venous hypertension in order to evaluate the expression pattern of leukocyte adhesion molecules involved in inflammation: LFA‐1 (CD11a), Mac‐1 (CD11b), p150,95 (CD11c), CD18, VLA‐4 (CD49d), and L‐selectin (CD62L). In the same patients, we used immunohistochemical methods to examine clinically unaffected skin and the skin near an ulcer, focusing on the adhesion molecules ICAM‐1, VCAM‐1, and E‐selectin. The microangiopathic changes observed with worsening clinical symptoms include a decrease in the number of capillaries, glomerulus‐like changes in capillary morphology, a drop in the oxygen content (tcpO2) of the skin, increased permeability of the capillaries to low‐molecular‐weight substances, increased laser Doppler flux reflecting elevated subcutaneous flow, and diminished vascular reserve. These microangiopathic changes worsen in linear proportion to the clinical severity of chronic venous insufficiency. In patients with venous ulcerations, the baseline expression of LFA‐1 and VLA‐4 on lymphocytes, Mac‐1 expression on the myeloid cell line, and L‐selectin expression on all three cell lines was not significantly different from that in healthy controls. During orthostatic stress, there was a significant reduction in the expression of L‐selectin in blood cells collected at foot level in the controls (p = 0.002), but not in the patients. Clinical improvement by compression therapy was accompanied by an increase in the number of nutritive capillaries, while the diameter of the capillaries and the dermal papillae was reduced. When ulcers healed in a short period (<6 weeks), we observed a concomitant increase in the number of capillaries (p < 0.05). Microangiopathy appears before trophic disorders of the skin develop. Even trophically normal skin areas may have dilated nutritive capillaries, an early sign of disturbed skin perfusion. These changes represen...

Evaluation of pain associated with chronic venous insufficiency in Spanish postmenopausal women

“…16,17 For the photoplethysmography test, women performed a series of calf exertion exercises to empty the veins, with 10 dorsiflexion movements of the ankle in both limbs in time with a metronome. This numerical quantification of venous function is significantly influenced by the pumping ability of the calf muscle.…”

Lower Extremity Venous Disorders

“…21 As the microangiopathy persists, there is leakage of micromolecules and macromolecules into the interstitial tissues, causing damage to the dermis and adipose tissue. 22,28 When the inflammatory process becomes chronic, there is a release of cytokines, which encourages vascular proliferation. 24 This process is similar to that of inner vein wall damage from the monocyte-macrophage system, neutrophils, T-lymphocytes, and plasma cells that produce intravascular lesions within the veins.…”

Systemische medikamentöse Therapie von chronischen Venenerkrankungen

“…1). In spä te ren Sta di en der CVI fin det sich eine Ra re fi zie rung der Ka pil lar dich te [19,31].…”

“…Ein we sent li cher pa tho ge ne ti scher Faktor sind au ßer dem die ver mehr te Ad hä sion von Leu ko zy ten am Ge fäßendo thel und kon se ku ti ve Me cha nis men [8,19,29]. > Das Zu sam men spiel der pa tho phy sio lo gi schen Me cha nis men führt zu ei nem stän dig er höh ten Ge webs druck Das Zu sam men spiel der pa tho phy sio lo gischen Me cha nis men führt zu ei nem stän-dig er höh ten Ge webs druck, dem Ab bau elas ti scher Struk tu ren in Ve nen, Lymphge fäßen und im Ge we be.…”

“…1). In spä te ren Sta di en der CVI fin det sich eine Ra re fi zie rung der Ka pil lar dich te [19,31].In der Fol ge des Über drucks im ve nö-sen Sys tem kommt es au ßer dem zu Ver än-de run gen der Ge fäß wand be schaf fen heit; der Aus tritt von Fib rino gen aus dem Kapil lar raum in den Pe ri ka pil lar raum wird be güns tigt. Das ver mehrt aus tre ten de Fibrino gen po ly me ri siert ne ben den Ka pilla ren als Fib rin und nimmt eine man schetten ar ti ge An ord nung als pe ri ka pil lä re Fibrin man schet te an.…”