Endothelial dysfunction Venous insufficiency and varices
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1 Endothelial dysfunction Venous insufficiency and varices Roman Gardlík, MD, PhD Institute of Pathophysiology Institute of Molecular Biomedicine
2 Endothelium A type of epithelium that lines the interior surface of blood vessels and lymphatic vessels Single layer of squamous endothelial cells with tight junctions
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5 Figure 1. Endothelium and permeability. William C. Aird Circ Res. 2007;100: Copyright American Heart Association, Inc. All rights reserved.
6 Endothelial cell Large amounts of vesicles and caveolae along the luminal surface - transendothelial transport of biologically active substances
7 Endothelium Mesodermal origin EC are aligned and elongated in direction of flow EC line the entire circulatory system one of the largest organ systems Unique functions
8 Endothelium Fluid filtration (glomeruli) Barrier function Blood vessel tone (vasodilation and vasoconstriction) Hemostasis Hormone trafficking Inflammation - neutrophil recruitment Angiogenesis Secretion of mediators normal vascular function
9 Barrier function
10 Figure 2. Endothelium and leukocyte trafficking. William C. Aird Circ Res. 2007;100: Copyright American Heart Association, Inc. All rights reserved.
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12 Figure 4. Mechanisms of EC heterogeneity. William C. Aird Circ Res. 2007;100: Copyright American Heart Association, Inc. All rights reserved.
13 Endothelial dysfunction Systemic pathological state of the endothelium Imbalance between vasodilating and vasoconstricting substances produced by the endothelium Shift of the balance in favour of vasoconstrictive, pro-inflammatory and pro-thrombotic effects Mainly due to reduced bioavailability and bioactivity of nitric oxide (NO)
14 Vasodilation Nitric oxide EDHF Prostacyclin Acetylcholine Bradykinin
15 Nitric oxide Most abundant free radical in the body Halflife of NO is affected by its chemical reaction and inactivation by superoxide anion. O NO ONOO -
16 Shear stress A stress state where the stress force is paralell to the surface of the vessel (ass opposed to normal stress, where the stress is vertical) Force exerted on vessel wall / cross-sectional area NO is released after shear stress in the vessel vasodilation NO mediated vasodilation decreases shear stress If shear stress is chronic upregulation of inflammatory cytokines endothelial dysfunction
17 Protective effects of NO Smooth muscle relaxation and vasodilation Lowering blood pressure Reducing proliferation of vascular smooth muscle Inhibition of platelet aggregation Inhibition of expression of VCAM and ICAM
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19 Vasoconstriction Endothelin-1 Prostaglandin H 2 Thromboxane A 2 ROS Endothelium-bound ACE angiotensin II
20 Regulatory Functions of the Endothelium Normal Dysfunction Vasodilation NO, PGI2, EDHF, BK, C-NP Thrombolysis tpa, Protein C, TF-I, vwf Vasoconstriction ROS, ET-1, TxA2, A-II, PGH2 Thrombosis PAI-1, TF-α, Tx-A2 Platelet Disaggregation NO, PGI2 Adhesion Molecules CAMs, P,E Selectins Antiproliferation NO, PGI2, TGF-, Hep Lipolysis LPL Growth Factors ET-1, A-II, PDGF, ILGF, ILs Inflammation ROS, NF- B Vogel R
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23 Consequences of ED EC as progenitor of atherosclerosis (ED is present long before onset of symptoms) EC as predictor of future cardiovascular events
24 Oxidative stress Imbalance between production of reactive oxygen species and ability of the system to detoxify the reactive intermediates or to repair the damage Key mechanism of endothelial dysfunction OS + ED are major factors for atherosclerosis
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29 ED in disease Cardiovascular disease Diabetes Transplant vasculopathy Autoimmune diseases Celiac disease and irritable bowel syndrome Hematologic disorders Neurocognitive disorders Cirrhosis
30 1. ED in diabetes T1DM, T2DM Pathogenesis unclear Multifactorial etiology of ED 1. Insulin resistance 2. Pro-inflammatory signalling 3. Oxidative stress 4. Protein kinase C 5. Hyperglycemia
31 Insulin resistance in ED Insulin activates vasoprotective pathways PI3K/Akt enos expression and activation In contrast, MAPK/ERK pathway promotes ET-1 and cellular proliferation In physiological conditions PI3K predominates Insulin resistance PI3K deficiency, MAPK predominates proatherogenic signalling
32 Roberts and Porter 2013
33 Pro-inflammatory signalling in ED Adipose tissue produces inflammatory cytokines TNFalpha, free fatty acids, RAGE activate NFkB that further stimulates expression of inflammatory genes in endothelium Reduction of NO expression
34 Oxidative stress in ED OS as a unifying mechanism of endothelial injury OS leads to diminished NO bioavailability Direct degradation of NO Alterations in functional capacity of enos
35 Protein kinase C in ED PKCbeta is endothelial isoform of serin/threonine kinase Main contributor to ED observed in diabetes High FFA and glucose high DAG (de novo from glucose) activation of PKCbeta induction of downstream events: ET-1 VCAM ICAM NADPH oxidase NFkB Inhibition of PI3K and enos
36 Hyperglycemia in ED 1. PKC activation 2. Activation of hexosamine pathway PKC 3. Activation of polyol pathway PKC 4. Formation of advanced glycation end-products Unifying mechanisms is ROS overproduction
37 2. ED in hypertension ED as an early event in pathophysiology of essential hypertension that contributes to subclinical target organ damage and progression of atherosclerosis Defective endothelial L-arginine/NO pathway Impaired responsiveness to exogenous NO Reduced generation of platelet NO In the presence of oxidatove stress Pro-inflammatory, pro-atherosclerotic, prothrombotic phenotype
38 Mechanism of ED in hypertension Hypertension as cause rather than consequence of endothelial dysfunction Hypertension-induced oxidative stress
39 Measuring endothelial function 1950s endothelium as a dynamic organ with diverse capabilities Invasive methods 1992 Celermajer et al. proposed first non-invasive method for assessment of endothelial function - diameter of superficial femoral and brachial arteries At rest During reactive hyperemia (endothelium-dependent dilatation) After sublingual nitroglycerin (endothelium-independent dilatation)
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41 Vascular markers of ED Quantitative coronary angiography MRI PET Invasive measurement of forearm blood flow (FBF) by venous occlusion plethysmography
42 Vascular markers of ED Non-invasive measurement Flow-mediated dilation (FMD) macrovascular function Peripheral arterial tonometry microvascular function Laser Doppler flowmetry
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45 Biomarkers of ED Assymetric dimethylarginine ADMA endogenous competitive inhibitor of NO synthase Oxidized LDL Endothelial microparticles Endothelial progenitor cells
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47 ED in periodontitis
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51 ED treatment Treatment should target the underlying comorbidity that lead to ED Life style modification diet, exercise, smoking weight reduction NO pathways L-arginine, PDE-I Receptor and enzyme pathways beta blockers, ACE-I, angiotensin receptor blockers, statins, aspirin
52 Secondary endothelial therapy Preserve the function of the already injured endothelium to delay progression of cardiovascular disease Statins, ACE-I, beta blockers, endothelin antagonists
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54 Control questions What are the 3 main vasodilators? Define shear stress How oxidative stress leads to ED? Which functions of endothelium are dysbalanced / predominate in ED? What is the standard method for measurement of endothelial dysfunction?
55 Endothelial barrier dysfunction in septic shock NO and vasodilation Vascular endothelium uram vascular-endothelium/
56 A short break
57 Venous insufficiency Varices
58 Venous system of lower limbs Superficial Perforator Deep
59 Chronic venous disease Condition in which the veins cannot pump enough blood back to the heart 20% of Western population Varicose veins Chronic venous insufficiency
60 Chronic venous disease Causes: Deep vein thrombosis Arteriovenous fistula Phlebitis Thrombophilia Obesity
61 Varicose veins Dilated, often palpable, subcutaneous veins with reversed blood flow Mostly in legs 30% of population (18% men, 42% women) Risk factors: unknown, age, sex, pregnancy, obesity, family history
62 Pathogenesis Reflux Obstruction Varicose veins: Increased amount of collagen Decreased number of smooth muscle cells and elastin Disorganization of muscle components, disruption of elastin fibres and fibrosis Weakness of vein wall leads to dilatation and enlargement of the valve ring the vein is unable to work properly - reflux
63 Pathogenesis Descending theory the process starts proximally and expands distal Ascending theory tributaries become dilated and incompetent and only thereafter the main trunks and junctions
64 Pathogenesis Obstruction Acute obstruction occurs in deep vein thrombosis Chronic obstruction caused by post-thrombotic changes stenosis, occlusion, rigidity of vein wall Obstruction + reflux in 55% of symptomatic patients
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66 Evaluation Clinical features: limb pain, swelling, stasis, skin changes, ulceration Symptoms: itching, restless legs, nocturnal leg cramps, heaviness, discomfort Pain
67 Pain Assessed by visual-analogue scale, type and frequency of analgesic use Absent in 20% patients The only feature in 10% patients Is relieved by leg elevation, support stockings, walking
68 CEAP classification Clinical Etiologic Anatomical Pathophysiological CVI = C 3 -C 6
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70 CEAP
71 Adjunctive scoring system
72 Imaging Duplex ultrasound scan
73 Complications Deep vein thrombosis Skin changes Leg ulcers (3% patients) Bleeding Thrombophlebitis thrombus in superficial vein
74 Treatment
75 Treatment Goals: Alleviate symptoms Prevent severe complications (ulcers) 1. Endothermal ablation of the saphenous vein burn the vein from inside (radiofrequecy or laser) 2. Foam sclerotherapy 3. Surgery 4. Compression hosiery (only if no other intervention is suitable)
76 Advice Weight loss Light to moderate physical activity Avoid factors that make symptoms worse When and where to seek further medical help
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78 Treatment in pregnancy Pregnancy can exacerbate symptoms of varicose veins and cause new ones No intervention in pregnancy (increases risk of thrombosis) Compression hosiery should be used
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80 Control questions Two mechanisms of CVI What does CEAP mean? What is the link between CVI and ED? Diagnostic methods How to know the most up-to-date methods of therapy?
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