UNI ED Diseases of peripheral vessels l Lower limb ischemia Usually manifests by a pain during physical effort (walk, run) - intermittent claudications Intermittent claudication distance - can be walked by the patient before stopping due to ischemic pain In later stages steady pain - critical limb ischemia, skin defects, „marble" skin, necrosis Smoking and badly compensated DM play important roles in the etiology Lower limb ischemia - Fontaine classification • I) asymptomatic • II) intermittent claudications • Ha) above 200m lib) below 200m • III) pain at rest • IV) skin defects, gangrene Hemodynamically significant stenosis -narrowing by approx. 50 % Peripheral Arterial Disease Steal syndromes •Occur in case when a collateral vessel bypass a stenosis (incl. artificial bypass) •''Robin Hood'' - vasodilation in ischemic area redirects the blood supply from healthy part of circulation (''the poor stealing from the rich'') • subclavian steal syndrome - arm "steals" from the brain via vertebral artery -> loss of consciousness •^Reversed Robin Hood'' - drug-induced vasodilation in healthy area redirects the blood supply from ischemic area (here, the vasodilatory mechanisms are already at maximum - ''the rich stealing from the poor'') • coronary steal syndrome - strong vasodilators may paradoxically worsen ischemia (e.g. combination of nitrates with sildenafil) Steal syndromes - examples Subclavian steal syndrome Circle of Willis Coronary steal syndrome Other atherosclerotic diseases Renovascular hypertension (unilateral/bilateral stenosis - Goldblatt model) Intestinal infarction, renal infarction, abdominal angina... Treatment of atherosclerosis Treating rise factors (lifestyle intervention, antihypertenzives, antidiabetics) Systemic 1) Treatment of lipid metabolism disorders Statins (block cholesterol synhesis) Ezetimib (blocks cholesterol absorbtion) PCSK9 inhibitors (upregulate LDL-R) Fib rates (decrease VLDL production) Gene therapy in monogennic dyslipidemia 2) Treatment of inflammatory response IL-1 blockers Treatment 2 Local PTA - percutaneous transluminal angioplasty POBA: plain old bo loon angioplasty BMS: bare metal stent DES: drug-eluted stent covered by a cytostatic to prevent neointimal hyperplasia and restenosis BVS: bio-vascular scaffold degradable, lower inflamatory response and risk of thrombosis Bypass Arterial Venous graft Endarterectomy Balloon angioplasty or percutaneous transluminal angioplasty Balloon-tipped catheter Expanded stent ® 123RF.com Artery In-stent restenosis Result of smooth muscle cells proliferation But: some degree of proliferation is necessary to cover the stent and stabilize the subendothelial space, otherwise the risk of thrombosis increases I risk of restenosis in DES is accompanied by f risk of thrombosis in early phase, local cytostatics are clinically efficient only in a range of years Vasospastic disorders Disorders of small arterioles •spasms <-+ vasodilation •| sympathetic activity •Raynaud phenomenon • White: vasoconstriction, lack of blood, cold skin • Blue: | deoxyHb in capillary vasodilation and hypoxia • Red: blood flow restored, pain • Can be provoked by stress or cold Secondary vasospastic disorders Result from other diseases •Atherosclerosis •Connective tissue diseases •Vasculitis •Frostbites •Vibrations •Treatment: reduction of cod and stress, vasodilators Vasculitis • Inflammatory disorders based on immune pathology • Often immune complexes - 111 rol type in Gell and Coombs classification • Affects both microcirculation and larger vessels • Many vascular segments (x atherosclerosis) • Primary x secondary (rheumatoid arthritis, SLE, Sjogren syndrome) • Complications: Vasospasms Development of aneurysms Microthrombi Chronic venous insufficiency ^hydrostatic pressure at the venous end of a capillary Most often caused by venous valves insufficiency Deep venous thrombosis - asymmetric oedema Leg ulcers - most often of venous origin Increased filtration -> increased capillary permeability -> protein leak -> „fibrin cuff"-> tissue ischemia -> ulcer CVI classification Widmer: 1st stage: oedema 2nd stage: stiff oeadema with hyperpigmentation (hemosiderin -degradation product of ferritin) 3. stage: leg ulcer CEAP (clinical-etiology-anatomy-patophysiology) classification - detailed