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Heparin and Its Derivatives in the Treatment of Arterial Thrombosis: a Review

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Heparin and Its Derivatives in the Treatment of Arterial Thrombosis: a Review Veterinarni Medicina, 55, 2010 (11): 523–546 Review Article Heparin and its derivatives in the treatment of arterial thrombosis: a review M. Dvorak1, M. Vlasin2, M. Dvorakova3, P. Rauser2, L. Lexmaulova2, Z. Gregor1, R. Staffa1 12nd Department of Surgery, St. Anne’s University Hospital, Faculty of Medicine, Masaryk University, Brno, Czech Republic 2Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences, Brno, Czech Republic 3Department of Internal Medicine, Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic ABSTRACT: Arterial occlusion due to thrombosis caused by ruptured atherosclerotic plaques (Baba et al., 1975) has been recognized as a major cause of morbidity and mortality in western populations. Thrombosis may occur in various sections of arterial circulation, peripheral arteries of the limbs, coronary arteries, brain arteries, or both major and minor vessels within the abdominal cavity. The ultimate consequence is varying degrees of organ failure, mostly of ischemic origin. Arterial thrombosis represents a continuous problem, debilitating patients and decreasing their quality of life. Moreover, along with chronic heart failure, it can significantly decrease patient life expectancy. Arterial thrombosis results in ischemia, with serious systemic consequences, such as metabolic breakdown. The major goal of treatment remains fast and efficient recanalization – surgical, interventional or thrombolytic. To be able to prevent acute reocclusion with severe consequences (rhabdomyolysis, compartment syndrome, excessive tissue necrosis leading to limb amputation, etc.), several adjunctive treatment regimens have been advocated. Among others, thrombin inhibitors and platelet inhibitors have been widely used for both prophylaxis and adjunctive treatment. Direct thrombin inhibitors and antithrombin stimulators have been recognized as typical antithrombotic drugs. Direct (antithrombin-independent) thrombin inhibitors can be divided into two main categories: monovalent, active site inhibitors (argatroban, efegatran, inovastan, melagatran) and bivalent (hirudin, hirugen, hirulog, bivalirudin), while antithrombin stimulators represent standard (unfractionated) heparin (UFH) and its depolymerizing products – low molecular weight heparins (LMWH’s). Recently, a clear change in the main use of heparin, as well as low-molecular weight heparins has been advocated representing a shift from treatment and prophylaxis of deep vein thrombosis to prophylaxis of thromboembolic disease following vascular, cardiovascular or orthopedic surgery, treatment of unstable angina and prevention of acute myocardial infarction. The main effect of heparins lies in their anticoagulant activity. Heparins are involved in different pathways of the coagulation cascade with anticoagulant, antithrombotic, profibrinolytic, anti-aggregative, as well as anti-inflammatory effects. Moreover, there is a little doubt about their anti-proliferative and anti-ischemic activity (Penka and Bulikova, 2006). Unlike standard heparin, low-molecular weight heparins do not affect the patient’s general coagulation profile. Obviously, the difference in molecular weight results in different pharmacokinetic and pharmacodynamic properties of the agents. Key words: coagulation; arterial thrombosis; standard heparin; low-molecular weight heparins List of abbreviations ABI = axillary/...index, t-PA = tissue-type plasminogen activator, ADP = adenosin diphosphate, AG = angiography, AMI = acute myocardial infarction, APSAC = acylated plasminogen streptokinase activator complex, APTT = activated partial thromboplastin time, AS = acute stroke, AT = antithrombin, ATD = acute thromboembolic disease, CNS = central nervous system, DNA = deoxyribonucleic acid, DSA = digital subtractional angiography, DVT = deep vein thrombosis, FDP’s = fibrin – fibrinogen degradation products, HCII = heparin cofactor II, HIT = 523 Review Article Veterinarni Medicina, 55, 2010 (11): 523–546 heparin-induced thrombocytopenia, IHF = ischemic heart failure, LDL = low density lipoproteins, LLID = lower limb ischemic disease, LMWH = low-molecular weight heparin, LMWH’s = low-molecular weight heparins, MRA = magnetic resonance angiography, PAT = percutaneous aspiration thrombectomy, PDGF = platelet-derived growth factor, PTA = percutaneous transluminal angioplasty, PTCA = percutaneous transluminal coronary angioplasty, SCu-PA = single chain urokinase-type plasminogen activator, TFPI = tissue factor pathway inhibitor, UFH = unfractionated heparin, USG = ultrasonography, VSMC’s = vascular smooth muscle cells Contents 3.1. Effect of heparin on the coagulation cascade 3.2. Limitations of heparin 1. Atherosclerosis as the main cause of thrombosis 3.3. Pharmacokinetics of heparin 2. Arterial thrombosis of lower extremities 3.4. Monitoring of treatment by heparin 2.1. Definition and pathogenesis of arterial 3.5. Antidotes of heparin thrombosis 3.6. Effect of heparin on vascular smooth muscle 2.2. Etiology of an acute arterial thrombosis, cell proliferation Virchow’s triad 3.7. Indications of heparin 2.2.1. Thrombophylia 3.8. Side-effects of heparin 2.3. Clinical observations 3.8.1. Heparin-induced thrombocytopenia 2.4. Diagnostic protocol for patients with sus- – HIT pected acute peripheral thrombosis 3.8.2. Osteoporosis 2.5. Treatment options for acute peripheral 4. Low molecular weight heparins – LMWH’s thrombosis 4.1. Anticoagulation properties of LMWH’s 2.5.1. Surgical revascularization 4.2. Pharmacokinetics of LMWH’s 2.5.2. Interventional endovascular proce- 4.3. Efficacy and safety of LMWH’s in an animal dures model 2.5.3. Thrombolysis 4.4. LMWH’s in the prevention of arterial throm- 2.5.3.1. First generation thrombolytic bosis – clinical studies agents 4.5. Administration and monitoring of LMWH’s 2.5.3.2. Second generation thrombo- 5. Summary lytic agents 6. Conclusions 3. Heparin 7. References 1. Atherosclerosis as the main cause (IS), or peripheral thromboembolic disease, most of thrombosis frequently lower limb ischemic disease (LLID), ca- rotid and/or renal artery occlusion. Occlusion of peripheral vessels is in more than 90% Atherosclerosis can be defined as a degenerative of cases caused by atherosclerosis leading to throm- process, typically with inflammatory infiltration bosis. Chronic vasculitis, small aneurysms, acute of the vessel wall, accumulation of triglycerides embolic disease, or external compression of arter- and proliferation of fibrotic tissue. The early stage ies is observed less frequently. Atherosclerosis can of atherosclerosis is more or less characterized affect arteries of the lower limbs, carotid arteries, by penetration of atherogenic lipoproteins and brain arteries and, last but not least, coronary arteries inflammatory cells through the endothelial layer (Ferrieres et al., 2006). On the other hand, upper limb and their accumulation in the sub-endothelial arteries are only affected in extremely rare cases. space. Later on, fibro-proliferative and degenera- The development of atherosclerosis is rather long tive processes take place, as a reaction to high levels and without clinical signs. Atherosclerotic plaques of lipoproteins and inflammatory mediators. The can subsequently obstruct the blood stream within development of atherosclerotic plaques currently the vessel by narrowing its diameter. According to depends on the effect of atherogenic lipoproteins the vessels affected, clinical consequences may in- in combination with endothelial damage and local clude: ischemic heart failure (IHF), ischemic stroke inflammatory process. 524 Veterinarni Medicina, 55, 2010 (11): 523–546 Review Article Based on pathophysiology, three main stages Acute arterial thrombosis can be defined as sud- of atherosclerosis are described: (1) early lesions den impairment in the perfusion of legs or acute with fatty stripes, (2) fibrotic and atherosclerotic exacerbation of pre-existing chronic ischemia of plaques, (3) stage of complication development the legs, typically manifested by severe pain, par- (Hansson et al., 2002). To be able to control athero- esthesia, as well as motor deficiency of various sclerosis, one must pay due attention to so called degrees, depending on extent and localization of “risk factors”. Risk factors are recognized as reduc- arterial occlusion. ible and non-reducible. To reducible risk factors be- As mentioned before, the most frequent (85% to long insufficient physical activity, smoking (Lekakis 95%) cause of arterial occlusion is atherosclerosis et al., 1997), arterial hypertension (Rizzoni et al., and its direct consequences, mainly acute throm- 1998), hyperglycemia, high concentrations of non- bosis (Puchmayer and Roztocil, 2000). Typically, enzymatic protein glycation products (Meeking affected patients have recently undergone a pe- et al., 1999), hyperhomocysteinemia, central-type ripheral vascular bypass. In clinical practice there obesity and, most of all, high concentrations of is a distinction between prosthetic and venous atherogenous low-density lipoprotein (LDL) par- bypasses; in a prosthetic bypass there is a higher ticles (Creager et al., 1990). As non-reducible risk probability of platelet-rich thrombus than in ve- factors are classified: genetic factors (family history nous grafts. In the rest of cases, there is some other of ischemic heart failure – IHF, or other manifesta- cause of occlusion, and occasionally the origin re- tion of atherosclerosis in a close relative), gender
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