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Percutaneous Coronary Intervention In armacolo Ph gy r : O Narasimha et al., Cardiovasc Pharm Open Access 2016, 5:6 la u p c e n s a A DOI: 10.4172/2329-6607.1000202 v c o c i e d r s a s C Cardiovascular Pharmacology: Open Access ISSN: 2329-6607 Review Article Open Acces Percutaneous Coronary Intervention in Patients with Heparin Induced Thrombocytopenia: Case Report and Review of Literature Narasimha D, Jutzy K and Hilliard A* Cardiac Catheterization Laboratory, Loma Linda University, USA Abstract Heparin Induced Thrombocytopenia (HIT) is a rare disorder, which manifests as acute onset thrombocytopenia within five to fifteen days after exposure to heparin. The milder version of the disease may manifest as asymptomatic thrombocytopenia, which resolves with cessation of heparin. The more severe form presents with arterial and venous thrombi, profound thrombocytopenia and is associated with devastating consequences such as myocardial infarction, stroke, limb ischemia etc. The management of patients with HIT undergoing revascularization in the form of Percutaneous Coronary Intervention (PCI) and/or Coronary Artery Bypass Grafting (CABG) can be challenging and complicated by acute stent thrombosis and early graft closure. Management strategy consists of immediate discontinuation of all heparin products, alternative anticoagulation, and lifelong avoidance of heparin products. Here we describe the various challenges specifically associated with coronary re-vascularization in these patients, and the current treatment options available. Keywords: HIT; Direct thrombin inhibitors; PCI; Bivalirudin; in platelet count. Thrombosis occurs in about 20-50% of patients. Heparin Induced Thrombocytopenia (HIT) The diagnosis of HIT includes a history of heparin exposure over the past few days to months, clinical signs and symptoms of thrombosis, Introduction and laboratory data. The 4T scoring system can be used as an aid to diagnosis (Table 1) [5]. Heparin Induced Thrombocytopenia (HIT) is defined as a decrease in platelet count <150,000 or over 50% of baseline occurring 5-15 days Laboratory diagnosis and management after the use of Unfractionated Heparin (UFH), or low-molecular weight heparin (LMWH) caused by an immune response [1]. HIT Various laboratory tests are available for the diagnosis of HIT when associated with thrombosis (HITT) can have devastating with varying sensitivities and specificities. These include Enzyme consequences due to the formation of arterial and venous thrombi. In Immunoassay (EIA) for polyclonal antibodies (IgG, IgA, and IgM) cardiac patients requiring Percutaneous Coronary Intervention (PCI) which have a low specificity as it is not specific for IgG, but this test can be used as a screening test [1]. Other tests include platelet activation and/or Coronary Artery Bypass Grafting (CABG) management of HIT tests such as Serotonin Release Assay (SRA) or heparin-induced can be, challenging given that anticoagulation is imperative for these platelet activation testing (HIPA testing). These have high specificities procedures. In addition, there is a high risk for stent thrombosis and but are performed only in certain laboratories, and usually take several graft occlusion following re-vascularization. We present a case report days to report. Once HIT is suspected all heparin products should be highlighting the clinical and therapeutic challenges faced in a patient stopped, including heparin coated catheters, heparinized flushes, etc. with HIT undergoing both PCI and a CABG, and review the current Alternative anticoagulants such as Direct Thrombin Inhibitors (DTI) literature in regards to management of these patients. should be started (Table 2) [5]. Warfarin should generally not be started Pathophysiology and clinical presentation until the thrombocytopenia resolves, as there is a high risk for skin and limb gangrene. Platelet transfusions are contraindicated, as this can HIT occurs in around 5-10% of patients treated with heparin lead to further thrombosis, unless the patient has major bleeding [1]. [1]. It usually occurs 5-15 days after heparin administration. Thrombocytopenia occurring more than two weeks after exposure Case Report to heparin is usually not due to HIT but can be considered in the A 73-year-old male with Coronary Artery Disease (CAD) was differential if other causes are ruled out. HIT can occur from the admitted on 12/23/2011 with a Non-ST Segment Elevation Myocardial intravenous or subcutaneous administration of heparin, and also Infarction (NSTEMI). He was found to have a low platelet count on with the use of heparin coated catheters and heparin flushes [2,3]. In HIT patients who have received heparin before, re-administration of heparin has been associated with a higher risk for significant *Corresponding author: Anthony Hilliard, Associate Chair of Cardiology, Director of thrombocytopenia and thrombosis [4]. UFH is also more likely to Cardiac Catheterization Laboratory, Associate Professor of Medicine, 11234 Anderson cause HIT compared with LMWH. Heparin and platelet factor four Street, Suite 2426, Loma Linda University, Loma Linda, CA 92354, USA, Tel: +1 909 (PF 4) form a complex that triggers the production of immunoglobulin 558 4498; E-mail: [email protected] G (IgG) against this complex [3]. Platelets express the Fc receptor on Received November 24, 2016; Accepted December 05, 2016; Published their surface, which binds to this IgG resulting in enhanced platelet December 12, 2016 aggregation and thrombocytopenia. In addition, this complex causes Citation: Narasimha D, Jutzy K, Hilliard A (2016) Percutaneous Coronary Intervention in the release of pro-coagulant factors such as Thromboxane A2 from Patients with Heparin Induced Thrombocytopenia: Case Report and Review of Literature. Cardiovasc Pharm Open Access 5: 202. doi: 10.4172/2329-6607.1000202 the platelets, which stimulates thrombosis. This manifests as arterial and venous thrombosis and can present as deep venous thrombosis, Copyright: © 2016 Narasimha D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits stroke, limb ischemia, or myocardial infarction. Clinically HIT can also unrestricted use, distribution, and reproduction in any medium, provided the be asymptomatic without thrombotic features and only mild decrease original author and source are credited. Cardiovasc Pharm Open Access journal Volume 5 • Issue 6 • 1000202 ISSN: 2329-6607 Citation: Narasimha D, Jutzy K, Hilliard A (2016) Percutaneous Coronary Intervention in Patients with Heparin Induced Thrombocytopenia: Case Report and Review of Literature. Cardiovasc Pharm Open Access 5: 202. doi: 10.4172/2329-6607.1000202 Page 2 of 7 Score Criteria 2 1 0 Degree of Decreased platelet count by >50% and Decreased platelet count by 30-50% or Decreased platelet count by <30% or thrombocytopenia* min. platelet count ≥20 g L-1 min. platelet count 10−19 g L-1 min. platelet count <10 g L-1 Probably 5-10 days (e.g., lack Timing from heparin inclusion to a drop in 5-10 days or ≤1 day ( if the patient was of laboratory results), >10 days ≤4 days when recently not platelet count exposed to heparin within 30 last days) or ≤1 day when unexposed to exposed to heparin heparin within previous 30-100 days Confirmed thrombosis at new location, Aggravation or recurrent thrombosis, skin Thrombosis or other skin necrosis, acute systemic reaction lesions without necrosis (erythematous) Absent symptoms of HIT following intravenous bolus of suspicion of thrombosis unfractionated heparin Other causes of Absent Possible Present thrombocytopenia Table 1: 4T Criteria for heparin induced thrombocytopenia. Combined with Drug and its short characteristics Dosage form Dosage Monitoring thrombin Lepirudin A synthetic analogue of hirudin (detected in Powder for preparing intravenous Saturating dose (bolus): 0.4 mg secretion of medical leeches) solution: kg' (not obligatory).followed by APTT (1.5-2.5-fold Irreversible complexes Half-life 60-80 min, increasing in an Vials 20 mg continuous infusion prolongation) unpredictable way in patients with renal Vials 50 mg 0.15 mg kg'' h'' dysfunction Bivalirudin Without a saturating A synthetic molecule consisting of two Powder for preparing venous dosexontinuous infusion 0.15- APTT (1.5-2.5-fold fragments of hirudin solution: 0.20 mg loll h'' (during PCI Irreversible complexes prolongation) Half-life 25 min. It is decomposed by Vials 250 mg bolus 0.75 mg kg', followed by proteolytic degradation in plasma continuous infusion 1.75 mg kg' Without a saturating dose, continuous infusion 2 pg Argatroban min.' (in critically ill patients, APTT A synthetic derivative of 1-arginine Half-life Intravenous form: Ampoules 250 those after cardiac Irreversible le (1.5-3-folds 40-50 min; almost completely metabolised by mg surgical procedures complexes prolongation) the liver or with hepatic failure, an infusion pg kg' min"' is recommended Dabigatran Pro-drug. Its structure is similar to that of benzamidine thrombin inhibitor (serine Oral form: Capsules 75 mg 220-300 g day' (decreased protease) Therapeutic concentration 2-4 h Irreversible Capsules 110 mg Capsules 150 doses suggested in the elderly Not necessary after administration complexes mg and patients with renal failure) Terminal half-life in healthy volunteers- approximately 8 h whereas in elderly individuals with renal failure-12 h Table 2: Direct thrombin inhibitors [5]. further work-up and a HIT panel was ordered on suspicion of HIT. lesions. He presented with unstable angina 9 months later, in
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