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ISSN: 1734-9338
Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej
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1/2012
vol. 8
 
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Infarct-related artery filled with thrombus cleared completely after tirofiban therapy

Serkan Bulur
,
Hakan Özhan
,
Yasin Türker
,
Șule Bulur

Post Kardiol Interw 2012; 8, 1 (27): 75–77
Online publish date: 2012/04/12
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Introduction



Coronary atherosclerosis is the most frequent cause of ischaemic heart disease, and plaque disruption with superimposed thrombosis is the main cause of acute coronary syndrome (ACS) [1]. The clinical manifestation of an ACS thrombotic event is determined by the balance between the propensity for thrombus formation and the efficacy of the endogenous thrombolytic processes [2]. An invasive strategy of coronary angiography, with revascularization when appropriate, is recommended for high-risk patients who have an acute coronary syndrome [3].

Tirofiban is a non-peptide tyrosine derivative which belongs to the class of glycoprotein (GP) IIb/IIIa inhibitors (GPI). By preventing the binding of fibrinogen and von Willebrand factor to the GP IIb/IIIa receptor on the surface of the platelet, GPIs are currently regarded as the most potent inhibitors of platelet aggregation [4].

Herein, we present the effect of tirofiban infusion on an infarct-related artery with high thrombotic burden.



Case report



A 73-year-old woman was admitted to our hospital with fluctuating crushing chest pain. The electrocardiogram (ECG) revealed normal sinus rhythm and negative T waves on V1-V2 and aVL. Her medical history revealed hypertension. She was taken to the catheterization laboratory for percutaneous coronary intervention with the diagnosis of acute coronary syndrome. Coronary angiography showed that the right coronary artery was filled with thrombus (Figure 1). The left anterior descending and circumflex arteries were normal. The culprit lesion could not be identified. Therefore, tirofiban infusion 0.40 µg/kg/min for the first 30 min plus 0.10 µg/kg/min infusion was started and continued for 48 h. In addition, aspirin, clopidogrel and low molecular weight heparin were given for ACS therapy. At the end of the infusion, the coronary angiogram was repeated. The right coronary artery was completely cleared (Figure 2). Creatine kinase (CK), CK-MB and troponin values did not increase during hospital follow-up. The patient was symptom-free after discharge from the hospital and was doing well at her 6-month follow-up visit with aspirin 100 mg, metoprolol 50 mg, clopidogrel 75 mg, atorvastatin 10 mg and perindopril 10 mg/day therapy.



Discussion



The presence of angiographically detected thrombosis in patients presenting with ACS is associated with a higher incidence of in-hospital and long-term adverse cardiac events [5]. In the setting of ACS or when faced with a thrombotic lesion for which percutaneous coronary intervention (PCI) is being considered, adjunctive pharmacological therapy delivered intravenously or via the intracoronary route should aim at the prevention of thromboembolic events associated with PCI, and the reversal of such events if they occur. The interventional cardiologist is faced with the hard task of managing lesions with high thrombotic burden, which is more prevalent when earlier catheterization is performed [6]. The mechanical manipulation of such lesions is associated with a high incidence of periprocedural complications at least in part due to a high incidence of distal embolization [7]. Intravenous antiplatelet GP IIb/IIIa inhibitors are frequently administered to patients with ACS undergoing PCI, a strategy supported by several randomized clinical trials [3]. In our index patient, PCI was delayed due to very high thrombus burden and mismatch of ECG changes with the coronary anatomy. However, aggressive antiplatelet treatment with tirofiban, a potent inhibitor of GP IIb/IIIa receptors, in combination with low molecular weight heparin was administered. The result was a perfectly cleared coronary artery without a need for PCI. Therefore, invasive cardiologists should always keep in mind that GP IIb/IIIa receptor blockers may avoid unnecessary percutaneous coronary intervention in patients with acute coronary syndrome complicated with very high intracoronary thrombus burden. In such cases “cooling” the lesion with appropriate antithrombotic therapy may help to achieve better results and even prevent unnecessary interventional procedures.



References



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 2. Saraf S, Christopoulos C, Salha IB, Stott DJ, Gorog DA. Impaired endogenous thrombolysis in acute coronary syndrome patients predicts cardiovascular death and nonfatal myocardial infarction. J Am Coll Cardiol 2010; 55: 2107-2115.

 3. Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA focused update of the guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011; 123: 2022-2060.

 4. Topol EJ, Byzova TV, Plow EF. Platelet GPIIb-IIIa blockers. Lancet 1999; 353: 227-231.

 5. Freeman MR, Williams AE, Chisholm RJ, Armstrong PW. Intracoronary thrombus and complex morphology in unstable angina. Relation to timing of angiography and in-hospital cardiac events. Circulation 1989; 80: 17-23.

 6. Matar F, Mroue J. The management of thrombotic lesions in the cardiac catheterization laboratory. J Cardiovasc Transl Res 2011; Oct 21.

 7. Henriques JP, Zijlstra F, Ottervanger JP, et al. Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction. Eur Heart J 2002; 23: 1112-1117.
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