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Year : 2021  |  Volume : 10  |  Issue : 4  |  Page : 144-146

BailOut angioplasty in a case of thrombus migration

Department of Cardiology, Grant Medical College and Sir JJ Group of Hospitals, Mumbai, Maharashtra, India

Date of Submission06-Jan-2021
Date of Decision31-May-2021
Date of Acceptance05-Jul-2021
Date of Web Publication24-Dec-2021

Correspondence Address:
Dr. Rohit Rai
Department of Cardiology, Grant Medical College and Sir JJ Group of Hospitals, Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcpc.jcpc_1_21

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Acute myocardial infarction with high thrombus burden poses a challenge to the operating surgeon. Thrombus migration can worsen the clinical condition by further occluding flowing vessels. In our case of acute anterior wall myocardial infarction, thrombus migration from left anterior descending (LAD) caused obstruction of the left circumflex artery (LCX), and ramus. Bailout percutaneous transluminal coronary angioplasty (PTCA) was done to LCX, ramus, and left main which helped the patient hemodynamically but soon succumbed to sudden cardiorespiratory arrest. Hence, bailout PTCA remains a challenging procedure.

Keywords: Angioplasty, cardiogenic shock, thrombus migration

How to cite this article:
Rai R, Jalkote SP, Shaikh SS, Gupta AV, Bansal NO. BailOut angioplasty in a case of thrombus migration. J Clin Prev Cardiol 2021;10:144-6

How to cite this URL:
Rai R, Jalkote SP, Shaikh SS, Gupta AV, Bansal NO. BailOut angioplasty in a case of thrombus migration. J Clin Prev Cardiol [serial online] 2021 [cited 2022 Nov 26];10:144-6. Available from: https://www.jcpconline.org/text.asp?2021/10/4/144/333698

  Introduction Top

Acute closure of the coronary artery during angioplasty is a life-threatening condition. The patient may suddenly go into cardiogenic shock, heart failure, or ventricular tachycardia and may require support. Increased thrombus burden and altered characteristics of leukocytes and platelets in the thrombus make angioplasty a challenging procedure. They are also associated with worse outcomes. This case had 100% thrombotic occlusion of infarct-related artery and how bailout percutaneous transluminal coronary angioplasty (PTCA) was done following thrombus migration. This is a rare case as similar case has not been reported in coronary angioplasty.

  Case Report Top

A 50-year-old male patient presented with anterolateral wall myocardial infarction and was thrombolyzed with streptokinase on admission following which his chest pain got relieved.

Blood pressure on admission was 120/80 mmHg and pulse rate of 88/min. Hemoglobin was 15.1 g%, white blood cell (WBC) counts were 19,200/mm3, and Platelet count was 2.94 lacs/mm3. The patient had fever, but his COVID reverse transcription-polymerase chain reaction (RT-PCR) was negative. He was given intravenous (IV) antibiotics and his WBC counts came down to 5800/mm3 and fever subsided. His urine routine examination and chest X-ray were within the normal limits. He was observed for 1 week for recurrence of fever and repeat COVID RT-PCR was also negative. The patient was on unfractionated heparin and his activated partial thromboplastin time was maintained between 2 and 3 times normal. He was taken for angiography which revealed left main distal plaque, LAD proximal 100% occlusion, ramus proximal 70% lesion, LCX proximal 70% lesion, and right coronary artery (RCA) mid 50% plaque [Figure 1].
Figure 1: Initial coronary angiography

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The patient was taken for angioplasty, a bolus of 5000 units of heparin was given and wire was passed across the lesion in LAD and predilated with PTCA balloon of 2 mm × 12 mm size following which thrombus migrated to left main and ostioproximal LAD. Thrombus was crushed in left main and proximal LAD with PTCA balloon 3.5 mm × 8 mm. Check shoot revealed ostioproximal LAD, proximal LCX, and proximal ramus 100% total occlusion [Figure 2]. Systolic blood pressure of the patient dropped to 20–30 mmHg. The patient was intubated and cardiopulmonary resuscitation (CPR) started with high-dose of dopamine and noradrenaline. Another bolus of 2000 units of heparin was given.
Figure 2: Coronary angiography following balloon dilation of LAD

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As a bailout procedure PTCA wire was passed across lesion in the ramus and stented with 2.75 mm × 38 mm drug-eluting stent following which the systolic blood pressure increased to 50–60 mm Hg [Figure 3]. Another PTCA wire was passed across the lesion in LCX and predilated with 2 mm x 12 mm size balloon. The lesion in LCX was stented with 2.5 mm × 16 mm drug-eluting stent following which the systolic blood pressure increased to 80–90 mmHg [Figure 4]. The lesion in left main artery was stented with 4 mm × 15 mm drug-eluting stent [Figure 5]. The blood pressure increased to 120/80 mmHg. A 2 mm × 12 mm size PTCA balloon was dilated in LAD but resulted in no flow in LAD. Hence, the procedure was abandoned and the patient was put on tirofiban infusion.
Figure 3: Bail out percutaneous transluminal coronary angioplasty to Ramus

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Figure 4: Bail out percutaneous transluminal coronary angioplasty to LCX

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Figure 5: Bail out percutaneous transluminal coronary angioplasty to left main

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The final result displayed ostioproximal 100% occlusion of the LAD and TIMI III flow across ramus and LCX [Figure 6]. Blood pressure of the patient was 120/80 mmHg [Figure 7]. Three hours postprocedure, the patient went into sudden cardiorespiratory arrest and could not be revived after cardiopulmonary resuscitation (CPR).
Figure 6: Angiography result after percutaneous transluminal coronary angioplasty to ramus, LCX and left main

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Figure 7: Postprocedure electrocardiogram

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  Discussion Top

In cases of acute myocardial infarction, large thrombus burden is common. Proximal migration and distal embolization following balloon dilation is also known. Bailout procedure by stenting no-reflow vessels is a lifesaving maneuver. Movahed also reported a case of proximal migration of thrombus in RCA in a case of acute inferior wall myocardial infarction.[1]

Thrombus can grow during percutaneous coronary intervention (PCI) by manipulation of guidewires, stasis of blood, stents or balloons, inadequate antithrombotic, or anticoagulant therapy resulting in the “angry clot” phenomenon. Hyperglycemia and leukocytosis may also accentuate thrombosis.[2] Massive hostile thrombus is rich with active procoagulants, adherent to vessel wall, voluminous, elastic yet friable, multi-layered, contains aggressive platelets, and discharges vasospastic mediators.[3]

After ischemia, arteriolar endothelial dysfunction and diffuse capillary swelling occurs. In addition, intracellular edema and clogging of vessels is contributed by activated leukocytes. Following reperfusion sudden rush of leukocytes and distal atheroemboli also contribute to impaired tissue perfusion.[4] The higher the thrombus burden the more is the distal embolization leading to obstruction of flow in distal vessels leading to no-reflow.[5] Morishima et al. showed that in the long run angiographic no-reflow is associated with more complications of acute myocardial infarction possibly related to left ventricular remodeling.[6]

Use of glycoprotein IIb/IIIa platelet receptor inhibitors, shortening the door to balloon time and distal protection devices are known to prevent no-reflow. Distal intracoronary injections of adenosine, verapamil, or nitroprusside may also improve intracoronary blood flow. Patients may require hemodynamic support till coronary blood flow improves.[4]

Devices used for thrombus aspiration such as Angiojet rheolytic thrombectomy, X-sizer catheter, hydrolyser thrombectomy catheter, and pronto catheter have failed to show benefit when they were used routinely in the setting of acute myocardial infarction.[7] Intracoronary residual thrombus after PCI is associated with worse outcomes.[8] Use of intracoronary thrombolytics have also failed to show any benefit.[9]

Bailout stenting as done in this case is essential to save the life of patients, especially in cases of thrombus migration. The sudden deterioration of the patient 3 h postangioplasty could be presumed to be due to reocclusion of the stents. Hence, bailout PTCA remains a challenging procedure.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Movahed MR. Persistent and proximal migration of a large coronary thrombus during percutaneous coronary intervention in the setting of acute Q-wave myocardial infarction. Cardiovasc Revasc Med 2006;7:48-50.  Back to cited text no. 1
Srikanth S, Ambrose JA. Pathophysiology of coronary thrombus formation and adverse consequences of thrombus during PCI. Curr Cardiol Rev 2012;8:168-76.  Back to cited text no. 2
Krishnaswami A, Carr ME Jr., Jesse RL, Kontos MC, Minisi AJ, Ornato JP, et al. Patients with coronary artery disease who present with chest pain have significantly elevated platelet contractile force and clot elastic modulus. Thromb Haemost 2002;88:739-44.  Back to cited text no. 3
Rezkalla SH, Kloner RA. Coronary No-reflow phenomenon. Curr Treat Options Cardiovasc Med 2005;7:75-80.  Back to cited text no. 4
Henriques JP, Zijlstra F, Ottervanger JP, de Boer MJ, van 't Hof AW, Hoorntje JC, et al. Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction. Eur Heart J 2002;23:1112-7.  Back to cited text no. 5
Morishima I, Sone T, Okumura K, Tsuboi H, Kondo J, Mukawa H, et al. Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol 2000;36:1202-9.  Back to cited text no. 6
Singh M, Tiede DJ, Mathew V, Garratt KN, Lennon RJ, Holmes DR Jr., et al. Rheolytic thrombectomy with Angiojet in thrombus-containing lesions. Catheter Cardiovasc Interv 2002;56:1-7.  Back to cited text no. 7
Harjai KJ, Grines C, Stone GW, Boura J, Turco M, Brodie B, et al. Frequency, determinants, and clinical implications of residual intracoronary thrombus following primary angioplasty for acute myocardial infarction. Am J Cardiol 2003;92:377-82.  Back to cited text no. 8
Ambrose JA, Almeida OD, Sharma SK, Torre SR, Marmur JD, Israel DH, et al. Adjunctive thrombolytic therapy during angioplasty for ischemic rest angina. Results of the TAUSA Trial. TAUSA Investigators. Thrombolysis and Angioplasty in Unstable Angina trial. Circulation 1994;90:69-77.  Back to cited text no. 9


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]


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