|Year : 2020 | Volume
| Issue : 2 | Page : 180-183
Reactive thrombocytosis leading to stent thrombosis
Piyush Kalantri, Aniruddha Kaushik, Rahul Singla, Arun Bade, Narendra Omprakash Bansal
Department of Cardiology, Grant Govt. Medical College and Sir JJ Group of Hospitals, Mumbai, Maharashtra, India
|Date of Submission||26-Jun-2020|
|Date of Decision||17-Jul-2020|
|Date of Acceptance||22-Jul-2020|
|Date of Web Publication||27-Aug-2020|
Dr. Piyush Kalantri
Room No. 2, 300 Residential Quarters, J.J. Hospital Campus, Byculla, Mumbai - 400 008, Maharashtra
Source of Support: None, Conflict of Interest: None
Percutaneous coronary intervention is associated with many complications, and stent thrombosis is the most feared among them. Common etiologies of stent thrombosis include high angiographic thrombus burden, inadequate antiplatelet dosing, total stent length, diabetes, and renal diseases. Rarely, it can be associated with thrombocytosis. We report a rare case of stent thrombosis associated with reactive thrombocytosis. Although acute coronary events have been documented due to essential thrombocytosis, very few cases of reactive thrombocytosis leading to acute coronary syndrome are reported. Thrombocytosis as a possible etiology is suspected when other risk factors including antiplatelet resistance is ruled out. In these cases, adequate treatment of both stent thrombosis and thrombocytosis needs to be administered simultaneously and the possible etiology of thrombocytosis should be sorted out and treated.
Keywords: Acute coronary syndrome, reactive thrombocytosis, stent thrombosis
|How to cite this article:|
Kalantri P, Kaushik A, Singla R, Bade A, Bansal NO. Reactive thrombocytosis leading to stent thrombosis. J Pract Cardiovasc Sci 2020;6:180-3
|How to cite this URL:|
Kalantri P, Kaushik A, Singla R, Bade A, Bansal NO. Reactive thrombocytosis leading to stent thrombosis. J Pract Cardiovasc Sci [serial online] 2020 [cited 2021 Aug 1];6:180-3. Available from: https://www.j-pcs.org/text.asp?2020/6/2/180/293529
| Introduction|| |
Stent thrombosis is the most feared complication of coronary stenting because of its immediate morbidity and mortality. Its etiology is multifactorial commonly such as high angiographic thrombus burden, total stent length, diabetes, renal insufficiency, and preprocedural inadequate thienopyridine administration, and there is a rare possibility with thrombocytosis. Here, we report a case of acute stent thrombosis in a patient who developed stent thrombosis within 24 h of left anterior descending artery (LAD) stenting associated with reactive thrombocytosis despite adequate antiplatelet therapy with aspirin and clopidogrel.
| Case Report|| |
A middle-aged female patient, nonhypertensive and nondiabetic, was admitted to our hospital with chest pain for the last 2 h, with electrocardiogram (ECG) suggestive of ST segment elevation in the inferior leads [Figure 1] and reciprocal changes in the anterolateral leads with quantitative Troponin T value of 540 pg/ml, with no other associated risk factors. Her routine investigation was unremarkable except for hemoglobin 9.0 g/dL, with platelet count being 1.68 lakhs/mm3. After loading with aspirin, clopidogrel, and atorvastatin, the patient was considered for urgent coronary angiography, which showed right coronary artery (RCA) 100% thrombotic occlusion [Figure 2] and LAD 80% lesion across the diagonal [Figure 3]. Primary angioplasty was carried out to the RCA with 3.5 mm × 48 mm drug-eluting stent (DES) from the proximal to the mid-RCA with TIMI III flow [Figure 4] under the cover of required dose of heparin and antiplatelets. LAD percutaneous coronary intervention (PCI) was decided to be carried out at a later stage. On second stage after 1 week, PCI to the LAD was carried out with 3.5 mm × 43 mm DES with good result TIMI III flow [Figure 5] (under the cover of required dose of heparin and antiplatelets). On the 2nd day of the LAD PCI about 20 h from the procedure, the patient developed sudden chest pain with profuse sweating with systolic blood pressure of 90 mmHg. ECG showed ST-segment elevations in the anterior leads and quantitative Troponin T of around 6000 pg/ml, reflecting acute anterior wall myocardial infarction. The patient was rushed to the cath lab where the left shoots showed acute LAD stent thrombosis [Figure 6]. Thromboaspiration failed, so the patient was thrombolyzed with intracoronary reteplase after informed consent and TIMI III flow was established [Figure 7]. LAD patency showed good result. The patient's resistance to clopidogrel was tested, which was negative. The patient's platelet count trend as shown [Table 1] was suggestive of reactive thrombocytosis on the day of stent thrombosis, which subsequently resolved thereafter administering cytoreductive therapy along with antibiotics. The patient was observed for 48 h in the intensive coronary care unit and subsequently discharged after 2 weeks with normal platelet count.
|Figure 1: Electrocardiogram – Q wave with ST elevation in leads II, III, and aVF with T wave inversion in V4–V6.|
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|Figure 2: Angiography showing proximal right coronary artery total occlusion.|
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|Figure 3: Angiography showing proximal left anterior descending artery 80% lesion.|
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|Figure 6: Check shoot showing left anterior descending artery instent thrombotic occlusion.|
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|Figure 7: Postintracoronary thrombolysis of left anterior descending artery showing TIMI III flow.|
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| Discussion|| |
Stent thrombosis is one of the fatal complications of the PCI if it occurs acutely. Stent thrombosis is defined based on the timing of the stent thrombosis and the level of certainty of the event.
Based on the timing of event, acute stent thrombosis occurs between 0 and 24 h after coronary stent implantation. The subacute stent thrombosis occurs between 24 h and 30 days after coronary stent implantation. Late stent thrombosis occurs between 30 days and 1 year after coronary stent implantation. Finally, very late stent thrombosis occurs 1 year after coronary stent implantation.
Angiographic confirmation of stent thrombosis: The presence of intracoronary thrombus that originates in the stent or in the segment 5 mm proximal or distal to the stent and presence of at least 1 of the following criteria within a 48-hour time window:
- Acute onset of ischemic symptoms at rest
- New ischemic ECG changes
- Typical rise and fall in cardiac biomarkers
- Nonocclusive thrombus
- Intracoronary thrombus
- Occlusive thrombus
- TIMI 0 or TIMI 1 flow intrastent or proximal to a stent up to the most adjacent proximal side branch or main branch.
Stent thrombosis has a multifactorial etiology, and one of the rare etiologies is thrombocytosis which should be suspected when all other common etiologies are ruled out. As our patient belongs to acute stent thrombosis category and was not having other risk factors such as excessive thrombus burden, stent landing zone on plaque, and dissection, we looked for possible etiology as thrombocytosis as platelet count was 9.86 laths/mm3 when the patient had stent thrombosis.
Based on etiology, thrombocytosis can be of two types: essential (primary thrombocytosis) and reactive thrombocytosis (secondary). Essential thrombocytosis is a rare disorder which is associated with abnormal megakaryocytic in the circulation.,, It is associated with events such as strokes, transient ischemic attacks, retinal artery or retinal vein occlusions, digital ischemia, and acute coronary syndrome (ACS). Only few case reports of coronary artery thrombosis associated with essential thrombocytosis have been previously described in literature.
Reactive thrombocytosis is caused by elevated thrombopoietin level and other cytokines, such as interleukin-6. Patients with reactive thrombocytosis do not usually require cytoreductive medication or antiplatelet treatment, but in some circumstances, they may require antiplatelet treatment given the potential risk of ACS, stroke, pulmonary embolism, or pulmonary hypertension. Our literature search identified very little case reports describing reactive thrombocytosis following the episode of myocardial infarction leading to recurrent ACS. In our case, the patient might have developed reactive thrombocytosis due to iron deficiency anemia and urinary tract infection. In our patient, we went ahead with intracoronary thrombolysis as studies have shown it to be effective in case of high thrombus burden and failed thromboaspiration.,
It is well documented that essential thrombocytosis is a predilection to myocardial infarction. Our patient might have developed another episode of ACS from reactive thrombocytosis. Hence, the pathophysiology of stent thrombosis in this case is probably not from atherosclerosis or plaque rupture but due to elevated platelet count from reactive thrombocytosis, resulting in a second myocardial infarction. Another possibility is that he might have primary resistance to clopidogrel, so we did an enzyme-resistant assay which turned out to be negative. In this scenario, the reactive thrombocytosis appears to be the culprit. We decided to substitute clopidogrel with a newer antiplatelet medication ticagrelor, and therapeutic doses of enoxaparin were started to treat the recurrence of ACS. Hydroxyurea, aspirin, and ticagrelor were initiated on consultation with a hematologist. Antibiotics were given for the treatment of urinary tract infection. Enoxaparin and hydroxyurea were discontinued when his platelet count returned to his baseline. This case highlights the potentially underrecognized danger of reactive thrombocytosis and stresses the need for comprehensive evaluation of the pathophysiology, consequences, and management of reactive thrombocytosis.
| Conclusion|| |
Reactive thrombocytosis can be a rare cause of ACS including stent thrombosis. A thorough vigilance for thrombocytosis as a possible etiology should be sorted to not miss it especially if patient is not having other cardiac risk factors.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initial will not be published, and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.
I am deeply indebted to Dr. Narendra Omprakash Bansal, HOD, Department of Cardiology, Sir J.J Groups of Hospital, for helping and guiding us in this study.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]