Heliyon 9 (2023) e22301
Available online 17 November 2023
2405-8440/© 2023 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Simultaneous acute portal vein thrombosis and ST elevation myocardial infarction in a Covid-19 patient – Case report
Ensieh Nournia
a,*, Hamid Abbasi
b, Maziar Bazrafshan
caCardiologist at Be’sat Hospital, Hamedan University of Medical Sciences, Hamedan, Iran
bAuckland Bioengineering Institute, University of Auckland, Auckland, 1010, New Zealand
cVascular Surgeon at Be’sat Hospital, Hamedan University of Medical Sciences, Hamedan, Iran
A R T I C L E I N F O Keywords:
Covid-19
Acute portal vein thrombosis ST elevation myocardial infarction NonVitamin K antagonist oral anticoagulants (NOAC)
Case report
A B S T R A C T
Background: Covid-19 infected patients without any risk factors and family history of a thrombotic event can be still at risks of developing thrombotic and/or other Covid-19-related complications, and therefore, there is a substantial need to study such cases.
Case presentation: In this study, we present a 60-years-old Covid-19 patient with mild symptoms who was admitted to the hospital with simultaneous arterial and venous thrombotic event, with chief complaint of chest pain and vague abdominal pain. The patient was diagnosed with Covid- 19 two weeks before admission to the ICU. A 12-lead electrocardiogram revealed pathologic Q- wave ST-segment elevation and T-wave inversion in II, III, aVF, and T inversion in V5 and V6.
Quantitative troponin was elevated which confirmed inferior ST-elevation MI. Abdominal color Doppler sonography and CT scan with contrast demonstrated an absent flow in the portal vein and thrombosis. A chest CT scan illustrated a normal pattern. We started IV unfractionated heparin (UFH), dual antiplatelet, beta-blocker, statin, intravenous nitrate, and angiotensin- converting enzyme inhibitor. Coronary angiography showed the right coronary artery was totally cut off at the proximal part.
Here we report three main un-common characteristics associated with our patient compared to other similar studies. First, the thrombotic event in our case occurred without pulmonary involvement and the patient only had a flu-like symptom two weeks before admission. The second main difference is that the patient’s arterial and venous thrombotic events had simultaneously happened, which is not common in most cases. Patient presented simultaneous portal vein thrombosis and recent ST-segment elevation Myocardial Infarction (MI). Finally, both MI and portal vein thrombosis symptoms were subtle and confusing, which could cause misdiagnosis. A post two-weeks color Doppler sonography follow-up showed portal vein thrombosis recanaliza- tion and myocardial perfusion scan had no viability and reversible ischemia in RCA territory.
Conclusions: This report addresses that a cautious diagnosis of Covid-19 at the time of admission can play a vital role in preventing cardiovascular events; where even asymptomatic to mildly infected patients could be still at higher risks of developing clinical complications (e.g., throm- botic events).
* Corresponding author.
E-mail address: [email protected] (E. Nournia).
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Heliyon
journal homepage: www.cell.com/heliyon
https://doi.org/10.1016/j.heliyon.2023.e22301
Received 13 August 2022; Received in revised form 8 November 2023; Accepted 9 November 2023
1. Background
The Covid-19 pandemic has been one of the most severe health issues in the world in the recent decade. Several factors including exaggerated inflammatory response, endothelial cell dysfunction, hypoxia, and immobility lead to susceptibility to thrombotic events in patients with severe Covid-19 infection. Studies indicate that a higher incidence of thromboembolic disorders in Covid-19 cases may cause an increase in the mortality and morbidity of such patients. Around 20 to 40% of patients show non-pulmonary involvement [1].
One of such complications is coagulation disorders. Several reports have indicated the increased risk of thrombotic complications during the disease course caused by immune system hyperactivity, cytokine storm, and local and systemic inflammatory reactions. The prognosis is worse with thromboembolic events [2].
In this work, we report a case with unique features associated with three major factors. Here we present a case a thrombotic event had occurred to a patient with mild Covid-19 symptoms with no pulmonary involvement. This finding is important as in most other Covid-19 cases a thrombotic event occurs in patients with moderate to severe infection who have pulmonary involvement. Moreover, our patient was complicated with simultaneous arterial and venous thrombotic events, which is not a commonly seen event in most cases. Furthermore, the subtle and confusing symptoms of Myocardial Infarction (MI) and portal vein thrombosis, in this case, could have resulted in misdiagnosis, if missed.
2. Case presentation
A 60-year-old male patient was admitted to Emergency Room with a chief complaint of abdominal pain, nausea, myalgia and chills, and fever for two weeks. He had a chief complaint of chest pain and vague abdominal pain, which had been predominant in the epigastric area since a couple of days before admission. The patient was infected by Covid-19 two weeks before and was in quarantine.
A nasopharyngeal swab specimen was positive for SARS-COV2 before two weeks of quarantine. The patient’s past medical history, family history, and psycho-social history were normal. The patient had no history of Covid-19 vaccination.
The patient was of average weight (BMI:23). At presentation, the blood pressure was 140/80, and the heart rate was 80 beats per minute. The body temperature was 37C, and the oxygen level in a pulse oximeter was 99% without oxygen therapy. The physical examination showed a soft abdomen without tenderness and rebound tenderness. Table 1 provides the timeline for the study.
A 12-lead electrocardiogram was performed on admission. It revealed pathologic Q wave STsegment elevation and T wave inversion in II, III, aVF, and T inversion in V5 and V6. Laboratory tests showed normal liver function test, cell blood count, renal function test, ESR, and CRP. D-dimer and quantitative troponin were elevated, the results of antithrombin III, protein C, protein S activity tests were in normal range and evaluation of Factor V Leiden, Prothrombin G20210A and anti-phospholipid antibody showed negative result, which proved, there was no hereditary or acquired hypercoagulable state (Table 2). Abdominal color Doppler so- nography demonstrated an absent flow in the portal vein and thrombosis. The computed tomography scan (CT) with contrast was performed for better evaluation. It revealed an acute portal vein thrombosis without splenic vein, superior mesenteric vein extension, and increased portal vein diameter (Fig. 1A–B and Fig. 1C–D, respectively, show the longitudinal and transverse sections of CT scan with portal vein thrombosis on admission). A chest CT scan illustrated a normal pattern on admission, with no pulmonary involvement.
Echocardiographic findings showed hypokinesia of the inferior wall and mild mitral valve regurgitation, with acceptable left and right ventricular ejection fractions LVEF: 45–50 %.
Coronary angiography was performed a day after admission and showed ectatic left anterior descending and left circumflex arteries (Fig. 2A). The right coronary artery was totally cut off at the proximal part with retrograde filling via the right and left systems (Fig. 2B–C).
The patient was admitted to the ICU. The patient was hydrated, and then we started IV unfractionated heparin (UFH) 80u/kg stat 18/kg/hr infusion, ASA 80mg/day Clopidogrel 75 mg/day, metoprolol 25 mg twice a day, Atorvastatin 40 mg/day, captopril 25 mg twice a day. During the hospital course, there was no chest pain, dyspnea, or other cardiac symptoms after the third day of hospi- talization. The abdominal pain was relieved six days after that.
We discontinued IV heparin two days before discharge and an oral anticoagulant (NOACs) was started. After clinical improvement, the patient was discharged on the tenth day of admission. The patient experienced more than one ischemic event in one episode.
Therefore, we preferred to start and continue triple therapy, including DAPT and Rivaroxaban 20 mg/day for three months, and then change to a single antiplatelet (Clopidogrel 75mg daily) and oral anticoagulant, at least for the next three months after that. This was performed to reduce the risks of major bleeding. The patient was referred for ischemia and viability assessment.
Two weeks after discharge, the patient visited the clinic and the follow-up color Doppler sonography showed portal vein throm- bosis recanalization. Liver function test, blood urea nitrogen (BUN), creatinine, and potassium were normal.
Table 1 Study timeline.
Time Procedure
Day 0 The patient was admitted to the ICU, and receieved UFH, dual anti-platelet, beta-blocker, and statin.
Day 1 Coronary Angiography was performed
Day 8 UFH was discontinued, and NOAC started (see therapeutic intervention section) Day 10 Patient discharged
Day 24 OPD follow-up: The patient re-visited the clinic with their lab reports and imaging data (including color Doppler sonography, myocardial perfusion scan)
Myocardial perfusion scan showed no viability and reversible ischemia in RCA territory. Thus, the continuation of anti-ischemic treatment was suggested.
No adverse and/or unanticipated events were observed during the patient’s visit in the follow-up session. Also, physical exami- nation and diagnostic assessments at the follow-up session showed patient improvement, confirming patient tolerability and medical treatment adherence.
3. Discussion and conclusion
Several studies report an increased rate of thromboembolic events in patients infected by SARSCoV-2. It may be originated from the activation of exaggerated inflammatory response and the direct effect of the virus on endothelial cells [3]. Therefore, it is critical to be cautious about the diagnosis of Covid-19. Current literature indicates a few related cases of portal vein thrombosis due to infections caused by the Covid-19. However, there are many other reported cases of patients who have suffered from a simultaneous Covid-19 infection and vascular events such as ischemic and hemorrhagic cerebrovascular events, ST and NonST myocardial infarction, acute coronary syndrome, etc.
A relatively similar case to this study has been recently reported for a Covid-19 patient admitted to the hospital with portal vein thrombosis and no pulmonary involvement [4]. However, their follow-up process, intervention, and treatment approaches differ from our strategies. On the one hand, intravenous anticoagulation for the patient in Ref. [4] was changed to Vitamin K antagonist oral anticoagulant (target PT INR 2.5–3.5); whereas in this study, we continued anticoagulant treatment with NOACs for the patient. In fact, we were obliged to start triple therapy after two simultaneous vascular events (i.e., portal vein thrombosis and ST-elevation MI).
Therefore, we decided to prescribe NOACs instead of Vitamin k antagonists with DAPT 1) to reduce the risks of bleeding, 2) it does not require serial lab tests, and 3) it has minimal interference with food and other medications. We believe this was one of the strengths of our treatment strategy. On the other hand, the patient in study [4] had a positive IgM result following a SARS-CoV2immunoserology test. A repeated 2-weeks follow-up test in Ref. [4]also shows a positive IgM and a positive IgG, confirming Covid-19 infection in their patient. In contrast, the Covid-19 test in the current study was performed through an antigen nasopharyngeal swab which has a limited and uncertain reliability. This is because nasopharyngeal swabs should be deeply inserted to collect adequate viral RNA for optimal reliability. Our patient was infected by Covid-19 two weeks before admission and had been in isolation. We did not perform repeated follow-up Covid-19 serology and PCR tests. This could be a limitation of our study.
A different study has reported a Covid-19 case with inferolateral ST-elevation MI while the patient was infected with Covid-19 Table 2
Laboratory test results.
Standard value Patient’s Laboratory results
AST (3–45 U/l) 27
ALT (0–45 U/l) 26
Alkaline phosphatase (80–306 mg/dl) 275
Total bilirubin (0.1–1.2 mg/dl) 0.6
ESR (0–15 mm/h) ~13
CRP (0–6 mg/l) 3
White blood count (5000–10000) 6700
Total cholesterol (<200 mg/dl) 155
HDL (30–85 mg/dl) 40
LDL (up to 110 mg/dl) 93
Triglyceride (<200 mg/dl) 162
Hemoglobin (13.5–18.0 g/dl) 14.4
Platelets (150–450 G/l) 150
Creatinine (0.4–1.3 mg/dl) 1
Blood urea nitrogen (5–23 mg/dl) 14
Albumin (3.5–5.5 g/dl) 4.6
PT (12–15 sec) 14
INR (1–1.06 ratio) 1
PTT (30–35 sec) 34
D-dimer (<0.5 mg/l) 4.2
Quantitative Troponin (<19 ng/l) 23
LDH (<265 U/l) 270
Protein C (65–145) 100
Protein S (>1yr & adult 55–160) 73
Anti-thrombin ш (75–125) 97
Factor V Leiden Negative
Anti-Phospholipid IgG (Negative <12 Eguivocal 12-18
Positive >18)
Negative
Anti-Phospholipid IgM (Negative <12 Eguivocal 12-18
Positive >18)
Negative
Prothrombin G20210A Negative
(similar to our case) but with pulmonary involvement and a decreased O2 saturation (unlike our case) [5]. Generally, thrombolytic therapy and conservative treatment are the priority choices for Covid-19 positive patients with ST-elevation MI and NonST-elevation MI, respectively. However, percutaneous coronary intervention (PCI) should be performed on patients who are diagnosed with a critical need for an invasive strategy. Of course, a PCI approach must be only considered after careful risks and benefits evaluations for the patient.
An acute MI had occurred to the patient in Ref. [5] during hospitalization (2–3 days after admission), making the patient eligible for Fig. 1.Longitudinal (A–B) and transverse (C–D) sections of CT-scan with portal vein thrombosis on admission (yellow arrows). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2.Coronary angiography: one-day post-admission assessment showed ectatic left anterior descending and left circumflex arteries (A), and the right coronary artery was totally cut off at the proximal part with retrograde filling via the right and left systems (B, C).
thrombolytic therapy. This is unlike our patient, who had experienced MI during their quarantine period and was referred to the hospital with a relatively long delay. Hence, we choose conservative treatment for our patient. Unlike the study [5], no Streptokinase or any other thrombolytic medication were prescribed for our patient due to recovering chest pain and improving evolving MI. Also, no coronary angiography has been performed for the patient in Ref. [5] due to the patient’s Covid-19 infectious phase with much higher contagious risks. In contrast, in our case, we were able to perform angiography because the patient was at their final days of infection, closer to the end of quarantine.
Furthermore, brain natriuretic peptide (BNP) can be assessed for risk stratification in patients with the acute coronary syndrome.
The use of BNP is one of the strengths of the study [5], which was not performed for our patient due to the lack of availability of the assessment kit and out of routine procedure.
There are three main characteristics associated with our case which are not common in most other similar studies. First, the thrombotic event in our case occurred in patients without pulmonary involvement (The patient only had a flu-like symptom two weeks before admission), whereas thrombotic events are associated with pulmonary involvement in most other cases. The second main difference is that the patient’s arterial and venous thrombotic events had simultaneously happened, which is not common in most cases. Finally, the last main difference is that both MI and portal vein thrombosis symptoms were subtle and confusing, which could cause misdiagnosis. Therefore, during the current pandemic, it is necessary to rule out Covid-19 confidently to prevent its associated probable complications. For example, early diagnosis of portal vein thrombosis leads to the prevention of intestinal ischemia and infarction, and early diagnosis of MI leads to the prevention of heart failure, arrhythmia, and other complications of cardiac ischemia.
In the current report, we discussed that although some cases may not show common Covid-19 symptoms, but they can still be at risks of developing thrombotic and/or other Covid-19-related complications. Most such patients may not go to the medical centers due to various reasons. For example, the patient in this study had a delayed referral to the hospital. This was different to most other studies which have been focused on reporting the hospitalized patients with severe Covid-19. These differences may need different diagnosis, prognosis, and interventions strategies. Also, it is possible that the number of thrombotic events are over estimated. For example, difficulties in distinguishing acute type I MI from type II MI and/or myocarditis, could lead to an overestimation of MI in Covid-19 patients [6].
Overall, the patient in the current report did not have any risk factors and family history of a thrombotic event, therefore, infection due to Covid-19 can be an independent new risk factor for cardiovascular events. This indicates that there is a substantial need to report patients with mild Covid-19 symptoms who may be at risk of developing cardiovascular events following a Covid19 infection. Finally, we suggest modification for other cardiovascular risk factors more than before, since the combination of Covid-19, as a new risk factor, with other factors can be more dangerous for the patients, during the current pandemic.
Ethics approval and consent to participate
This study has been performed under the ethical principles and the national standards for conducting Medical Research in Iran. The study holds ethics approval from the Research Ethics Committee of Hamedan University of Medical Sciences (IR.UMSHA.
REC1401.168). Informed consent was obtained from the patient(s) (or relative/guardian) for the publication of all images, clinical data and other data included in the manuscript.
Consent for publication Available.
Informed consent
Available on request from the author.
Funding
This research has not received support from any grants from any funding sources.
Data availability statement
Data associated with this study has not been deposited into a publicly available repository.
Data will be made available on request.
Additional information
No additional information is available for this paper.
CRediT authorship contribution statement
Ensieh Nournia: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Project
administration, Methodology, Investigation, Data curation, Conceptualization. Hamid Abbasi: Writing – original draft, Writing – review & editing. Maziar Bazrafshan: Investigation, Data curation.
Declaration of competing interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Abbreviations
BUN Blood urea nitrogen CRP C-reactive protein
CT scan Computed tomography scan DAPT Dual antiplatelet therapy ESR Erythrocyte sedimentation rate IgG Immunoglobulin G
ICU Immunoglobulin M (IgM) Intensive care unit IV Intravenous
MI Myocardial infarction
NOAC Non-vitamin k antagonist oral anticoagulant PCI Percutaneous coronary intervention PCR Polymerase chain reaction RNA Ribonucleic acid
RCA Right coronary artery
SARS-COV2 Severe acute respiratory syndrome – coronavirus 2 UFH Unfractionated heparin
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