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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 23  |  Issue : 4  |  Page : 221-225  

Acute ST-Elevation myocardial infarction in patient with severe uncontrolled hyperthyroidism complicated by thyroid storm


1 Department of Cardiology, Hamad Medical Corporation, Doha, Qatar
2 Department of Internal Medicine, Hamad Medical Corporation, Doha, Qatar

Date of Submission04-Feb-2022
Date of Acceptance09-Oct-2022
Date of Web Publication17-Nov-2022

Correspondence Address:
Dr. Khaled Al Khodari
Heart Hospital, Hamad Medical Corporation, Doha
Qatar
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartviews.heartviews_8_22

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   Abstract 


Acute ST-elevation myocardial infarction is a life-threatening medical emergency that needs to be recognized early and treated properly to prevent deleterious complications, including death. A thyroid storm (TS) is a rare but severe manifestation of uncontrolled hyperthyroidism that might present with serious cardiovascular or neurological problems. We described a case of a 40-year-old male patient, known to have uncontrolled hyperthyroidism, who presented with acute onset of central chest pain, agitation, tachycardia, and pulmonary congestion. Fast atrial fibrillation with ST-segment elevation in anterior leads was detected on electrocardiogram. Thyroxin level (T4) was very high with undetectable thyroid stimulating hormone. Initially, the patient refused any type of coronary revascularization; therefore, he was admitted to the cardiology intensive care unit, and medical treatment was commenced for both TS and acute coronary syndrome. High-risk coronary angiography was done 2 h later because he had worsening persistent chest pain and started to develop signs of heart failure. It showed embolic occlusion of the distal left anterior descending artery that was treated medically with anti-coagulation. There were no complications. Chest pain and thyroid function tests settled down during his hospital stay with close cardiology and endocrinology follow-up.

Keywords: Coronary angiogram, hyperthyroidism, iodine load, myocardial infarction, thyroid storm


How to cite this article:
Al Khodari K, Tahtouh RA, Hamid T. Acute ST-Elevation myocardial infarction in patient with severe uncontrolled hyperthyroidism complicated by thyroid storm. Heart Views 2022;23:221-5

How to cite this URL:
Al Khodari K, Tahtouh RA, Hamid T. Acute ST-Elevation myocardial infarction in patient with severe uncontrolled hyperthyroidism complicated by thyroid storm. Heart Views [serial online] 2022 [cited 2022 Dec 8];23:221-5. Available from: https://www.heartviews.org/text.asp?2022/23/4/221/361405




   Introduction Top


Acute myocardial infarction (MI) is defined as an elevation of cardiac troponin that demonstrates a rise and/or falls pattern with evidence of acute myocardial ischemia that manifests as symptoms of chest pain, new electrocardiogram (ECG) changes, and/or cardiac regional wall motion abnormalities confirmed on cardiac imaging.[1]

Complications of MI include heart failure (HF), arrhythmias, cardiogenic shock, free wall rupture, acute mitral regurgitation, ventricular septal defect, and others.[2]

Thyroid storm (TS) is a rare, life-threatening complication of severe uncontrolled hyperthyroidism that is associated with a high mortality rate.[3] The presenting features may include fever, diarrhea, tachycardia, hypotension, signs of decompensated HF, agitation, seizures, coma, and even death.[4] TS can happen without clear precipitating factors or induced by an acute event such as sepsis, surgery, trauma, acute iodine load, acute cardiovascular disease, or noncompliance with anti-thyroidal drugs which is the most common reason based on a nationwide survey in Japan.[5]

The coexistence of MI and TS is life-threatening, and it makes acute management more challenging because both diseases might be associated with hemodynamic instability, and acute MI requires immediate coronary angiography (CAG) that needs iodinated contrast media. Such intervention was considered heavy iodine load which may exacerbate the hemodynamic and clinical complications of TS.


   Case Presentation Top


A 40-year-old male patient with a past medical history of hypertension, atrial fibrillation (AF), and previous severe uncontrolled hyperthyroidism complicated with TS, that required medical intensive care unit admission and intubation 1 year before this current presentation. He is not compliant with his medications and stopped taking them 2 months before this admission.

He presented to our emergency department (ED) complaining of central chest pain and palpitation that started 2 h earlier. The pain was progressive, pressure-like, and associated with agitation and nausea without vomiting. Initial ED evaluation revealed blood pressure (BP) was 181/112 mmHg, pulse was irregularly irregular with heart rate (HR) around 140 beats/min, tachypneic with the respiratory rate (RR) around 38/min, and the temperature was 37.6°C. Oxygen saturation was very low on room air, around 85%, which improved to 96% on 5 L of oxygen therapy. On physical examination, he was anxious and agitated with visible diffuse goiter. His skin was clammy and warm. Bibasilar crackles were detected on chest auscultation without lower limb edema. ECG exhibited fast AF and ST-segment elevation from V3 to V6 [Figure 1].
Figure 1: ECG at time of presentation showing atrial fibrillation with rapid ventricular response (heart rate around 130 beats/min), ST segment elevation from V3 to V6, and PVC. ECG: Electrocardiogram, PVC: Premature ventricular beat

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Blood investigations revealed mild leukocytosis with normal hemoglobin, platelets, renal, and liver function tests. ProBNP (pro B-type natriuretic peptide) was 1100 pg/Ml which decreased to 280 pg/Ml upon inpatient follow-up. Thyroid-stimulating hormone was undetectable and serum Thyroxin (T4) was more than 100 pmol/L. He scored 60 on Burch-Wartofsky Point Scale for TS possibility (more than 45 is highly suggestive of TS).[6] Serum troponin T level was 1200 ng/L then went down to <200 ng/L within 3 days.

Acute anterior wall MI combined with TS was diagnosed. Benefits and possible complications of both ways of revascularization, CAG with/without percutaneous coronary intervention (PCI) and thrombolytic therapy, was discussed extensively with the patient who opted for medical treatment and refused to proceed with any type of intervention.

Dual antiplatelet therapy (DAPT), aspirin and clopidogrel, and unfractionated heparin infusion were started. The endocrinology team stated that CAG/PCI might increase the risk of clinical deterioration of patient's status because of iodine load and started the patient on propylthiouracil (PTU) 200 mg every 4 h, hydrocortisone 200 mg stat dose followed by 100 mg every 8 h, cholestyramine 4 mg every 6 h, and Lugol's solution 10 drops every 8 h. Beta-blockers were not started because of hypervolemia secondary to HF. Isosorbide dinitrate (ISDN) infusion was started at a rate of 25 mcg/min and a bolus dose of intravenous (IV) furosemide 40 mg was given.

During the next 2 h, chest pain was progressing and the patient started to be more tachypneic; therefore, the patient received another dose of IV furosemide, and the ISDN infusion rate increased to 50 mcg/min. A prolonged re-discussion among treating physicians (primary cardiologist, interventionist, and endocrinologist) and the patient about the need for revascularization resulted to proceed with high-risk CAG with/without PCI. High-risk consent was obtained, the anesthesia team was kept on standby for any possible emergency, and the procedure was performed through femoral access. The contrast solution was diluted with normal saline (50;50), and only a minimal dose of 15 ml was used for the procedure to diminish iodine loading. CAG revealed single vessel disease, distal left anterior descending artery 100% embolic occlusion, TIMI 3, and blood flow was restored when the guidewire crossed the lesion. Chest pain settled down, and ECG changes improved to baseline. The echocardiogram showed an ejection fraction (EF) of 35% with anterior wall motion hypokinesia, grade 2 diastolic dysfunction, and moderately dilated left atrium.

The patient's clinical status stabilized markedly over time in terms of chest pain, palpitation, oxygenation, and signs of both HF and TS. Patient's BP improved to 130/80; heart rate, and RR improved to between 70 and 80 beats/min, and <20 times/min, respectively. Oxygen saturation in room air improved to more than 96%. Bisoprolol was started and titrated up gradually which helped to control the patient's sympathetic activity, and IV furosemide was changed to oral 40 mg once daily. Upon discharge, ECG exhibited AF with controlled ventricular response and T wave inversion in anterior leads [Figure 2].
Figure 2: ECG on discharge revealed atrial fibrillation with controlled heart rate of 72 beats/min, resolution of ST segment elevation, and T-wave inversion from V3 to V6. ECG: Electrocardiogram

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Improvement in thyroxin (T4) level was observed to 67 pmol/L within 1 week; therefore, hydrocortisone was tapered down, cholestyramine and Lugol's solution stopped, and PTU switched to carbimazole 20 mg twice daily which continued as an outpatient. Discharge medications included DAPT and rivaroxaban for 1 month, then he was kept on clopidogrel and rivaroxaban for 1 year, rosuvastatin 20 mg, furosemide 40 mg once daily, bisoprolol 10 mg, spironolactone 25 mg, and valsartan 160 mg once daily. The patient understood the importance of medication compliance to improve his clinical status and prevent any possible complications.

The patient was clinically stable upon close endocrinology and cardiology follow-up. He is compliant with medications. ECG revealed AF with a controlled heart rate after 1 month. Repeated T4 level dropped to 23 pmol/L and EF improved to 49%, 6 weeks and 3 months after discharge, respectively.


   Discussion Top


Both hyperthyroidism and hypothyroidism might cause or worsen cardiovascular diseases, including arrhythmias, coronary artery disease, and HF which increases the risk of morbidity and mortality.[7] Dilated cardiomyopathy complicated with pulmonary edema could be the initial presentation of hyperthyroidism which can be reversed completely with appropriate treatment of excess thyroid hormone.[8] Increased risk of total and coronary heart disease mortality was concluded in a cohort study that was conducted to evaluate the effect of subclinical hyperthyroidism on cardiovascular diseases.[9]

In a large retrospective cohort study to assess the cardiovascular events in hospitalized patients with TS, 3895 out of 6380 patients (61%) had cardiovascular events, of which arrhythmia was the most common (around 3770 patients) than HF, and finally ischemic heart events which happened in around 150 patients (2% of the total study population). It concluded that patients with cardiovascular events have a higher risk of in-hospital mortality, longer hospital stay, and more cost. That was more obvious if ischemic events or HF developed.[10]

Acute thromboembolic events, like acute MI, can happen in patients with TS secondary to AF or an increase in activity of procoagulant factors, such as factor VIII, Von Willebrand factor, or tissue plasminogen activator inhibitor-1.[11]

Heavy iodine load, which can be given through iodinated contrast media used during a coronary angiogram, may induce or exacerbate TS complications in a patient with uncontrolled hyperthyroidism.[12]

Our patient was already diagnosed with acute anterior wall MI combined with a TS. Chest pain was progressing coinciding with persistent ST elevation on ECG and signs of HF. That's why high-risk CAG was commenced. We diluted iodinated contrast media with normal saline (1:1 ratio), aiming to decrease contrast exposure as possible, and used only 15 ml of contrast media to do the procedure through femoral access which was preferred in case of any emergency during the procedure that needs urgent intervention, like intra-aortic balloon pump insertion. Fortunately, there were no complications, the patient's clinical status improved significantly over time, and he was discharged in stable condition.


   Conclusion Top


Acute MI and TS are a dangerous and life-threatening combination that requires careful monitoring in the intensive care unit and close multidisciplinary team follow-up to achieve the best management based on the patient's clinical status and hemodynamic stability. Routine check-up of thyroid status might be considered in symptomatic patients who presented with acute cardiac events.

Ethical approval

Ethical approval to report this case was obtained from Hamad Medical Corporation ethics committee named ABHATH. MRC-04-21-801.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Executive group on behalf of the joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) task force for the universal definition of myocardial infarction. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol 2018;72:2231-64.  Back to cited text no. 1
    
2.
Bajaj A, Sethi A, Rathor P, Suppogu N, Sethi A. Acute complications of myocardial infarction in the current era: Diagnosis and management. J Investig Med 2015;63:844-55.  Back to cited text no. 2
    
3.
Carroll R, Matfin G. Endocrine and metabolic emergencies: Thyroid storm. Ther Adv Endocrinol Metab 2010;1:139-45.  Back to cited text no. 3
    
4.
Misra M, Thyroid storm. Practice Essentials, Pathophysiology, Etiology 2022. Available from https://emedicine.medscape.com/article/925147-overview. Retrieved October 18, 2022.  Back to cited text no. 4
    
5.
Akamizu T, Satoh T, Isozaki O, Suzuki A, Wakino S, Iburi T, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid 2012;22:661-79.  Back to cited text no. 5
    
6.
Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am 1993;22:263-77.  Back to cited text no. 6
    
7.
Cappola AR, Desai AS, Medici M, Cooper LS, Egan D, Sopko G, et al. Thyroid and Cardiovascular Disease Research Agenda for Enhancing Knowledge, Prevention, and Treatment. Circulation (2019).doi: 10.1161/CIRCULATIONAHA.118.036859.  Back to cited text no. 7
    
8.
Goland S, Shimoni S, Kracoff O. Dilated cardiomyopathy in thyrotoxicosis. Heart 1999;81:444-5.  Back to cited text no. 8
    
9.
Collet TH, Gussekloo J, Bauer DC, den Elzen WP, Cappola AR, Balmer P, et al. Subclinical hyperthyroidism and the risk of coronary heart disease and mortality. Arch Intern Med 2012;172:799-809.  Back to cited text no. 9
    
10.
Waqar Z, Avula S, Shah J, Ali SS. Cardiovascular events in patients with thyroid storm. J Endocr Soc 2021;5:bvab040.  Back to cited text no. 10
    
11.
Min T, Benjamin S, Cozma L. Thromboembolic complications of thyroid storm. Endocrinol Diabetes Metab Case Rep 2014;2014:130060.  Back to cited text no. 11
    
12.
Bjekic MJ, Zdravkovic M, Vukasin T, Ivanovic N, Crevar-Marinovic S, &amp Sasa H. Primary percutaneous coronary intervention induced thyroid storm and acute coronary syndrome: A case report. Endocrine Abstracts 2020. Available from https://www.endocrine-abstracts.org/ea/0070/ea0070aep936. Retrieved October 18, 2022.  Back to cited text no. 12
    


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  [Figure 1], [Figure 2]



 

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