Hyperthyroidism-induced myocardial infarction: a case of coronary spasm

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CASE REPORT

Hippokratia 2024, 28(3): 126-128

Xu ZW, Zhao XZ
Department of Cardiology, Affiliated Hospital of Hebei University, Baoding, China

Abstract

Background: In the etiology of coronary artery spasm (CAS), elevated thyroid hormone levels have been implicated, disrupting cardiac homeostasis and precipitating acute myocardial infarction (AMI). We report a case of AMI secondary to CAS in a male with hyperthyroidism without other classical cardiovascular risk factors.

Case Description: A 48-year-old male with a known history of hyperthyroidism but no other known classical cardiovascular risk factor urgently attended the hospital with suggestive symptoms of an AMI. The diagnostic process revealed CAS; he was managed successfully with intracoronary nitrates. We noted his elevated thyroid hormone levels, thus linking the hyperthyroid state to the CAS and subsequent AMI.

Conclusion: The reported case highlights the diagnostic complexities in patients suffering from hyperthyroidism and presenting with atypical AMI and emphasizes the importance of thyroid function evaluation in such cases. The management includes treatment of the AMI and long-term normalization of the thyroid function, and this case emphasizes the critical interaction between these conditions, advocating for a multidisciplinary approach to managing atypical coronary events in the context of underlying endocrine disorders. HIPPOKRATIA 2024, 28 (3):126-128.

Keywords: Coronary artery spasm, acute myocardial infarction, hyperthyroidism, interaction, endocrine system, cardiovascular system

Corresponding author: Xingzhou Zhao, Department of Cardiology, Affiliated Hospital of Hebei University, 212 Yuhua Road, 071000 Baoding, China. Tel.: +8613582216006, e-mail: 693809370@qq.com

Introduction

Hyperthyroidism is known to manifest various cardiovascular symptoms commonly, as the interaction between thyroid function and the cardiovascular system has long been recognized. The excess of thyroid hormones is anticipated to potentially provoke adverse cardiac effects, justifying the need to exclude thyrotoxicosis in patients presenting with new-onset atrial fibrillation and idiopathic congestive heart failure. Hyperthyroidism is also associated with other cardiovascular conditions, such as pulmonary hypertension, occurring in up to 35 % of hyperthyroid patients and frequently related to Graves’ disease1. Acute myocardial infarction (AMI) due to hyperthyroidism-induced coronary artery spasm (CAS) is an intriguing and rather rare clinical entity2, with the first reported case relating hyperthyroidism to CAS presented in the mid-20th century, and subsequent studies indicating a prevalence rate approximately 7.4 % for such spasms in patients with hyperthyroidism3,4. Interestingly, such cases often lack the classical risk factors associated with coronary artery disease, challenging the diagnostic process.

This report presents a notable case of AMI in a patient with hyperthyroidism, emphasizing the absence of classical cardiovascular risk factors and focusing on the diagnostic and management challenges associated with this rare clinical entity. While most clinical reports document non-obstructive spasms or spasms inferred through clinical suspicion, we notably confirmed the presence of reversible obstructive CAS through coronary angiography during the patient’s chest pain episode.

Case presentation

A 48-year-old male with a known history of hyperthyroidism urgently attended the hospital with intermittent chest pain over three days, unrelated to exertion. The pain, crushing in nature, located behind the sternum, was accompanied by sweating and lasted for several minutes. After a year of methimazole treatment, during which he felt well, he discontinued the medication two months before his presentation. He had no history of hypertension, coronary artery disease, diabetes, smoking, or alcohol use. Physical examination and electrocardiogram (ECG) were unremarkable (Figure 1A), with normal levels of cardiac troponin I and N-terminal pro–B-type natriuretic peptide (NT-proBNP). However, the echocardiogram indicated slight hypokinesia in the anterior wall of the left ventricle.

Figure 1: Electrocardiographic (ECG) images showing A) the outpatient ECG before admission displaying no significant ST-T changes, and B) subsequent ECG when the patient experienced a recurrence of the chest pain accompanied by sweating, revealing ST-segment elevation in leads V1-V6.

The patient was diagnosed with acute coronary syndrome and was treated with aspirin, clopidogrel, atorvastatin, and intravenous nitroglycerin. In the afternoon, he experienced a recurrence of the chest pain accompanied by sweating. A subsequent ECG revealed ST-segment elevation in leads V1-V6 (Figure 1B). Emergency angiography showed a 20 % stenosis in the left main coronary artery and complete occlusion in the anterior descending branch, with no significant issues in other branches. The administration of 200 μg of intracoronary nitroglycerin restored blood flow, confirming the diagnosis of CAS (Figure 2). Post-interventional, diltiazem and nicorandil were added for spasm treatment.

Figure 2: Emergency angiography images showing A) a complete occlusion of the mid-segment of the anterior descending branch (white arrow), and B) reperfusion (green arrow), and no significant narrowing of the mid-segment of the anterior descending branch after administering 200 μg of nitroglycerin intracoronary. Image C shows no significant narrowing observed in the right coronary artery.

On the second day of hospitalization, thyroid function tests displayed abnormal results: elevated free triiodothyronine (FT3) at 16.23 [normal range (NR): 3.1-6.8] pmol/L, elevated free thyroxine (FT4) at 68.74 (NR: 12-22) pmol/L, and suppressed thyroid-stimulating hormone (TSH) at 0.005 (NR: 0.27-4.2) μIU/mL, indicating hyperthyroidism. Consequently, treatment with Methimazole was reinstated. No further chest pain occurred during hospitalization, and a one-year follow-up showed well-controlled hyperthyroidism without chest pain recurrence.

Discussion

The pathophysiological mechanisms linking hyperthyroidism to CAS and consequent AMI are multifaceted and complex. Elevated levels of thyroid hormones, particularly T3 and T4, disrupt normal cardiovascular homeostasis in hyperthyroid patients. These hormones enhance cardiac muscle contractility and heart rate, raising myocardial oxygen demand. This heightened demand, coupled with the vasodilatory effect on peripheral vessels, can result in a mismatch between myocardial oxygen supply and demand, potentially precipitating ischemic events5.

Moreover, hyperthyroidism induces a hyperadrenergic state characterized by increased catecholamine sensitivity, which further contributes to CAS. Elevated thyroid hormone levels potentiate the vasomotor response to endogenous vasoconstrictors such as serotonin and norepinephrine, heightening the risk of CAS6. Additionally, thyroid hormones induce changes in vascular endothelial function, leading to endothelial dysfunction, a key factor in developing CAS7. This dysfunction is marked by an imbalance between endothelial-derived relaxing and contracting factors, increased oxidative stress, and an inflammatory milieu within the vascular wall8,9.

Thyrotoxicosis-related CAS presents clinically as non-exertional chest pain, increasing rapidly over time and ceasing abruptly with control of the thyrotoxicosis. Indicative of the diagnosis is finding a reversible coronary artery stenosis on coronary angiography. Nevertheless, previous reports are not supportive of using coronary angiography as the foremost diagnostic test in chest pain patients with underlying uncontrolled hyperthyroidism, as using iodine-containing agents has the potential to induce thyrotoxicosis10. However, in clinical practice, coronary angiography is often unavoidable to rule out coronary artery disease definitively or to exclude myocardial infarction in the context of acute coronary syndrome presentations.

Our case highlights the clinical challenge of diagnosing AMI secondary to CAS in hyperthyroidism, particularly in the absence of classical cardiovascular risk factors. The atypical presentation underscores the importance of considering hyperthyroidism as a potential etiological factor in patients with chest pain and the absence of significant atheromatosis. Previous reports of cases often involve non-obstructive spasms or suggest coronary artery spasms based on clinical suspicion without significant stenosis identified through imaging techniques such as coronary angiography or coronary computed tomography angiography. Notably, we confirmed the presence of reversible obstructive CAS through coronary angiography during the patient’s chest pain episode, which underscores the necessity of timely invasive examinations for such patients.

The management of CAS in the context of hyperthyroidism involves addressing the acute coronary event and the underlying thyroid disorder. Immediate AMI management includes using anti-anginal and anti-ischemic agents such as nitrates and calcium channel blockers. However, long-term management should focus on restoring and maintaining euthyroid status through antithyroid medications or other definitive therapies for hyperthyroidism. Furthermore, a multidisciplinary approach involving cardiologists, endocrinologists, and primary care physicians is crucial for the holistic management of these patients.

In conclusion, this case report sheds light on a rare clinical scenario and underscores the intricate interplay between endocrine and cardiovascular systems. It highlights the need for an integrated approach to diagnosing and managing atypical presentations of coronary artery disease, especially in the context of underlying endocrine disorders.

Conflict of interest

The authors declare no conflicts of interest.

Acknowledgement

Informed consent for this publication was obtained from the patient before submitting this case report. 

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