"Severe coronary artery blockages that vanished with a simple nitrate injection revealed a dangerous mimic: artery spasm triggered by excess thyroid hormone from medication, underscoring the critical need for precise hormone level monitoring."
A routine diagnostic workup for chest pain took a surprising turn for a 61-year-old woman, whose diagnostic tests initially indicated critical blockages in the very arteries supplying her heart muscle. However, a crucial intervention—the injection of a nitrate medication—swiftly dissolved these apparent obstructions, revealing a far less common but equally dangerous condition: severe coronary artery spasm. This case, reported by cardiologists at Gyeongsang National University hospitals in South Korea, highlights the potential for iatrogenic thyrotoxicosis, or thyroid hormone excess caused by medical treatment, to precipitate life-threatening cardiac events that can be easily mistaken for obstructive coronary artery disease. The findings, published in Frontiers in Cardiovascular Medicine, emphasize the vital importance of recognizing nitrate responsiveness as a diagnostic tool and carefully selecting cardiovascular medications to avoid potentially unnecessary and invasive procedures like stenting or bypass surgery.
The patient’s ordeal began with three days of chest pain that occurred specifically during physical exertion. While her resting electrocardiogram (ECG) appeared normal, the subsequent treadmill stress test elicited significant discomfort. Crucially, her ECG during the test displayed ST-segment elevation in lead aVR and the anterior leads, coupled with ST depression in the inferior leads. This specific pattern on an ECG is a significant red flag, often raising immediate concern for compromised blood flow to the left main coronary artery, the primary vessel responsible for supplying a substantial portion of the heart muscle. Concurrently, blood tests revealed an elevated level of troponin, a biomarker indicative of heart muscle damage, further intensifying the urgency of the situation.
The diagnostic pathway then led to coronary angiography, a procedure that visualizes the heart’s arteries. The angiogram presented a grim picture, showing severe narrowing at the ostia, the openings of both the right coronary artery and the left main artery. Such simultaneous severe narrowing at the origin of these major vessels would typically suggest advanced, critical atherosclerotic disease, necessitating immediate intervention.
However, before proceeding with potentially invasive treatments, the cardiology team administered a diagnostic test designed to differentiate between fixed plaque buildup and dynamic artery narrowing. They injected a small dose of nitrate (200 micrograms) directly into the right coronary artery and subsequently into the left main artery. The response was dramatic and immediate. Within seconds, both of the apparent severe narrowings resolved completely, and normal blood flow was restored. This unequivocal demonstration of nitrate responsiveness confirmed that the issue was not static plaque obstruction but rather severe, dynamic spasm of the coronary arteries at their ostia. The authors of the report noted the particularly perilous nature of bilateral coronary ostial spasm, as it can lead to global subendocardial ischemia, a condition where the inner layer of the heart muscle is deprived of adequate blood supply.
The subsequent investigation delved into the underlying cause of this severe vasospasm. The patient revealed a significant medical history: her thyroid had been removed 18 years prior due to thyroid cancer, and she was consequently taking a daily dose of 75 micrograms of levothyroxine, a synthetic thyroid hormone. Thyroid hormone replacement therapy is common, but meticulous monitoring is essential to ensure the correct dosage. In this patient’s case, her thyroid-stimulating hormone (TSH) level was profoundly suppressed at 0.07 mIU/L (normal range typically 0.4-4.0 mIU/L), indicating that her pituitary gland was sensing an overabundance of thyroid hormone and significantly reducing its own signal to the thyroid. Further blood tests confirmed this suspicion: her free thyroxine (free T4) level was nearly double the upper limit of the normal range, and her free triiodothyronine (free T3) level was almost triple the upper limit. While tests for antibodies associated with Graves’ disease, an autoimmune cause of hyperthyroidism, were negative, the clinical picture pointed clearly to iatrogenic thyrotoxicosis – an excess of thyroid hormone resulting from medical treatment.
The researchers explained that this excess thyroid hormone can make the smooth muscle of blood vessels hyper-responsive to endogenous stress hormones. This heightened sensitivity can precipitate severe, bilateral coronary ostial spasm, effectively mimicking the appearance of significant obstructive coronary artery disease on diagnostic imaging.
To address the root cause, the patient’s levothyroxine dosage was reduced. At a three-month follow-up, her TSH levels had returned to the normal range, and importantly, she reported no further episodes of chest pain, no recurrent ischemic ECG changes, and no further hospital visits for cardiac symptoms. This outcome underscored the direct link between her overtreatment with levothyroxine and her cardiac event.
Adding another layer to this complex case was the recent initiation of carvedilol, a non-selective beta-blocker, about a month prior to her cardiac symptoms. Carvedilol was prescribed to manage palpitations, a common symptom of thyroid imbalance. While beta-blockers are foundational in the management of many cardiovascular conditions, their use can be problematic in the context of coronary artery spasm. The authors explained that non-selective beta-blockade can diminish beta-2 mediated vasodilation, a mechanism that helps arteries relax and widen. This reduction in vasodilatory tone can lead to a relative dominance of alpha-adrenergic signaling, which promotes vasoconstriction (artery tightening). In simpler terms, by blocking certain signals that would normally help arteries relax, the medication may inadvertently allow the signals that tighten arteries to become unopposed, potentially exacerbating coronary spasm. This concern is echoed by clinical guidelines, such as those from the National Library of Medicine’s StatPearls, which advise against non-selective beta-blockers in cases of vasospastic angina and recommend calcium channel blockers as a first-line treatment.
While the authors interpret the carvedilol as potentially exacerbating the spasm, they acknowledge that as a single case report, it establishes an association rather than definitive cause and effect. Nevertheless, the clinical decision was made to discontinue the carvedilol and initiate a calcium channel blocker, a class of drugs known to effectively relax arterial smooth muscle and are considered a primary treatment for coronary vasospasm. This medication-based management, avoiding stenting or surgery, proved successful.
Thyroid-related coronary spasm, though uncommon, is a recognized phenomenon. A 2025 systematic review published in Biomedicines identified 35 cases and studies of acute coronary syndromes linked to thyrotoxicosis between 2007 and 2025. In approximately half of these reported instances, angiograms revealed either normal coronary arteries or diffuse spasm. Graves’ disease was the most frequent underlying cause, with only a small number of cases attributed to drug-induced hyperthyroidism, making this patient’s medication-related excess somewhat atypical. Furthermore, women constituted 57% of the patients in the review, with an average age of around 40, positioning this 61-year-old patient as an older demographic for this specific presentation.
The issue of overtreatment with thyroid hormone medication is more prevalent than often realized. The National Institute of Diabetes and Digestive and Kidney Diseases estimates that about 1 in 100 Americans aged 12 and older have hyperthyroidism. They also note that some individuals taking thyroid hormone for hypothyroidism may inadvertently receive a dose that is too high. A study conducted in Germany and published in the European Thyroid Journal in May indicated that approximately one-third of individuals taking thyroid hormone exhibited low TSH levels, a finding suggestive of either overtreatment or a questionable indication for the medication.
It is crucial to emphasize that millions of individuals take levothyroxine safely and effectively. This case does not warrant self-adjustment of medication doses. Instead, it powerfully illustrates the indispensable role of regular thyroid function blood tests in ensuring appropriate dosing and highlights the importance of prompt medical evaluation for new or worsening chest pain or palpitations, particularly in individuals on thyroid hormone replacement therapy. Such symptoms should always prompt a comprehensive review of thyroid hormone levels.
Key Questions Answered
What happened to the woman?
Initially, diagnostic tests indicated critical blockages at the openings of both major coronary arteries. However, upon injecting nitrate, these apparent blockages dissolved entirely, revealing severe artery spasm as the underlying cause.
What caused the spasm?
Her doctors attributed the spasm to excess thyroid hormone stemming from her levothyroxine dosage. The recent addition of a non-selective beta-blocker may have also contributed to worsening the spasm.
Why does nitrate testing matter?
Nitrates have the effect of relaxing arterial smooth muscle. If a severe narrowing observed on an angiogram resolves after nitrate administration, it strongly suggests vasospasm rather than fixed plaque obstruction, potentially sparing patients from unnecessary interventions like stents or bypass surgery.
How was she treated?
Her levothyroxine dose was reduced, the beta-blocker was discontinued, and a calcium channel blocker was initiated. Three months later, she was symptom-free.
Should people on thyroid medication worry?
Most individuals taking thyroid medication do so without issue. Regular blood tests are essential for maintaining the correct dosage, and patients should never alter their medication regimen without consulting their doctor. Any new onset of chest pain requires immediate medical attention.
