ArticleCureus2026
Premature Myocardial Infarction in Severe Hypothyroidism: A Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
Hypothyroidism exerts significant effects on the cardiovascular system through alterations in lipid metabolism, endothelial function, vascular resistance, and myocardial performance. Both overt and subclinical hypothyroidism have been associated with an increased risk of atherosclerosis and premature coronary artery disease, particularly in women and in individuals with markedly elevated thyroid‑stimulating hormone (TSH) levels. We report the case of a 60‑year‑old woman with long‑standing hypothyroidism, noncompliant with levothyroxine therapy for about six months before presentation. The patient arrived at the emergency department with acute substernal chest pain and was found to have a rapidly rising high‑sensitivity troponin level, which peaked at 125,000, with no ST elevation on electrocardiogram (ECG), consistent with non-ST‑elevation myocardial infarction (NSTEMI). Coronary angiography revealed a critical proximal left anterior descending artery occlusion requiring percutaneous coronary intervention. Echocardiography demonstrated reduced left ventricular ejection fraction (15-20%) and elevated left ventricular end‑diastolic pressure (>16 mmHg), indicating combined systolic and diastolic dysfunction. Thyroid function testing confirmed profound hypothyroidism (TSH >500). This case illustrates the multifactorial cardiovascular consequences of untreated hypothyroidism and highlights its potential association in precipitating premature ischemic events, even in the absence of traditional cardiovascular risk factors. The patient's presentation aligns with established pathophysiologic mechanisms linking thyroid hormone deficiency to endothelial dysfunction, dyslipidemia, increased systemic vascular resistance, and myocardial impairment. This report emphasizes the importance of recognizing hypothyroidism as a modifiable contributor to cardiovascular disease. Routine assessment of thyroid function should be considered in patients presenting with acute coronary syndromes, particularly when traditional risk factors are absent or insufficient to explain the severity of the disease. Early diagnosis and adherence to thyroid hormone replacement therapy may reduce cardiovascular risk and prevent serious complications.
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