The Authors Reply We would like to thank Uehara et al. for their insightful indications regarding this case presentation (1).
The patient's hemoglobin level was 11 g/dL (normal: 11.6-14.8), and this level of anemia is unlikely to cause significant myocardial ischemia. The thyroid function was normal, with a free thyroxine 4 level of 1.5 ng/dL (normal: 0.9-1.7) and thyroid stimulating hormone level of 1.02 mIU/L (normal: 0.61-4.23). Echocardiography showed that both the interventricular septal and posterior wall thickness was 11 mm. Coronary angiography revealed 25% stenosis of the left main trunk, which under physiological conditions was unlikely to induce myocardial ischemia.
Of course, the concordance of other cardiovascular diseases cannot be completely excluded. A return to normal sinus rhythm, however, immediately normalized the ST-T segment changes, hemodynamics, symptoms, and cardiac enzymes. The patient's heart rate was relatively high at 123 beats/min. Parwani et al. showed that atrial fibrillation is often accompanied by high cardiac troponin I levels and that patients with elevated cardiac troponin I levels had higher heart rates during atrial fibrillation than those without elevation (2). Thus, the primary cause of the ST-T changes and elevated cardiac enzymes was presumed to be relative ischemia of the myocardium due to tachycardic atrial fibrillation.
It is also possible that the persistence of myocardial ischemia was one cause of the elevated myocardial enzyme levels, and indeed, the duration of atrial fibrillation was relatively long at approximately four hours. In addition, the patient's HbA1c value was 6.3%, but she had been diagnosed with diabetes mellitus at another hospital. Several factors, such as diabetes mellitus, can cause microvascular dysfunction in coronary arteries, and this may have played a role in this incident (3).
The authors state that they have no Conflict of Interest (COI).
References
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